Dr Athakorn Kirakul MD30th May 2012
Chronic kidney disease Acute kidney injury Contrast induced
nephropathy Nephrogenic systemic
fibrosis Cardiorenal syndrome Hepatorenal syndrome Intra-abdominal
hypertension amp Abdominal compartment syndrome
Topics
ไต 1 ขางมประมาณ 1-13 ลาน nephron
Normal GFR in youngmale is 120 mlminOR 180 Lday
Normal RBF1000 mlmin
Normal RPF625 mlmin
Normal urine output 1 mlkghr
The Kidney
Chronic kidney disease Acute kidney injury Contrast induced
nephropathy Nephrogenic systemic
fibrosis Cardiorenal syndrome Hepatorenal syndrome Intra-abdominal
hypertension amp Abdominal compartment syndrome
Topics
ไต 1 ขางมประมาณ 1-13 ลาน nephron
Normal GFR in youngmale is 120 mlminOR 180 Lday
Normal RBF1000 mlmin
Normal RPF625 mlmin
Normal urine output 1 mlkghr
The Kidney
ไต 1 ขางมประมาณ 1-13 ลาน nephron
Normal GFR in youngmale is 120 mlminOR 180 Lday
Normal RBF1000 mlmin
Normal RPF625 mlmin
Normal urine output 1 mlkghr
The Kidney
The Kidney
คณ คะhellipคณคอจดออนท13สดของทม เชญคะ
1 Kidney damage for ge3 months as defined by structural or functional abnormalities of the kidney with or without decreased GFR manifest by either
Pathological abnormalities or Markers of kidney damage including
abnormalities in the composition of the blood or urine or abnormalities in imaging tests
2 GFR lt60 mlmin173 m2 for ge3 months with or without kidney damage
Chronic Kidney Disease (CKD)
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Markers of Kidney Damage
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential RF for Susceptibility to and
Initiation of CKDClinical Factors Socio-demographic Factors
DiabetesHypertension
Autoimmune diseasesSystemic infections
Urinary tract infectionsUrinary stones
Lower urinary tract obstructionNeoplasm
Family history of chronic kidney disease
Recovery from acute kidney failureReduction in kidney massExposure to certain drugs
Low birth weight
Older age
US ethnic minority status ieAfrican American American
Indian Hispanic Asian or Pacific Islander
Exposure to certain chemical and environmental conditions
Low incomeeducation
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Staging
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Stage 5
CKD Stage 4
CKD Stage 3
CKD Stage 2
CKD Stage 1
Stage
Description GFR(mlmin173 m2)
1 Kidney damage with normal or uarrGFR
ge 90
2 Kidney damage with mild darrGFR
60-89
3 Moderate darrGFR 30-59
4 Severe darrGFR 15-29
5 Kidney failure or ESRD lt 15 or RRT
Measurement of GFR with exogenous filtration markers Inulin 125I Iothalamate 51Cr-
EDTA 125mTc-DTPA Iohexol 99mTc-DTPA 99mTc-MAG3
Estimation of GFR with endogenous filtration markers Creatinine Cystatin C
Equations used to estimate GFR Cockroft-Gault formula MDRD formula CKD-EPI equation
Assessment of Kidney Function
N Engl J Med 2006354(23)2473-2483
Imaging 2005171-18
Relationship Between Serum Cr and GFR
Nephrology Rounds 20064(2)
Factors That Affect Serum Creatinine Level
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
1 Kidney damage for ge3 months as defined by structural or functional abnormalities of the kidney with or without decreased GFR manifest by either
Pathological abnormalities or Markers of kidney damage including
abnormalities in the composition of the blood or urine or abnormalities in imaging tests
2 GFR lt60 mlmin173 m2 for ge3 months with or without kidney damage
Chronic Kidney Disease (CKD)
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Markers of Kidney Damage
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential RF for Susceptibility to and
Initiation of CKDClinical Factors Socio-demographic Factors
DiabetesHypertension
Autoimmune diseasesSystemic infections
Urinary tract infectionsUrinary stones
Lower urinary tract obstructionNeoplasm
Family history of chronic kidney disease
Recovery from acute kidney failureReduction in kidney massExposure to certain drugs
Low birth weight
Older age
US ethnic minority status ieAfrican American American
Indian Hispanic Asian or Pacific Islander
Exposure to certain chemical and environmental conditions
Low incomeeducation
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Staging
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Stage 5
CKD Stage 4
CKD Stage 3
CKD Stage 2
CKD Stage 1
Stage
Description GFR(mlmin173 m2)
1 Kidney damage with normal or uarrGFR
ge 90
2 Kidney damage with mild darrGFR
60-89
3 Moderate darrGFR 30-59
4 Severe darrGFR 15-29
5 Kidney failure or ESRD lt 15 or RRT
Measurement of GFR with exogenous filtration markers Inulin 125I Iothalamate 51Cr-
EDTA 125mTc-DTPA Iohexol 99mTc-DTPA 99mTc-MAG3
Estimation of GFR with endogenous filtration markers Creatinine Cystatin C
Equations used to estimate GFR Cockroft-Gault formula MDRD formula CKD-EPI equation
Assessment of Kidney Function
N Engl J Med 2006354(23)2473-2483
Imaging 2005171-18
Relationship Between Serum Cr and GFR
Nephrology Rounds 20064(2)
Factors That Affect Serum Creatinine Level
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Markers of Kidney Damage
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential RF for Susceptibility to and
Initiation of CKDClinical Factors Socio-demographic Factors
DiabetesHypertension
Autoimmune diseasesSystemic infections
Urinary tract infectionsUrinary stones
Lower urinary tract obstructionNeoplasm
Family history of chronic kidney disease
Recovery from acute kidney failureReduction in kidney massExposure to certain drugs
Low birth weight
Older age
US ethnic minority status ieAfrican American American
Indian Hispanic Asian or Pacific Islander
Exposure to certain chemical and environmental conditions
Low incomeeducation
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Staging
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Stage 5
