Abstract: TH-PO0430
A Case of Concurrent Acid-Base Disorders with No Apparent Etiology
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Umar, Sumayya, St Vincent's Medical Center, Bridgeport, Connecticut, United States
- Bhat, Nuthan, St Vincent's Medical Center, Bridgeport, Connecticut, United States
- Pena Zapata, Oscar Yasser, St Vincent's Medical Center, Bridgeport, Connecticut, United States
- Singh, Shashwat, St Vincent's Medical Center, Bridgeport, Connecticut, United States
Introduction
Gastric outlet obstruction (GOO) typically presents with intractable vomiting and metabolic alkalosis due to gastrointestinal (GI) losses. Here, we present a diagnostically challenging case of GOO with no apparent GI symptoms, with a profoundly deranged acid-base profile and renal dysfunction.
Case Description
A 39-year-old female with alcohol use disorder presented to our hospital with extreme fatigue. She hadn't eaten for 5 days, no bowel movements in 14 days, and urinated twice in the past week. She denied any nausea, vomiting, or diarrhea. Labs revealed a complex acid-base disorder indicative of coexisting metabolic alkalosis and high-anion-gap metabolic acidosis. She had severe hypokalemia (1.9), hypochloremia (56), and elevated bicarbonate (34) indicating chloride-depletion metabolic alkalosis, likely driven by chronic volume depletion with resulting hyperaldosteronism. The anion gap was elevated at 32, suggesting superimposed high anion gap acidosis, due to uremia (BUN 155, Cr 8.5). An elevated serum osmolality (335) with normal glucose and ethanol levels pointed toward an osmolar gap, likely reflecting retained unmeasured solutes such as phosphate or other uremic toxins. Her alkalemic pH (7.49) with low pCO2 (21) was consistent with concurrent respiratory alkalosis. Urinary electrolytes showed inappropriately high sodium (65), potassium (35), and chloride (51) despite volume depletion, suggesting intrinsic tubular injury with no plausible cause evident as per history or any apparent GI losses. CT abdomen showed a markedly distended stomach with circumferential thickening of the pylorus and first portion of the duodenum concerning for gastric outlet obstruction, finally revealing the etiology of the complex acid-base disorder.
Discussion
GOO is classically associated with metabolic alkalosis, but concurrent advanced kidney dysfunction can mask the traditional acid-base pattern. Delay in recognizing this reversible cause of electrolyte derangements risks irreversible injury and life-threatening complications such as arrhythmias or seizures.
Coronal and transverse views of the CT abdomen and pelvis demonstrating a profoundly distended stomach