Metabolic complications of the use of stomach for urinary reconstruction

A total of 34 children with normal renal function underwent either gastrocystoplasty or continent urinary reservoirs with stomach at our institutions. Severe hypochloremic hypokalemic metabolic alkalosis developed in 2 patients, manifested by intractable seizure disorder in 1 and altered mental status with respiratory depression in 1. Symptoms developed at 4 and 6 months, respectively. Despite severe alkalosis, urinary pH was less than 5.0 and fractional excretion of chloride remained high in both patients. Resuscitation with sodium chloride, arginine hydrochloride and potassium chloride restored electrolyte balance in less than 48 hours in both patients. Serum gastrin was slightly elevated in 1 patient (137 pg./ml., normal 0 to 125) who responded to long-term histamine-blocker therapy. The other patient had significant hypergastrinemia (624 pg./ml.) with secondary hyperaldosteronism. Maximum doses of histamine blockers, oral replacement of sodium chloride and potassium chloride, and the proton pump inhibitor omeprazole failed to control recurrent bouts of severe hypochloremic metabolic alkalosis. This patient ultimately underwent removal of three-quarters of the gastric augmentation and replacement with ileum. Postoperatively, serum gastrin levels and electrolytes reverted to normal. The pathophysiology of this potentially lethal complication is further discussed.