CKD Stage 4
CKD Stage 3
CKD Stage 2
CKD Stage 1
Stage
Description GFR(mlmin173 m2)
1 Kidney damage with normal or uarrGFR
ge 90
2 Kidney damage with mild darrGFR
60-89
3 Moderate darrGFR 30-59
4 Severe darrGFR 15-29
5 Kidney failure or ESRD lt 15 or RRT
Measurement of GFR with exogenous filtration markers Inulin 125I Iothalamate 51Cr-
EDTA 125mTc-DTPA Iohexol 99mTc-DTPA 99mTc-MAG3
Estimation of GFR with endogenous filtration markers Creatinine Cystatin C
Equations used to estimate GFR Cockroft-Gault formula MDRD formula CKD-EPI equation
Assessment of Kidney Function
N Engl J Med 2006354(23)2473-2483
Imaging 2005171-18
Relationship Between Serum Cr and GFR
Nephrology Rounds 20064(2)
Factors That Affect Serum Creatinine Level
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Potential RF for Susceptibility to and
Initiation of CKDClinical Factors Socio-demographic Factors
DiabetesHypertension
Autoimmune diseasesSystemic infections
Urinary tract infectionsUrinary stones
Lower urinary tract obstructionNeoplasm
Family history of chronic kidney disease
Recovery from acute kidney failureReduction in kidney massExposure to certain drugs
Low birth weight
Older age
US ethnic minority status ieAfrican American American
Indian Hispanic Asian or Pacific Islander
Exposure to certain chemical and environmental conditions
Low incomeeducation
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Staging
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Stage 5
CKD Stage 4
CKD Stage 3
CKD Stage 2
CKD Stage 1
Stage
Description GFR(mlmin173 m2)
1 Kidney damage with normal or uarrGFR
ge 90
2 Kidney damage with mild darrGFR
60-89
3 Moderate darrGFR 30-59
4 Severe darrGFR 15-29
5 Kidney failure or ESRD lt 15 or RRT
Measurement of GFR with exogenous filtration markers Inulin 125I Iothalamate 51Cr-
EDTA 125mTc-DTPA Iohexol 99mTc-DTPA 99mTc-MAG3
Estimation of GFR with endogenous filtration markers Creatinine Cystatin C
Equations used to estimate GFR Cockroft-Gault formula MDRD formula CKD-EPI equation
Assessment of Kidney Function
N Engl J Med 2006354(23)2473-2483
Imaging 2005171-18
Relationship Between Serum Cr and GFR
Nephrology Rounds 20064(2)
Factors That Affect Serum Creatinine Level
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
CKD Staging
KDOQI Guideline 2002 CKD AJKD 200239S1-226
CKD Stage 5
CKD Stage 4
CKD Stage 3
CKD Stage 2
CKD Stage 1
Stage
Description GFR(mlmin173 m2)
1 Kidney damage with normal or uarrGFR
ge 90
2 Kidney damage with mild darrGFR
60-89
3 Moderate darrGFR 30-59
4 Severe darrGFR 15-29
5 Kidney failure or ESRD lt 15 or RRT
Measurement of GFR with exogenous filtration markers Inulin 125I Iothalamate 51Cr-
EDTA 125mTc-DTPA Iohexol 99mTc-DTPA 99mTc-MAG3
Estimation of GFR with endogenous filtration markers Creatinine Cystatin C
Equations used to estimate GFR Cockroft-Gault formula MDRD formula CKD-EPI equation
Assessment of Kidney Function
N Engl J Med 2006354(23)2473-2483
Imaging 2005171-18
Relationship Between Serum Cr and GFR
Nephrology Rounds 20064(2)
Factors That Affect Serum Creatinine Level
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Measurement of GFR with exogenous filtration markers Inulin 125I Iothalamate 51Cr-
EDTA 125mTc-DTPA Iohexol 99mTc-DTPA 99mTc-MAG3
Estimation of GFR with endogenous filtration markers Creatinine Cystatin C
Equations used to estimate GFR Cockroft-Gault formula MDRD formula CKD-EPI equation
Assessment of Kidney Function
N Engl J Med 2006354(23)2473-2483
Imaging 2005171-18
Relationship Between Serum Cr and GFR
Nephrology Rounds 20064(2)
Factors That Affect Serum Creatinine Level
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Imaging 2005171-18
Relationship Between Serum Cr and GFR
Nephrology Rounds 20064(2)
Factors That Affect Serum Creatinine Level
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Nephrology Rounds 20064(2)
Factors That Affect Serum Creatinine Level
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Formula for eGFR Calculation
CKD-EPI Levey 2009 (N = 8254 3896 in validation set)
Ann Int Med 2009150(9)604-613httpwwwkidneyorgprofessionalskdoqigfr_calculatorcfm
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
CKD-EPI equation Most circumstances
Cockroft-Gault Elderly
24 hour urine Creatinine clearance Pregnancy Extreme age amp size Amputees Skeletal muscle disorders paraplegia
quadriplegia Vegetarian diet Severe malnutrition or obesity
So What to Use
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Proteinuria amp Albuminuria
แนวทางเวชปฏบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Equivalent Ranges for Urinary Protein Loss
Adapted from ABC of Kidney Disease 1st edition
Urine Dipstick
Albumin Excretion
Rate(mg24 hr)
Urine ProteinCr
Ratio(mgmg)
Urine Protein(mg24 hr)
Normal Neg 10-30 lt150 lt150
Microalbuminuria
Neg 30-300 lt150 lt150
Macroalbuminuria
+ gt300 150-299 150-299
Proteinuria 2+ 3+ NA 300-3500 300-3500
Nephrotic 4+ NA gt3500 gt3500
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ตวอยางการรายงานผล spot urine protein
รายงานตวนพอ
รายงานตวนพอ
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ตวอยางการรายงานผล 24 hour urine protein
รายงานแคนพอ
รายงานตวนดวย
Creatinine values lt 1 g24 hours for men or lt 09 g24 hours for women nearly always mean that the urine collection was incomplete
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
กอนนบเวลาใหถายปสสาวะท$งไปใหหมด และเร13มนบเวลา (จดเวลาท13เร13มเกบ) หลงจากน$นใหเกบปสสาวะท13ถายท$งหมดใสภาชนะท13เตรยมใหจนครบ 24 ช13วโมง
เชน เร13มเกบ 0800 น เวลาส$นสดคอ 0800 น วนร งข1$น ระหวางเกบใหเกบภาชนะตามใบคาแนะนาท13ระบไว เม13อครบเวลา 24 ช13วโมง ใหเกบปสสาวะท13ถายคร$งสดทายลงในภาชนะ รบนาสงหองปฏบตการทนท เจาะเลอดตรวจหาคาครอะตนนในเลอดดวย ยกเวน กรณมผลการตรวจคร$ง
