Severe Hypochloremic Metabolic Alkalosis After Gastric Augmentation Cystoplasty

Introduction: Augmentation cystoplasty (AC) is a surgical procedure done to enlarge the bladder using the body's native tissue. Intestinal or gastric tissue is typically used. We describe a young female with history of neurogenic bladder who underwent gastric AC ten years prior to presenting with severe hypochloremic metabolic alkalosis, found to be due to loss of HCl into the urine through the bladder's gastric mucosa. Case Description: A 33-year-old female with history of end stage kidney disease secondary to neurogenic bladder with a gastric AC 10 years prior and transplanted kidney presented to the emergency room for abnormal blood work. Her initial lab work revealed serum creatinine 7.0 mg/dL (baseline 3-4.0 mg/dL), bicarbonate 49 mmol/L, chloride 67 mmol/L, venous blood gas with pH 7.6, pCO2 52mmHg, and bicarbonate 51 mEq/L. She received 500cc of normal saline and was started on maintenance intravenous fluids at 75cc/hr. Over the next two days her serum chloride increases to 76mmol/L, bicarbonate decreases to 37mmol/L and creatinine decreases to 5.80 mg/dL. At this time, she eloped from the hospital. One week after initial presentation she returned to the hospital for a planned arterial-venous graft placement; at that time her serum chloride had improved to 93mmol/L, bicarbonate 30mmol/L, and creatinine 4.34mg/dL. Over the next few months, she was admitted to the hospital multiple times with similar lab findings. Treatment with proton pump inhibitor (PPI) and histamine type 2 receptor antagonist (H2 blockers) was initiated which resulted in normalization of serum bicarbonate. Discussion: Gastric AC uses gastric tissue which continues to secrete HCl- into the urine and can result in a severe metabolic alkalosis and hypochloremia. It is suggested that the electrolyte abnormalities tend to resolve over time, but in our patient, her metabolic derangements did not present until ten years after surgery. Treatment with PPIs and H2 blockers to suppress gastric acid production resulted in resolution of metabolic alkalosis. This case shows an uncommon etiology of metabolic alkalosis, where understanding of physiology resulted in effective treatment of severe life-threatening electrolyte abnormality.