Abstract: PUB110
Severe Metabolic Alkalosis from Gastric Acid Losses: Improvement with Acid Suppression
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Moise, Altagracia C., Stamford Health, Stamford, Connecticut, United States
- St Gilus, Rose H., Stamford Health, Stamford, Connecticut, United States
- Rosen, Raphael Judah, Stamford Health, Stamford, Connecticut, United States
Introduction
Metabolic alkalosis can be life-threatening due to associated electrolyte derangements, cardiovascular compromise and compensatory hypoventilation. The primary mechanism to manage metabolic alkalosis is renal excretion of excess bicarbonate. We present a case of severe metabolic alkalosis in a patient due to small bowel obstruction (SBO) with high nasogastric tube (NGT) output which was successfully ameliorated with acid suppression with proton pump inhibitors (PPI) and H2 blockers to decrease GI acid losses.
Case Description
An 80-year-old woman with prior incisional hernia repair and recurrent SBO presented after a fall with rib fractures, pneumothorax, and hemothorax. Her course was complicated by SBO requiring NGT decompression, with output up to 5 L over 24 h. She developed severe metabolic alkalosis with altered mental status, hypokalemia, AKI, prompting ICU transfer for aggressive fluid and electrolytes repletion.
Initial studies showed pH 7.60, pCO2 64 mmHg, serum bicarbonate 50 mEq/L (from 33 two days prior), potassium 2.8–3.3 mEq/L, chloride 83 mEq/L, and creatinine 1.4 mg/dL (baseline 0.8), with decreasing urine output. Urine chloride was <20 mEq/L. Labs suggested volume contraction with hemoconcentration. Aggressive saline administration with additional potassium chloride was initiated. Given ongoing gastric acid loss via continuous NGT suction, PPI therapy was initiated. With this therapy, gastric fluid pH increased from 5 to 7.5 after initiation. Due to slow improvement, an H2 blocker was initiated and a single dose of acetazolamide was given to attempt to accelerate renal excretion of bicarbonate. Subsequently, urine output improved and serum bicarbonate gradually normalized, with resolution of alkalosis, AKI and mental status changes.
Discussion
This case underscores the importance of targeting the underlying mechanism in metabolic alkalosis. In patients with significant gastric acid loss, such as high NGT output, suppression of gastric hydrogen ion secretion with PPIs and H2 blockers can reduce ongoing losses and facilitate correction. While volume and electrolyte repletion remain the cornerstone of therapy, acid suppression represents an effective adjunct in refractory cases. Recognition of risk factors, including diuretic use, vomiting, and NGT suction, is essential to guide timely and mechanism-based management.