สดทายไมเกน 2 วน ผ2ท13มรอบเดอน ใหเล13อนการตรวจปสสาวะ จนกวารอบเดอนจะหมด กรณท13ตองการถายอจจาระ ควรถายปสสาวะเกบกอน เพ13อป3องกนการปนเป4$ อน สารรกษาสภาพปสสาวะเป6นเคมอนตราย หามสมผส หามส2ดดม หามกลนกน
คาแนะนาการเกบปสสาวะ 24 ช13วโมง
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ตวอยางการรายงานผล 24 hour urine CCr
รายงานแคนพอ
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
KDOQI Guideline 2002 CKD AJKD 200239S1-226
Action Plan
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Action Plan
Stage
Description GFR(mlmin173 m2)
Action
1 Kidney damage with normal or uarrGFR
ge 90 Specific Rx based on DxRx comorbid conditionSlowing progressionRx of CVD and CVD RF
2 Kidney damage with mild darrGFR
60-89 Estimating progression
3 Moderate darrGFR 30-59 Prevention and Rx of complication
4 Severe darrGFR 15-29 Preparation of RRTReferral to nephrologist
5 Kidney failure or ESRD
lt 15 or RRT
Renal replacement RxKDOQI Guideline 2002 CKD AJKD 200239S1-226
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Cardiovascular Disease Mortality in General Population (GP) versus ESRD Patients
Am J Kidney Dis 199832S112-S119
Annual mortality from CVD is increased 5 - 500 times with kidney failure
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Control BP BP lt13080 (lt12575 mmHg if proteinuria gt1 g24 hr)
Control BS HbA1c lt7 (65) FBS 70-130 mgdl Post pandrial BS lt180 mgdl
Reduce lipid level LDL lt100 (70 mgdl) TG lt150 mgdl HDL gt40 (M) or gt50 (F) mgdl
Low salt diet Na lt24 gday (100 mmolday) Una
Moderate protein restriction 06 (CKD stage 4-5) - 08 (CKD stage 1-3) gkgday High biological value gt60
Slow Progression of CKD (1)
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Reduce proteinuria ACEI ARB Atorvastatin Correct metabolic acidosis HCO3 ge22 mEqL
Low to Moderate aerobic exercise Control BW BMI 185-249 kgm2
Stop smoking Avoid nephrotoxic agents eg CM NSAIDs COX-II
inh AG Herb Avoid pregnancy
Slow Progression of CKD (2)
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Anemia Hyperkalemia Metabolic acidosis 2 Hyperparathyroidism Hyperphosphatemia Hypocalcemia
Complications of CKD Hypertension Malnutrition Neurological changes Uremic bleeding Functioning and well being
Ca corrected = Ca measured + 08 (4 ndash Alb)
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Pathogenesis of Anemia in CKD patients
Semin Nephrol 200626261-8
Anemia
Erythropoietin deficiency
Iron deficiency
Chronic inflammation
Hemolysis
Folic acid B12 deficiency
Hyperparathyroidism with BM fibrosis
Carnitine deficiency
Aluminium intoxication
Drugs
Uremic suppression of erythropoiesisรายงานแคนพอ
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
IV Iron amp Erythropoietin
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Nat Clin Pract Nephrol 20073(3)138-153
DDAVP (Minirin)03 - 04 μgkg IV or SC as a single injection
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
อาหาร บาบดในผ2ป7วยโรคไตเร$อรงระยะกอนลางไตhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=186
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการลางไตทางชองทองhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=188
คาแนะนาเก13ยวกบ อาหารสาหรบผ2ป7วยไตวายเร$อรงท13ร กษาดวยวธการฟอกเลอดดวยเคร13องไต เทยมhttpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=187
อาหารสาหรบผ2ป7วยโรคไต
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
แนวทางเวชปฎบตสาหรบโรคไตเร$อรงกอนการบาบดทดแทนไต พศ 2552KDOQI Guideline 2004 HT AJKD 200443(5) Suppl 1S1-S290
ปรมาณโปแตสเซยมในผกและผลไม
CKD Stage 1-2K lt4 gday
CKD Stage 3-4K 2-4 gday
If K gt55 mEqLจากดผลไมทกชนด
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
JAMA 2011305(15)doi101001jama2011451
A Predictive Model for Progression of CKD to Kidney Failure
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
มคา eGFR นอยกวา 10 มลนาทตอ 173 ตารางเมตร หรออาจพจารณาเม13อ eGFR 10-15 มลนาทตอ 173 ตารางเมตรและมขอบงช$
มภาวะน$าเกนและหรอความดนส2งอยางรนแรงท13ไมตอบสนองตอยาขบปสสาวะหรอยาลดความดนขนาดส2ง
มภาวะโพแทสเซยมในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยา มภาวะเลอดเป6นกรดท13ไมตอบสนองตอการรกษาดวยดาง (ไบคารltบอเนต) มภาวะฟอสเฟตในเลอดส2งท13ไมตอบสนองตอการจากดอาหารและการใชยาจบฟอสเฟต มภาวะโลหตจางท13ไมตอบสนองตอการใชยาฮอรltโมนกระตนเมดเลอดแดง
(erythropoietin) และธาตเหลก สมรรถภาพรางกายหรอความสขสบายลดลงโดยไมมเหตอ13นท13ดกวาอธบายได มน$าหนกตวลดลงหรอมภาวะทพโภชนาการเกดข1$นใหม โดยเฉพาะถามอาการคล13นไส
อาเจยน หรอหลกฐานของกระเพาะลาไสอกเสบ มความผดปรกตของระบบประสาท เชน ปลายประสาทอกเสบ สบสน ซ1ม ชก มอาการทาง
จต มภาวะเย13อหมปอดอกเสบหรอเย13อหมหวใจอกเสบโดยไมมเหตอ13นท13ดกวาอธบายได มภาวะเลอดออกผดปรกตซ113งตรวจพบโดยม bleeding time ยาวนานกวาปรกต
เม13อไหรท13สมควรเร13มการฟอกไต
Handbook of Dialysis 4th editionขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
สทธบาบดทดแทนไต(Update
กพ2553)
httpwwwnephrothaiorgnewsnewsasptype=KNOWLEDGEampnews_id=194
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ใหผปวยเป นผตดสนใจ
การบาบดทดแทนไต
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Principle of Hemodialysis
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
AV Fistula (AVF) AV Graft (AVG) Permanent Catheter
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ผ2ป7วยโรคไตเร$อรงระยะท13 4 หรอ 5 ไมควรใชเสนเลอดดาบรเวณแขนท13กาหนดไวสาหรบทาเสนฟอกเลอดถาวรในการเจาะเลอด ใหสารน$าฉดยาทางเสนเลอด หรอใสสายสวนหลอดเลอดใดๆ
ผ2ป7วยท13ใช AVF ควรใชเวลาเตรยมประมาณ 4-6 เดอนกอนเร13มฟอกเลอดดวยเคร13องไตเทยม สวนในกรณท13เป6น AVG ควรใชเวลาเตรยมประมาณ 3-6 สปดาหltกอนเร13มฟอกเลอดดวยเคร13องไตเทยม ยกเวน graft บางชนด อาจเร13มใชไดทนทหลงผาตด
เสนฟอกเลอดท$งชนด AVF และ AVG ตาแหนงท13ควรเลอกใชจะไลจากปลายแขนข1$นมาตนแขน และสาหรบ graft ท13แขนสวนลางน$นแบบวงดกวาแบบตรง
เสน AVF ควรแนะนาการบรหารโดยการบบกามอหลงผาตดจนกวาเสนพรอมและสมบ2รณltสาหรบการลงเขม
ในกรณท13ใชสายสวนหลอดเลอดสาหรบการฟอกเลอด ควรเลอก internal jugular vein เป6นตาแหนงแรกและควรมการประเมนสายสวนหลอดเลอดกอนการใชงาน
