Critical Combine Conference R4 王建中 /VS 吳允升 Apr, 11 st, 2014

Critical Combine Conference

R4 王建中 /VS 吳允升Apr, 11st, 2014

A 49-year-old man with left upper abdominal

pain for about 3 months

Patient Profile Systemic disease:

Gastric adenocarcinoma, cT4bNxM1, inoperable and metastatic, pancreas invasion and peritoneal seedings/carcnomatosis with ileus, stage IV

Obstructive uropathy with hydronephrosis due to cancer

Operation: 2014/02/17: Port-A implantation, echo-guided

Allergy: NKA

Personal history: Smoking & alcohol use: Nil Education: Junior high school Marital status: Married

Patient Profile

Occupation:服務業 Drug history:

Nexium (40) 1 tab QD Strocain 1 tab TID Gascon (40) 1 tab TID

Family History

49 y/o

No HTN, CAD, Autoimmune Disease HX

49 y/o

20 y/o 19 y/o

77 y/o

Past History2013

Jan, 21

Dec

Left upper abdominal sharp pain Not correlated to oral intake Easy satiety and abdominal distention Visit 新泰 hospital: EGD : gastric ulce

2014 Persistent abdominal pain Weight loss about 9kgs in one months Bowel habit change was noted. 新光 H: EGD : one large ulcer about 1.5~2cm with elevated margin and folds convergence in the angle to the LC/posterior wall of lower body, suspected malignancy Biopsy performed CT scan : gastric cancer with peritoneal seeding

Past History2014

Jan, 21

Laparoscopic appentectomy was done for suspicious of acute appendicitis Peritoneal seeding was noted during surgical intervention Pathology: metastatic adenocarcinoma

Jan, 21

Feb, 12

NTUH MRI : infiltrative tumor with involvement of stomach and pancreas, probably arising from gastric cancer and directly invading the pancreas; multiple regional lymph nodes

Abdominal MRI (2014.02.12)

Infiltrative gastric tumor with involvement of stomach and pancreas; multiple regional lymph nodes

Physical Examination BH: 170cm BW:68.7Kg BMI:23.77 HEENT

Conjunctiva: not pale, Sclera: icteric (-) Pupil: isocoric, 4mm/4mm, midposition

Light reflex: R/L +/+, promptly Oral thrush(-), oral ulcers(-)

Neck Supple, tightness(-), JVE(-) , LAP(-), goiter(-) Kernig’s sign (-), Brudzinski’s sign(-)

Chest Symmetrically expanded, axillary LAP(-) Breath sound: clear over bilateral lower lung fields

Heart PMI displacement (-),RHB, thrill(-) Murmur(-), distant heart sound (-)

Abdomen Distended, normoactive bowel sound, Tenderness(+,

epigastric area) Hepatosplenomegaly (-),

Extremity Petechiae(-), purpura(-), cyanosis(-), cold (-) Leg edema(-), clubbing finger(-)

Physical Examination

CXR 201402/17

ECG (2014.02.14)

Past History2014

Port-A insertion Initiate TPN

Feb, 17

EGD: Advanced gastric cancer, Bormann type 3, angle to the LC-PW of lower body, s/p biopsy Pathology: adenocarcinoma, poorly-differentiated

Feb, 19

Double J (Tumor stent) insertion for left hydronephrosisFeb, 22

Past History2014

HDFL C1D1 NG decompensation: more than 2000ml gastric juice drained out per day Keep TPN and keep I/O balance

Feb, 25

Laboratory Data

2/27: Cl:93 mmol/L

Sp.Gr. PH Protein Glu Ketone OB Bil Uro bil

mg/dL mg/dL mg/dL mg/dL mg/dL mg/dL

1.031 6.0 100 (2+) - - 3+ - <1.5

RBC WBC Epith. Cast Crystal Nit. color

(/HPF) (/HPF) (/HPF) (/LPF)

>100 20-35 0-2 Granular cast - - cloudy, yellow

Urine exam 2014/02/24

Cre Na

mg/dL mmole/L

62 68

FENa =1.8% > 1%FENa =1.8% > 1%

Renal Echography (2014.02.27)

Right Size : normal 13.6

cm Shape : regular Cortical

echogenecity : increased chogenecity

Cortical thickness : Normal: 2.0 cm

Central echo : mildly seperated

Cystic lesion(s): Nil

Solid lesion : Nil

IMPRESSION : 1. Bilateral parenchymal renal disease 2. Moderate right hydronephrosis 3. Renal cyst, right 4. Engorged right renal vessels, r/o renal vein thrombosis

Left Size : normal 12.1

cm Shape : regular

Cortical echogenecity : increased echogenecity

Cortical thickness : Normal: 1.8 cm Central echo : mildly seperated

Cystic lesion(s): Nil Solid lesion : Nil

Acute kidney injury

Prerenal

Intrinsic

Postrenal

Hypovolemia Decreased cardiac output

Decreased effective circulating volume: -Congestive heart failure

-Liver failure Impaired renal autoregulation: NSAIDS, ACEI/ARB, cyclosporin

Gluomerular: acute glomerulonephritis

Tubules and interstitium

Vascular: vasculitis, malignant hypertension, TTP-HUS

Bladder outlet obstruction Bilateral pelvoureteral obstruction

(or unilateral obstruction of a solitary functioning kidney)

Harrison's Principles of Internal Medicine, 18e

Past History2014

Increased O2 demand suddenly NG decompression: about 2600-3300ml/day Suspected septic shock

