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8/9/2019 AKI MIU BCPS 2015
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Taher Hegab, PharmD, PhD, BCPS
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Define Acute Kidney Injury (AKI) Distinguish prerenal from intrinsic and
postrenal causes of AKI
Be able to assess a patient for AKI List most important diagnostic test used in
evaluating patients with AKI
Develop treatment protocols for AKI
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AKI is defined as a decrease in glomerularfiltration rate occurring over hours to days.The decline in GFR is often accompanied bydecline in urine output
Also termed acute renal failure (old term),now only used for severe AKI
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The most recent AKI guidelines define AKI as:
Increase in Scr by 0.3 mg/dl ( 26.5 mmol/l)within 48 hours
Or
Increase in Scr to 1.5 times baseline, which isknown or presumed to have occurred within theprior 7 days
Or Urine volume 0.5 ml/kg/h for 6 hours.
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Stage Serum creatinine Urine output
1 1.51.9 times baselineOR0.3 mg/dl (26.5 mmol/l) increase
0.5 ml/kg/h for 612hours
2 2.02.9 times baseline 0.5 ml/kg/h for >12hours
3 3.0 times baselineOR
Increase in serum creatinine to 4.0mg/dl (353.6 mmol/l)ORInitiation of renal replacement therapyOR, In patients
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Not common in community Dehydration, some disease states and some medication
increase the risk Individuals with CKD is at higher risk NSAIDS, ACEI, ARB, contrast media are common
medication associated with AKI
Common in acute care disease states Very common in ICU setting AKI is associated with increased morbidity and
mortality Risk of death increases with increase in RIFLE
category or AKI stage
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KI
Pre-renal
(Decreased renal
perfusion/ normal renal
tissue)
Intrinsic
(Damage to the kidney/
ischemic or toxin)
Post-renal
(Obstruction or urine flow
bellow kidney) 9
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Intravascular volume Depletion: Dehydration from vomiting, diarrhea, decreased
intake, glucosuria, diabetes insipidus
Diuretics (excessive loss)
Hemorrhage Hypoalbuminemia
Skin losses
Burns
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Arterial hypotension: Sepsis, anaphylaxis
Decreased cardiac output: CHF, sepsis, pulmonary hypertension, aortic stenosis
Renal hypoperfusion ACE inhibitors, ARBs, renal artery stenosis, rental artery
emboli
BUN: Scr ratio > 20:1 indicates prerenal condition
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Prerenal azotemia: Azotemia associated with prerenal AKI
Azotemia: high levels of nitrogen waste in the bloodcauses confusion, alertness, low or no urine
output.
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Critical to identify patient at risk
Administration of wrong medication or notadministering enough volume may invoke AKI
Once AKI identified, must treat as soon aspossible to minimize or prevent permanentdamage
Correct the fluid states to restore renalperfusion
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Damage to the kidney itself
Damage can affect: Vasculature
Vasculitis, emboli, thrombocytopenia purpurea, accelerated HTN,
Glomeruli Lupus, post-streptococcal glomerulonephritis
Tubules (Acute tubular necrosis) (85% of cases) Ischemic (hypotension, vasoconstriction)
Exogenous toxins (contrast dye, heavy metals, aminoglycoside)
Endogenous toxins (Myoglobin, hemoglobin)
Interstitium (acute interstitial nephritis) Drugs (PCN, ciprofloxacin, sulfonamides)
Infections
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Renal Vasculature Damage:
Thromboemboli obstruct blood flow and cause anischemic event (just like an MI)
Emboli can develop/occur on arterial or venous sidekidney
Common event during vascular procedures(angioplasties and aortic manipulations as well asrenal vascular manipulations)
Can result as atrial fibrillation complication or muralthrombus complication (left ventricle)
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Tubular Damage Majority of cases (85%) caused by ATN;
50% ischemic (extended prerenal)
35% direct toxins
Tubules, have high oxygen demands, yetreceive low delivery compared to cortex,hence most affected by ischemia
ATN can occur over hours to days
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Risk factors: CKD
Age > 65
Multi-organ system failure, sepsis
Drugs, infection, surgery, malignancy Bone marrow or solid organ transplantation
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Obstruction: Bladder outlet obstruction
Ureteral
Renal pelvis or tubules
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Outpatient: Change in urinary habits, sudden weight gain, or
flank pain
Inpatient: Usually recognized by clinician before the patient
Decrease in UOP
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Medical history Medical/medication history
Physical exam BP, weight, fluid status, urine output
Laboratory tests Chemistry, hematology, urine sediment, urinalysis,
serologic
Diagnostic Renal imaging
Renal biopsy (rarely)
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serum creatinine, BUN, K, and phosphorus. BUN: Scr ratio
> 20:1 may indicates prerenal condition
Ca and pH (metabolic acidosis)
in WBC if associated with sepsis
in eosinophil may indicate acute interstitialnephritis
Urine analysis: May contain cells, cast, andcrystals
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Urinalysis: Specific gravity: dilution or concentration of urine
(dehydration?)