ขอแนะนาเวชปฏบตการลางไตโดยการฟอกเลอดดวยเคร13องไตเทยม พศ 2555
การเตรยมหลอดเลอดสาหรบการฟอกเลอด
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Principle of Peritoneal Dialysis
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
httpthaipublicaorg201203statistics-patient-died-ambulatory-peritoneal-dialysis
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
httpthaipublicaorg201203nhso-campaign-peritoneal-dialysis
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Kidney Transplantation
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
N Engl J Med 19993411725-1730
Mortality Rate of Patients on Dialysis on Waiting List and Recipients of First CDKT
23275 1st CDKT recipients vs46164 pts on waiting list
26x17x
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hours
GFR lt15mlmin173m2 BSA or requirement for RRT
Acute Kidney Injury (AKI)
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138Curr Opin Crit Care 20028509ndash514
Kidney Failure
There are at least 35 definitions of acute renal failure (ARF)
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
RIFLE vs AKIN
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Causes of AKI Exposures and Susceptibilities for non-specific
AKIExposures Susceptibilities
SepsisCritical illness
Circulatory shockBurns
TraumaCardiac surgery (esp with CPB)
Major non-cardiac surgeryNephrotoxic drugs
Radiocontrast agentsPoisonous plants and animals
Dehydration or volume depletionAdvanced ageFemale gender
Black raceCKD
Chronic diseases (Heart Lung Liver)DM
CancerAnemia
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Test patients at increased risk for AKI with measurements of SCr and urine output to detect AKI
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
AKI Staging
Stage
Serum Creatinine Urine Output
1 15-19x Baseline OR
ge03 mgdl increase
lt05 mlkghr for 6-12 hr
2 20-29x Baseline lt05 mlkghr for ge12 hr
3 ge30x Baseline OR
Increase in SCr to ge4 mgdl OR
Initiation of RRT
lt03 mlkghr for ge24 hr
ORAnuria for ge12
hr
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Patients should be staged according to the criteria that give them the highest stage
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
A 29 year old Japanese model with a baseline creatinine of 14 receives a contrasted CT scan to determine the source of bleeding following a hysterectomy Her creatinine 2 days later is 22 Her urine output over the last 8 hours is 640 mL
Quiz
A 24 year old wakes up in a bathtub of ice water Scrawled on the bathroom mirror in blood is a message that both of her kidneys were removed and sold On exam she has bilateral nephrectomy scars and an ultrasound confirms absence of both kidneys She has been anuric since a foley was placed 14 hours ago her creatinine is 18
A 62 year old star has arthritis and HT She presents to her primary care doctor with symptoms of fatigue since starting ramipril for her blood pressure Her medications include ibuprofen 800 mg tid HCTZ 25 mg qd simvastatin 40 mg qd and ramipril 10 mg qd Her labs show a Cr of 32 (baseline 12) K of 66 She urinated a ldquonormal amountrdquo prior to coming to the office
A 57 year old british comedian is admitted for decompensated heart failure His baseline creatinine is 14 On admission his creatinine is 22 He is given furosemide and responds well His oxygen requirement decreases most of his edema improves but his creatinine has gone up to 32 His urine output in the last 8 hours is 460 mL
AKIN Stage 1
AKIN Stage 3
AKIN Stage 2
AKIN Stage 2
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Evaluate patients with AKI promptly to determine the cause with special attention to reversible causes
Monitor patients with AKI with measurements of SCr and urine output to stage the severity
Manage patients with AKI according to the stage and cause Evaluate patients 3 months after AKI for resolution new
onset or worsening of pre-existing CKD
Evaluation and General Management of Patients with and at Risk for AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Action Plan
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Aetiology of AKI
Outpatient
Hospital
58
38
4
7211
17
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ABC of Kidney Disease 1st edition
Prerenal
Postrenal
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ABC of Kidney Disease 1st edition
Intrinsic Renal
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Is this AKI or CKD
Has obstruction been excluded
Is the patient euvolemic
Is there evidence of renalparenchymal diseases(other than ATN)
Has a major vascularocclusion occurred
Complete anuriaPalpable bladderUS KUB
Pulse postural BP Daily BW JVPCVPFluid balanceDisproportional BUNCr ratioUrine Na FENa FEureaFluid challenge
Hx and PE (Systemic features)Urine exam (dipstick sediments)
Atherosclerotic vascular diseaseKidney asymmetryLoin painMacroscopic hematuriaComplete anuria
Hx and PE (DM HT)Previous SCrSmall kidneys in US
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Evaluation of AKI according to the stage and cause
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Am Fam Physician 200061(7)2077-2088
Algorithm for Dx and Rx of AKI
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Causes of AKI and Diagnostic Tests
Selected causes of AKI requiring immediate diagnosis and specific therapies
Recommended Diagnostic Tests
Decreased kidney perfusion
Volume status and urinary diagnostic indices
Acute glomerulonephritis vasculitis interstitial nephritis thrombotic microangiopathy
Urine sediment examination serologic testing and hematologic testing
Urinary tract obstruction Kidney ultrasound
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
