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Abstract: PO1184

A Case of Extreme Metabolic Alkalosis

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Author

  • Ajmal, Muhammad Suleman, Baylor College of Medicine, Houston, Texas, United States
Introduction

Metabolic alkalosis results from an increase in serum bicarbonate concentration due to loss of hydrogen ions and/or gain in bicarbonate ions. We present a case of extreme metabolic alkalosis due to multiple etiologies rarely co-existing.

Case Description

A 30-year-old male with Duchenne muscular dystrophy, chronic respiratory failure on mechanical ventilation via tracheostomy, gastrojejunostomy (G-J) tube dependent and genetic cardiomyopathy presented with drowsiness and lethargy for last 2 days per mother. His tube feed regimen was Nutren 1 can with 120 cc free water 4 times/day. He was recently started on Lasix 20 mg daily. Initial labs showed blood PH of 7.81, bicarb 66 and PCo2 53. He had AKI with Creatinine (Cr) of 2.66, BUN 266 and Cystatin C 11. His baseline Cr was 0.9-1.1. UA showed 3+ protein and no sediment. Urine (Ur) sodium 87, Ur chloride <15, Ur Cr <10 and Ur PH was 9. Chest Xray showed cardiomegaly with mild venous congestion and kidney ultrasound showed bilateral small echogenic kidneys.
He was treated with normal saline (NS) IV @100 cc/hr, acetazolamide IV, potassium IV, proton pump inhibitor to decrease gastric acid and minute ventilation was decreased to allow for compensatory hypercapnia. AKI improved with adequate diuresis and PH normalized (Image 1) by day 5. He had hypernatremia after 24 hours of IV NS and fluid were changed to hypotonic + free water via G-J tube. High daily output of ~700cc was recorded from the G-J tube. He was discharged home without diuretics and tube feeds were changed to Suplena + increase free water but was re admitted in 1 week with hyponatremia and severe metabolic alkalosis. He underwent G-J tube exchange during 2nd admission followed by persistent normalization of blood PH.

Discussion

This is a unique case of extreme metabolic alkalosis primarily due to the loss of gastric acid in the G-J tube, but volume depletion, hypokalemia, AKI, high protein tube feeds, lack of respiratory compensation due to ventilator dependence and loop diuretics contributed to the development and maintenance of metabolic alkalosis. We corrected his metabolic alkalosis and AKI with cautious use of IV fluids and Acetazolamide without needing dialysis, although metabolic alkalosis relapsed until the G-J tube was changed.

Daily PH and Cr