Protein: indicate kidney damage (nephrotic syndrome orLupus)
Glucose: glucose diuresis Ketones: DKA? Not eating/drinking?
Blood / RBCs kidney stone? Glomerular disease?
Nitrite : UTI? Leukocyte esterase UTI? WBCs UTI? Pyelonephritis? Bacteria UTI?
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Urine sodium and fractional sodium excretion FeNa = (Urine Na x Plasma Cr)
(Plasma Na x Urine Cr)
Used in evaluation of AKI with oliguria
If FeNa < 1% and urine sodium < 20 mEq/L itis likely prerenal
IF > 2% and urine sodium > 40 mEq/Lsuggests acute tubular necrosis
Loop diuretics can increase FeNa
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Diagnostic procedures may be necessary to assistdiagnosis Abdominal radiography including kidneys, ureters and
bladder
Cat Scan (CT) Ultrasonography
Identifies small/shrunken kidneys (CKD)
Postrenal obstruction visible on ultrasound or CT
Cystoscopy/Biopsy may be necessary to identifymalignancy, prostate hypertrophy, uterinefibroids, some stones
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Calculated GFR using any method willoverestimate renal function especially whenrenal function is rapidly changing.
Monitor Scr changes from baseline, look atthe trend not the just the value
Monitor urine output changes
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Pre-renal Volume expansion
Normal saline, to enhance renal perfusion (or LR)(guideline recommended over colloids)
Follow chemistry (BUN, creatinine), urine output
Hold BP meds to ensure good renal perfusion (withinreason)
Isotonic crystalloids generally preferred overcolloids
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Intrinsic renal Stop potentially offending agent Supportive care Immunosuppressives ( lupus, TTP)
Monitor electrolytes, UOP Biopsy as last resort, if indicated
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Post-renal Remove obstruction
Foley placement!
Follow BUN, creatinine
Should improve slowly over several days
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Stop nephrotoxic drugs Stop ACE inhibitor / ARB
No NSAIDs Avoid aminoglycoside if possible
Adjust dose of renally eliminated drugs Can have catastrophic consequences
Antibiotics like ciprofloxacin, levofloxacin, most penicillinsand cephalosporins, vancomycin, aminoglycosides,ranitidine, enoxaparin, and many others
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Question:At what creatinine level should the patient bedialyzed?