AKI a competency network Academy of Medical Royal College 2011
Chain of Respond
Recorder Recognizer PrimaryResponder
SecondaryResponder
TertiaryResponder
Communicaton amp Handover
Healthcareassistant
Trained staffnurse
DoctorAdvanced nurseCritical careoutreach nurse
Training gradedoctor in nonnephrologyspecialty
Nephrologyconsultant
A core component of the Chain of Response is the ability to recognise and respond to signs of deterioration in the patient and to escalate care to the next level if indicated
BPUAPhysiological observatonFluid balance
Risk of AKIUrea ElectrolytesUAPhysiological observatonFluid balanceUrethral cathMedicine manageAKI recovery
Risk of AKIVolume status assessmentUrea ElectrolytesUAFluid balanceAKI causesMedicine manageAKI complicationsAKI recovery
Risk of AKIMedicine manageInvestigationDiagnosis of AKIFluid balanceRenal referralCritical care referral
Risk of AKIUA UACR UPCRAKI causesMedicine manageKidney biopsyRRT
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Clinical Assessment of Volume Status
Postural vital signs Dry axillae Capillary refill time Moistness of mucous
membranes Skin turgor JVPCVP Changes in body weight Others ndash dryfurrowed
tongue sunken eyes
Urine output and fluid balance chart
Evidence of peripheral edema pleural effusions ascites or pulmonary oedema
Physiological response to a fluid challenge
Physiological response to passive leg raising
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Measurement requires a wait of two minutes before obtaining supine vital signs and one minute before obtaining erect vital signs
Postural pulse increment (HR gt30 beatsmin on standing)Sensitivity 22 (moderate) ndash 97 (severe) Specificity
98 Postural hypotension (BP ge20 mmHg on standing)
Sensitivity 9-27 (moderate) ndash (severe) Specificity Supine tachycardia (Pulse gt100 beatsmin)
Sensitivity 12 Specificity 96 Supine hypotension (SBP lt95 mmHg)
Sensitivity 50 (moderate) ndash 33 (severe) Specificity 97 Dry axilla
Sensitivity 50 Specificity 82 Capillary refill time
Sensitivity 6 Specificity 93
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Skin turgor No diagnostic value
Physiological Response to fluid challenge Changes in physiological parameters eg MAP HR
CVP after rapid administration of intravenous fluid over a short time
No data on the optimum technique or its diagnostic reliability
Physiological Response to Passive Leg raising Moving the patient from a semi-recumbent position
to a supine position with passive elevation of the legs to 45ordm above the horizontal
Maximal response is seen within 30-60s Descending aortic blood flow of ge10 or
echocardiographic subaortic flow of ge12 ---- fluid responsiveness
Utility of PLR outside the critical care environment is questionable
Clinical Assessment of Volume Status
AKI a competency network Academy of Medical Royal College 2011
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
JVP Indication of the pressure in the right atrium
NOT a direct measure of volume A measurement of gt3 cm from sternal angle (gt8 cm from
RA) is taken as evidence of high RA pressure in normal patients
Many conditions that can result in an elevated JVP eg RV failure TR or TS pericardial effusion or constrictive pericarditis SVC obstruction Volume overload
J Gen Intern Med 200217(11)852-6Chest 2008134(1)172-8
Am J Med198783(5)905-8
This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVPCVP to predict the hemodynamic response to a fluid challenge CVP should not be used to make clinical decisions regarding fluid management
Clinical assessment was only able to identify 47 of hypovolemic patients and 48 of normovolemic patients in the setting of hyponatremia whereas the spot urine Na clearly separated hypovolemic from normovolemic patients
RA distance to be 8 cm 97 cm and 98 cm at 30 45 and 60 degrees elevation respectively There is considerable inter-subject variability with dependent variables including age smoking status and AP chest diameter
Clinical Assessment of Volume Status
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
รายงานผลเป6น mmHg หรอ cmH2O (1 mmHg = 136 cmH2O)
วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด 4th ICS กบ mid axillary line ให IV fluid ไหลเขาไปในสาย extension ดานไมบรรทด โดยปAด
ดานผ2ป7วยไวกอน ควรให IV fluid อย2ในสาย extension ในระดบเกอบเตมสาย หรอมากกวาคาเดม (ประมาณ 5 cm) จากน$นหมนปAด three-way ดานไมบรรทด
นาไมบรรทดวางทาบท13ผ2ป7วย โดยใหตาแหนงของ zero หมน three-way เปAดเฉพาะดานผ2ป7วยกบไมบรรทด ปAดดาน IV การอานคา CVP ท13 work ด จะตอง fluctuate หรอมการเตนข1$น
ลงของระดบน$าในสายท13ไมบรรทดตามจงหวะการหายใจ วดตอนหายใจออกสด (End expiration) ใหปลดเคร13องชวยหายใจขณะอานคา ถาเป6นไปได กรณท13มการใส
PEEP จะทาใหคา CVP ส2งกวาคาจรงมากข1$น
การวด CVP
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Physical examination is a useful tool in assessing a patientrsquos volume status BUT individual clinical findings are often insensitive andor nonspecific
กระบampอสร ตกโกวควปาย (ส)สานกระบamp)หนกอนแรก - เกร$ยวกราดรนแรง ทาลายลางทกส13ง เม13อวยหนมฉกรรจlt ใชชงชยกบเหลาผ2กลาแควนฮอซวกหนกอนทampสอง - กระบ13ออนกหลาบหน2มวง ใชกอนอายสามสบ พล$งมอทารายผ2กลาฝ7ายธรรมะ ถอเป6นส13งอปมงคล โยนท$งลงส2กนหบเหว หนกอนทampสาม - กระบ13หนกไรคม ใชไดคลองแคลว ฝCมอการสรางไมประณต กอนอายส13สบใชพชตท$วแผนดนหนกอนส)ดทาย - หลงอายส13สบปC ไมย1ดตดกบวตถ แมแมกไมไผหนลวนถอเป6นกระบ13ได นบแตน$พากเพยรฝDกปรอ เร13มเขาส2หวงไรกระบ13เหนอกวามกระบ13
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ABC of Kidney Disease 1st edition
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
ค2มอการสงตรวจทางหองปฏบตการทางการแพทยlt ภาควชาพยาธวทยาคลนก
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
กรณทampสผดปรกตหร+อสงสยภาวะเฉพาะ เชน rhabdomyolysis
กรณทampสงสยมการตดเช+อกรณทampม AKI หร+อ polyuria
