Abstract: PUB518
Excessive Water Intake Causing Severe Metabolic Alkalosis
Session Information
Category: Trainee Case Report
- 902 Fluid and Electrolytes: Clinical
Authors
- Sanon, Julien, Einstein Healthcare Network, Cheltenham,, Pennsylvania, United States
- Bloom, Eric J., Albert Einstein Medical Center, Berwyn, Pennsylvania, United States
- Chewaproug, Daranee, Einstein Medical Center Philadelphia, Bryn Mawr, Pennsylvania, United States
- Dissanayake, Imara, Albert Einstein Medical Center, Berwyn, Pennsylvania, United States
Introduction
Severe metabolic alkalosis is one of the most dreaded acid-base disorders. It is defined as a pH of more than 7.60 with serum bicarbonate of more than 40 mmol/L. Clinical features include confusion, seizures, and cardiac arrhythmias. Mortality rate increases significantly with the severity of the alkalosis and can reach up to 80% with a pH of more than 7.60. We present a case of severe metabolic alkalosis with a pH up to 7.70 in a patient with a jejunostomy and a gastrostomy tube.
Case Description
The patient is an 82-year-old female with diabetes mellitus, cardiac arrhythmia and perforated gastric ulcer. She was admitted with syncope and found with severe metabolic alkalosis. Two months prior to her presentation, she had an open jejunostomy for tube feeds with a gastric tube for drainage. Formal instructions were to only take occasional sips of water. The day prior to admission, she had increased thirst and started to drink a large amount of water. She then noticed large drainage into her gastrostomy bag. Admission arterial gas showed a pH of 7.70, pCO2 of 70 mmHg. Blood work had sodium of 137 mEq/L, potassium of 2.5 mEq/L, chloride of 60 mEq/L, bicarbonate more than 50 mEq/Liter and glucose of 466 mg/dL. Urinalysis showed a pH of more than 9. EKG had atrial paced rhythm. CT of the abdomen had jejunostomy and gastric tube well positioned. The patient was treated aggressively with normal saline, potassium, Acetazolamide and Protonix. She improved significantly after 2 days with potassium of 3.1 mEq, chloride of 90 mEq/L, serum bicarbonate of 43.6 mEq/L.
Discussion
Our patient, had severe metabolic alklaosis secondary to massive gastrointestinal drainage in her gastric tube. In addition she was volume depleted contributing to her metabolic alkalosis. The excessive volume of water ingested prior to her presentation likely triggered the increased gastric secretion. We believe the gastric distension due to the ingsted water, resulted in excessive grastric secretions by stimulating the stretch receptor. The treatment includes aggressive hydration, potassium repletion, Proton Pump Inhibitor, Acetazolamide and hydrochloric acid infusion in refractory cases. Hemodialysis has also been used. Our case demonstrates that good outcome can be achieved with prompt, aggressive and appropriate treatment of severe metabolic alkalosis.