Answer:Creatinine level does not matter
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cidosis: metabolic
Electrolytes: hyperkalemia, hypermagnesemia
Intoxication: if dialyzable (lithium, salicylate,methanol, ethylene glycol, theophylline)
Overload: pulmonary edema, CHF
Uremia: pericarditis, altered mental status
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Intermittent hemodialysis: Most common, available everywhere
Rapid removal of fluid and solute
Rapid correction of acid base disorders
Hypotension can be a concern
Continuous renal replacement therapy For hemodynamically unstable patients
Not available at all facilities, more expensive
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In critically ill patients, we suggest insulintherapy targeting plasma glucose 110149mg/dl (6.18.3 mmol/l). (2C)
We suggest achieving a total energy intake of2030 kcal/kg/d in patients with any stage ofAKI. (2C)
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We suggest administering 0.81.0 g/kg/d ofprotein in noncatabolic AKI patients withoutneed for dialysis (2D), 1.01.5 g/kg/d inpatients with AKI on RRT (2D), and up to a
maximum of 1.7 g/kg/d in patients oncontinuous renal replacement therapy (CRRT)and in hypercatabolic patients. (2D)
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We recommend not using diuretics to preventAKI. (1B)
We suggest not using diuretics to treat AKI,except in the management of volumeoverload. (2C)
We recommend not using low-dosedopamine to prevent or treat AKI. (1A)
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We suggest not using aminoglycosides forthe treatment of infections unless no suitable,less nephrotoxic, therapeutic alternatives areavailable. (2A)
We suggest that, in patients with normalkidney function in steady state,aminoglycosides are administered as a singledose daily rather than multiple-dose dailytreatment regimens. (2B)
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We recommend monitoring aminoglycosidedrug levels when treatment with multipledaily dosing is used for more than 24 hours.(1A)
We suggest monitoring aminoglycoside druglevels when treatment with single-dailydosing is used for more than 48 hours. (2C)
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We suggest using topical or local applicationsof aminoglycosides (e.g., respiratory aerosols,instilled antibiotic beads), rather than i.v.application, when feasible and suitable. (2B)
We suggest using lipid formulations ofamphotericin B rather than conventionalformulations of amphotericin B. (2A)
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In the treatment of systemic mycoses orparasitic infections, we recommend usingazole antifungal agents and/or theechinocandins rather than conventional
amphotericin B, if equal therapeutic efficacycan be assumed. (1A)
We suggest not using N-Acetyl Cysteine(NAC) to prevent AKI in critically ill patientswith hypotension. (2D)
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We recommend i.v. volume expansion witheither isotonic sodium chloride or sodiumbicarbonate solutions, rather than no i.v.volume expansion, in patients at increased
risk for CI-AKI. (1A)
We suggest using oral NAC, together with i.v.isotonic crystalloids, in patients at increasedrisk of CI-AKI. (2D)
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We suggest not using diuretics to enhancekidney function recovery, or to reduce theduration or frequency of RRT. (2B)
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54yo M with AIDS (CD4 of 39) who presentsto the ED with altered mental status andneurologic deficits. CT scan with contrast wasordered to further investigate his condition.
His baseline creatinine is 1.4, but he returnsfrom the CT scan and now has creatinine of2.5, with decreased urine output
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Is this AKI? What type is it most likely to be?
How would you manage this?
Answers: Yes, ATN from contrast, supportive care
Bonus:
How might you have prevented this?
A: Pre-hydration and N-acetylcystine prophylaxis
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42yo F with no significant PMH presents to EDwith a cc of 4 days of nausea, vomiting anddiarrhea, with fever to 101OF. She has beenunable to keep any food down, and very little
in the way of liquids. Her son is in primaryschool and had similar symptoms 1 weekago. Creatinine is 2.0. Last one was 0.9about a year ago.
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Is this AKI? What type is it most likely to be? What tests might you order? How would you manage this?
Answers: Yes
pre-renal from dehydration / volume depletion
Orthostatic vitals, BUN:Scr ratio, Give fluids (saline saline saline!), follow creatinine
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75yo M with history of prostate cancerdiagnosed in 2 years ago. It was metastatic tohis ribs at the time, so he was not a candidatefor prostatectomy. He has done well since
then on hormone therapy, but presents toclinic today cc of abdominal pain anddecreased urine output over the last 5 days,as well as irritability and back pain. His
creatinine is 8.5, up from a baseline of 1.4.
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Is this AKI? What type is it most likely to be? What tests might you order? How would you manage this?
Answers: Yes
Post-renal, from prostatic obstruction
Bladder scan or post-void residual; renal ultrasound
Foley placement, give fluids, follow UOP and creatinine
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Pharmacotherapy: Principles and Practice,2013.