กรณทampม acidosis หร+อกาลงรกษาดวย urine alkalinization
อาจตองแปลผลรวมกบ Spgr และ sensitive กบ albumin เทานน
ควรตรวจ FBS รวมดวย ถาปรกตควรน2กถ2ง Fanconirsquos syndrome
กรณทampม acidosis esp DKA Alcoholic ketoacidosis
แปลผลคกบ RBC เสมอ อาจบงชถ2ง Rhabdomyolysis Hemolysis
กรณทampม hyperbilirubinemia
บงชถ2ง UTI จากเช+อเฉพาะบางชนดบอกถ2ง infectioninflammation
รายงานรปรางดวยเสมอ esp acanthocyte
ชวยแยก medical ndash surgical hematuria โดยอาศย cast proteinuria ดวยบอกถ2งการปนเป4 อนจากการเก5บ urine
การรายงานคาตางๆ ใน UA
อาจเป น UTI หร+อ contaminate ก5ได
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Differentiating Prerenal vs Intrinsic Renal
FENa () = UNa x SCr x 100
SNa x UCr
FEUrea () = Uurea x SCr x 100
BUN x UCr
None of the above criteria for the diagnosis of prerenal disease may be present in a patient with underlying
renal disease
No recent diuretics
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
In the absence of hemorrhagic shock use isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume
Use of vasopressors in conjunction with fluids in patients with vasomotor shock
Use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting or in patients with septic shock
Hemodynamic Monitoring and Support for Prevention and Management of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Am Fam Physician 200061(7)2077-2088
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Commonly Used IV Solutions
6 Voluven
10 Voluven
Haemaccel
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
NEJM 2010362(9)779-789
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
NEJM 2001345(19)1368-1377
I MAP ge65 mmHg II CVP 8-12 mmHg III Improvement in blood lactate level IV ScvO2 gt97 V urine output ge05 mlkghr
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Insulin therapy targeting plasma glucose 110ndash149 mgdl in critically ill patients
Achieve a total energy intake of 20ndash30 kcalkgd in patients with any stage of AKI
Avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT
Provide nutrition preferentially via enteral route in patients with AKI
Administer protein of 08ndash10 gkgd in noncatabolic AKI patients without need
for dialysis 10ndash15 gkgd in patients with AKI on RRT up to 17 gkgd in patients on CRRT and in
hypercatabolic patients
Glycemic Control and Nutritional Support
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Do NOT use diuretics to prevent AKI Do NOT use diuretics to treat AKI except in the management
of volume overload High dose furosemide (gt1 gday) may cause ototoxicity Continuous infusion of 05 mgkghr was not associated with
ototoxicity Do NOT use low dose dopamine (1ndash3 mgkgmin) to prevent
or treat AKI
Diuretics and Vasodilator Therapy in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on All-Cause Mortality
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Anaesthesia 201065283ndash293
Effect of Furosemide vs Control on Need for RRT
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Mortality
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Ann Intern Med 2005142510ndash524
Effect of Low-dose Dopamine on Need for RRT
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Do NOT use aminoglycosides to treat infections unless no suitable less nephrotoxic therapeutic alternatives are available
In patients with normal kidney function in steady state aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens
Monitor aminoglycoside drug levels when treatment with single-daily dosing is used for gt48 hours
Use topical or local applications of aminoglycosides (eg respiratory aerosols instilled antibiotic beads) rather than IV when feasible and suitable
Use azole agents echinocandins or lipid formulations rather than conventional formulations of amphotericin B if equal therapeutic efficacy can be assumed
Prevention of Aminoglycoside- andAmphotericin-related AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Initiate RRT emergently when life-threatening changes in fluid electrolyte and acid-base balance exist
Consider the broader clinical context the presence of conditions that can be modified with RRT and trends of laboratory tests rather than single BUN and creatinine thresholds alone to start RRT
Discontinue RRT when it is no longer required either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs or because RRT is no longer consistent with the goals of care
Do NOT use diuretics to enhance kidney function recovery or to reduce the duration or frequency of RRT
Dialysis Intervention for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Potential Applications for RRT
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Initiate RRT in patients with AKI via an uncuffed nontunneled dialysis catheter rather than a tunneled catheter
When choosing a vein for insertion of a dialysis catheter in patients with AKI consider these preferences- First choice = Right IJ vein Second choice = Femoral vein Third choice = Left IJ vein Last choice = SC vein with preference for the dominant side
Use a subclavian site rather than a jugular or a femoral site in adult patients to minimize infection risk for nontunneled CVC placement
Use ultrasound guidance for dialysis catheter insertion CXR after placement and before first use of IJ or SC catheter Use a CVC with the minimum number of ports or lumens
essential for the management of the patient
Vascular Access
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138CDC Guidelines for the Prevention of Intravascular Catheter-Related
Infections 2011
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Temporary Dialysis Catheter
Rt IJ 12-15 cmLt IJ 15-20 cmFemoral 19-24 cm
Femoral --- CRRT
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Use continuous and intermittent RRT as complementary therapies in AKI patients
