Abstract: SA-PO1002
Severe Metabolic Alkalosis After Cystogastrostomy in a Patient with Chronic Necrotizing Pancreatitis
Session Information
- Fellows/Residents Case Reports: Fluid, Electrolytes, Acid Base
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Wongboonsin, Janewit, University of Minnesota, Minneapolis, United States
- Elfering, Sarah L., University of Minnesota, Minneapolis, Minnesota, United States
Background
Hospital acquired metabolic alkalosis occurs in the setting of diuresis or other volume depleting conditions. Correction of volume depletion, hypochloremia and hypokalemia results in resolution of alkalosis. We present a case of severe metabolic alkalosis that was an unexpected complication of cystogastrostomy, a common procedure utilized in chronic pancreatitis.
Methods
A 68 year old man was hospitalized for chronic necrotizing pancreatitis managed with abscess drains and cystogastrostomy tube. On hospital day 154, he required restenting of cystogastrostomy tube. Following this, gastric output was 15 L in 5 days with an average net negative balance of 900 ml/day. Physical examination revealed blood pressure of 86/61 mmHg, heart rate at 88/min and normal mental status. Over 5 days, serum bicarbonate rose from 20 to >45 mmol/L and chloride decreased from 118 to 94 mmol/L. Serum creatinine rose from 1.0 to 1.4 mg/dL. Arterial blood gas revealed pH 7.61 pCO2 55 mmHg, pO2 71 mmHg and calculated bicarbonate at 55 mmol/L. Pertinent medications included fludrocortisone 50 mcg for chronic orthostatic hypotension. In addition to his obligate intake of ~4L/day it took aggressive chloride replacement with normal saline (15 L in 3 days) and potassium replacement with 430 mEq over 3 days to resolve the alkalosis.
Conclusion
Cystogastrostomy is a common procedure that is used to manage walled-off pancreatic fluid collections. Gastric irritation and excessive vomiting are not an expected complication of this procedure. This patient’s volume assessment was a challenge due to chronic hypotension with chronic orthostasis. It was not anticipated that he would require an extraordinary amount of isotonic sodium chloride to reverse the alkalemia. Direct chloride loss, volume depletion, hypokalemia and fludrocortisone therapy were likely mechanisms leading to such severe metabolic alkalosis. Neither acetazolamide nor HCl therapy was utilized given excellent response to aggressive fluid resuscitation. This case highlights the need to recognize and correct precipitating and maintenance factors in metabolic alkalosis in order to avoid hypercapnia and respiratory failure.