Mar, 04

Mar, 05 Consult nephrologist; transfer to MICU? DNR(+)

Mar, 05Mar, 05

Family decided to discontinue inotropic agents Passed away

Mar, 06

Final Diagnosis Gastric adenocarcinoma, cT4bNxM1, stage IV,

inoperable and metastatic, pancreas invasion and peritoneal seedings/carcnomatosis with ileus

Severe metabolic alkalosis secondary to hydrogen ion loss from vomiting (obstructive GI tract)

Acute kidney injury, AKIN stage 3 Septic shock, suspected IAI related Obstructive uropathy with hydronephrosis due to

cancer

Discussion--1. Metabolic alkalosis

2. The rule of dialysis for treatment for severe metabolic alkalosis

Metabolic alkalosis

F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135




SCNN1B geneKCNJ1 gene

HSD11B2 gene

Metabolic alkalosis

(1) Abnormal chloride losses (2) In states of mineralocorticoid

excess (3) Renal ion transport disrupted by

genetic abnormalities that lead to stimulation of collecting duct sodium reabsorption through ENaC (eg, Liddle syndrome)


Metabolic alkalosis Surreptitious vomiting or diuretic abuse should

always be considered Both aldosterone and renin levels should be

increased

Apparent mineralocorticoid syndrome Liddle syndrome HSD2 deficiency

Hypertension Hypokalemia Metabolic alkalosis Low aldosterone levels


Genetic analysis: gold standard Aldosterone antagonist: for 11HSD2

deficiency; no effect to Liddle syndrome Amiloride: blocks ENaC directly,

treatment for Liddle syndrome

Clinical course of a patient with CHF and metabolic

alkalosis

Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827

Case Present 68 y/o M, transferred to ICU: Af and pulmonary

edema s/p intubation HTN, CAD,CHF with preserved systolic function,

obesity Persistent signs of volume overload but

received only intermittent doses of furosemide Three days prior to transfer, developed more

overt signs of CHF, prompting more aggressive use of furosemide (40-80 mg intravenously [IV] twice daily)


Case Present

Remained volume overloaded and developed pulmonary edema requiring intubation during an episode of rapid Afib

Echocardiogram: atrial dilatation, moderate AR and MR, LVEF: 50% with mild posterobasal hypokinesis, and impaired diastolic filling

IV furosemide with gradual improvement in congestion progressive alkalemia and severe hypokalemia over the ensuing 5 days


Diagnosis: CHF; metabolic alkalosis due to heart failure and loop diuretic use; hypokalemia due to loop diuretic use and secondary

hyperaldosteronism from decompensated heart failure


Metabolic alkalosis of CHF

Diuretic therapy: chloride loss, decreased effective circulating volume, activation of the renin-angiotensin-aldosterone system

CHF: system sympathetic overactivity increased renal adrenergic tone activation of the sodium/hydrogen

ion exchanger in the proximal tubule




IV acetazolamide (250 mg every 6 hours for 24 hours or as a single dose of 500 mg)

Ex: 70 kg*0.5*10 mEq; infusion should not be faster than 0.2 mEq of hydrogen per 1 kg of body weight per hour;

F/U e-/ABG Q1-2H

The rule of dialysis for treatment for severe metabolic alkalosis

Case Present A 69-year-old woman, ESRD (secondary to

hypertensive nephrosclerosis); invasive SCC of the left pinna and ear with neck metastasis

Presented with confusion, lethargy, and low oxygen saturation (80%)

These symptoms preceded for several days of severe and profuse vomiting

Abdominal CT: proximal small-bowel dilatation measuring up to 3.3 cm in diameter, with a transition point noted in the left hemipelvis (narcotic use)

Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

Case Present Admitted to ICU:

NG insertion, pantoprazole therapy Dialysis: urgently for 3 hours without

ultrafiltration: using dialysate: Potassium : 4 mEq/L (4 mmol/L) Calcium(ionized): 5 mg/dL (1.25

mmol/L) Bicarbonate: 30 mEq/L (30 mmol/L)



iHD 2hoursNG

4700ml iHD



+


Vomiting and GI hydrogen ion loss High grade gastric distension due to outlet

obstruction causes cholinergic activation

Increased gastrin secretion, decreased somatostatin secretion

Increased hydrogen ion secretion and gastric fluid volume When stimulated, gastric fluid has a hydrogen ion

concentration of 100-170 mmol/L (pH 1.0) No stimulated: hydrogen ion concentration 10 mmol/L One millimole of bicarbonate is generated in body

fluids for each millimole of hydrogen ion lost in emesis


Hemodialysis for severe metabolic alkalosis Severe metabolic alkalosis (serum

bicarbonate concentrations > 50 mEq/L): Hemodialysis with a reduced bath bicarbonate

concentration is a safe and effective intervention Bicarbonate decreased to the lowest level

available No increase calcium concentration

Hydrochloric acid infusion is not an acceptable treatment alternative in patients without kidney function (large volume of fluid)



Take Home Message

Severe metabolic alkalosis (bicarbonate cncentration >50 mEq/L) + (all these severe case reports) with impairment of kidney function (due to volume loss)

Hemodialysis may be considered !

For metabolic alkalosis, treatment the underlying disease is most important

Thank you for your attention!

Documents

Critical Combine Conference R4 王建中 /VS 吳允升 Apr, 11 st, 2014