Use CRRT rather than standard intermittent RRT for hemodynamically unstable patients
Use CRRT rather than intermittent RRT for AKI patients with acute brain injury or other causes of increased intracranial pressure or generalized brain edema
Modality of RRT for Treatment of AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Advantages and Disadvantages of Each RRT Modality
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
The dose of RRT to be delivered should be prescribed before starting each session of RRT
Frequently assess of the actual delivered dose in order to adjust the prescription
Provide RRT to achieve the goals of electrolyte acid-base solute and fluid balance that will meet the patientrsquos needs
Deliver a KtV of 39 per week when using intermittent or extended RRT in AKI
Deliver an effluent volume of 20-25 mlkgh for CRRT in AKI
Dose of RRT in AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
1 Increase in SCr by ge03 mgdl within 48 hours2 Increase in SCr to ge15 times baseline
which is known or presumed to have occurred within 7 days
3 Urine volume lt05 mlkghr for 6 hoursafter administration of intravascular contrast
media
Contrast-induced AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Incidence 1-2 (Low risk) to 25 (High risk)
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Assess the risk of CI-AKI esp screen for pre-existing renal impairment in all patients who are considered for a procedure that requires IVIA administration of iodinated contrast media Serum Cr M ge13 F ge10 mgdl eGFR lt60
mlmin173m2
Dipstick testing for urine protein Risk factor questionniare
Other risk factors Advanced age DMPre-DM HT hyperuricemia metabolic syndrome CHF volume depletion hemodynamic instability use of concurrent nephrotoxic medications large volume CM high osmolar CM intraarterial administration
Assessment
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Tech Urol 1998465ndash69
Sample Questionnaire for CI-AKI Risk
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
J Am Coll Cardiol 2004441393-1399httpwwwzunisorgContrast-Induced20Nephropathy20Calculator2htm
CI-AKI Risk Score Model for PCI
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Repeated exposure of CM should be delayed for 48 hr in patients without risk factors for CI-AKI 72 hr in patients with DM or pre-existing chronic renal
dysfunction Stop nephrotoxic medications eg NSAIDs aminoglycosides
amphotericin B high dose loop diuretics acyclovir ACEIARBs can be continued Consider alternative imaging methods in patients at
increased risk Use the lowest possible dose of contrast medium in patients
at risk
Use iso-osmolar or low osmolar iodinated contrast media rather than high-osmolar iodinated contrast media in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Max CM dose = 5 x BW
SCr
CM ratio = Volume administered Max CM dose
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Do NOT use oral fluids alone in patients at risk IV Volume expansion with either isotonic NaCl or NaHCO3
solutions rather than no IV volume expansion in patients at increased risk
75 NaHCO3 200 ml + D5W 950 ml ( Na amp HCO3 153 mEqL each) IV drip 3 mlkghr (Max 300 mlhr) x 1 hr then 1 mlkghr x 6 hr NSS 1000 ml IV drip 1 mlkghr 8-12 hr before to after CM injection Use oral NAC together with IV isotonic crystalloids in patients
at risk Do NOT use prophylactic intermittent hemodialysis or
hemofiltration for CM removal in patients at risk
Prevention of CI-AKI
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Ann Intern Med 2009151631ndash638
Bicarbonate vs NSS and Risk of CI-AKI
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Circulation 20111241250-1259
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Non-pitting edema with blister and bullae
Peau drsquoorange skin changesCobblestoning and induration skin
Contracture
Gadolinium
Pathology
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Use of a macrocyclic chelate is preferred over linear chelate Gd
Use the lowest dosage possible to achieve the image Avoid repeat exposure with Gd Consider performing intermittent hemodialysis after exposure
and next 2 days in patients who are already maintained on HD
Demonstration of significant quantities of insoluble Gd in the skin of NSF patients months after exposure to Gd based contrast material and after extensive tissue processing
Prevention of NSF
KDIGO Guideline 2012 ndash AKI KI Supplements 20122(1)1-138
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Type 1 acute decrease in cardiac function leads to acute kidney injury
Type 2 chronic decrease in cardiac function leads to progressive CKD
Type 3 acute kidney injury leads to acute cardiac dysfunction
Type 4 chronic kidney disease leading to decreased cardiac function cardiac hypertrophy andor increased risk of adverse cardiovascular events
Type 5 Systemic condition (eg sepsis) causing both cardiac and renal dysfunction
Cardiorenal Syndrome
J Am Coll Cardiol 2008521527-1539
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Patient wakes up at five AM with acute shortness of breath and ldquoheartburnrdquo
He takes Lomicid and tries to go back to sleep despite continued pain
The pain continues off and on for the next 8 hours before he relents and follows his co-workers advice and goes to be evaluated by a doctor
In the ER he is found to have a troponin T of 15 His shortness of breath initially improved with IV Lasix but
over the next 24 hours it worsens along with increasing oxygen requirement
His SCr on admission was 14 and rises over the next few days to 34 mgdl with his worsening hemodynamics
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
N Engl J Med 2011364(9)797-805
Diuretic Strategies in Patients with Acute Decompensated Heart Failure
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
N Engl J Med 2011364(9)797-805
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
A 78 year old male has ischemic heart disease with left-sided heart failure
The patient had a series of admissions over the summer of 2010 due to recurrent decompensated heart failure but has since remained out of the hospital on the following regimen
bull Lasix 40 mg daily bull HCTZ 125 mg Mondays and Thursdays bull Carvedilol 25 mg bid bull Lisinopril 20 mg daily bull Aldactone 25 mg daily
Along with the improved heart failure management his creatinine has gradually risen from 14 to 28 and his BUN now runs around 70-80 mgdl
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
A 68 year old patient with compensated heart failure is maintained on the following regimen lisinopril 20 mg furosemide 40 mg bid metoprolol 100 mg bid
She presents to clinic with a blood pressure of 16595 labs show a potassium of 56 and a creatinine at baseline 16
Her internist adds HCTZ 25 mg daily for the potassium and blood pressure Her follow-up chemistries and blood pressure are improved and stable
She calls back 2 weeks later complaining of swollen hot red right big toe A diagnosis of acute gout is made and she is prescribed Celebrex 400 mg daily
Three days later she presents to the ER with shortness of breath palpitations and peripheral edema Her potassium is 68 and creatinine is 36
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
58 year old patient with diabetic nephropathy has been on dialysis for 3 years
He has finally agreed to explore kidney transplant As part of the work-up she gets a stress echocardiogram
He has a non-ischemic response but is found to have significant left ventricular hypertrophy
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
56 year old Caucasian woman is admitted with fever shortness of breath and one week of productive cough
CXR shows right middle lobe infiltrate
At admission her vitals were stable except for a temp of 1023 Soon after she decompensated and her blood pressure falls to 70 systolic She is started on dopamine
She is ultimately admitted to the MICU and intubated The following day her creatinine has risen from 12 to 25 and a bedside echo shows an LVEF of 30 down from 65 2 months ago
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Unique form of kidney injury resulting from renal vasoconstriction in the setting of systemic and splanchnic arterial vasodilatation in patients with advanced cirrhosis HRS type 1 SCr gt100 from baseline to gt25 mgdl
within 2 wks HRS type 2 SCr ge15 mgdl in patients with refractory
ascites that either steady or worsening but not fulfill HRS type 1
Functional defect with preserved tubular function and absence of significant histologic abnormalities
Trigger Bacterial infection esp SBP GI bleeding Large volume paracentesis (gt5 L) without albumin administration
Hepatorenal Syndrome
Gut 200756(9)1310-1318
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
N Engl J Med 2009361(13)1279-1290
SCrHyponatremiaLow UNaLow FENaHigh UosmHigh UosmSosm
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Use hemodynamic monitoring when possible to help with the management of fluid balance in patients with HRS
Resuscitate patients with HRS type 1 with albumin (initially 1 g of albuminkg for two days up to a maximum of 100 gday followed by 20 to 40 gday) in combination with a vasoconstrictor preferentially terlipressin
RRT should be avoided in HRS type 1 patients unless there is either an acute reversible component or a plan for liver transplantation
Management
Crit Care 201216R231-17
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Extracorporeal Liver Support System
Crit Care 201216R231-17
Treatment of HRS type 1 is vasoconstrictor + albumin liver transplantationTreatment of HRS type 2 is large volume paracentesis with albumin administration 8 g1 L of ascites removed liver transplantation
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Renal failure in an asthma attack
Specific collection of symptoms Alveolar hemorrhage Acute glomerulonephritis
Specific diagnosis Wegenerrsquos granulomatosis Goodpasturersquos syndrome SLE Microscopic polyangiitis
Pulmonary-renal Syndrome
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Intra-abdominal pressure (IAP) = pressure concealed within the abdominal cavity
Abdominal perfusion pressure (APP) = MAP ndash IAP Filtration Gradient (FG) = glomerular filtration
pressure (GFP) - proximal tubular pressure (PTP) = MAP ndash (2 x IAP)
Normal IAP 5-7 mmHg in critically ill adults IAH = sustained or repeated IAP ge12 mmHg 4 Grades
Grade I 12-15 mmHg Grade II 16-20 mmHg Grade III 21-25 mmHg Grade IV gt25 mmHg
Abdominal compartment syndrome (ACS) = sustained IAP ge20 mmHg (plusmnAPP lt60 mmHg) with new organ dysfunctionfailure
Intra-abdominal Hypertension
Intensive Care Medicine 200632(11)1722-1732
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Primary IAH injury or disease in the abdomino-pelvic regionSecondary IAH NOT originate from the abdomino-pelvic region
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
รายงานผลเป6น mmHg (1 mmHg = 136 cm H2O) วดในทานอนราบ (Supine) หาตาแหนงของ Zero ท13จดตด iliac crest กบ mid axillary
line ใส NSS ไมเกน 25 ml ลงทาง Foley catheter ลงไปใน
bladder เร13มวด 30-60 วนาทหลงจากใส NSS ลงไปเพ13อใหกลามเน$อกระเพาะ
ปสสาวะคลายตว วดตอนหายใจออกสด (End expiration) วดขณะท13ผ2ป7วยไมมการหดเกรงของกลามเน$อทอง
การวด Intra-abdominal pressure
Intensive Care Medicine 200632(11)1722-1732
Intensive Care Medicine 200733(6)951-962
Intensive Care Medicine 200733(6)951-962
Recommended
