Abstract: PUB098
Bridging to Transplantation: Tolvaptan for Refractory Hyponatremia in Decompensated Cirrhosis
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Mbolu, Chika Miriam, Westchester Medical Center, Valhalla, New York, United States
- Chugh, Savneek S., Westchester Medical Center, Valhalla, New York, United States
- Gupta, Sanjeev, Westchester Medical Center, Valhalla, New York, United States
- Okebugwu, Prosper Chisom, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States
Introduction
Hyponatremia is a common and serious complication of advanced cirrhosis caused by impaired free water excretion from non-osmotic arginine vasopressin (AVP) release. Portal hypertension and splanchnic vasodilation cause effective arterial underfilling, activating the renin-angiotensin-aldosterone system, sympathetic nervous system, and AVP secretion. This leads to water retention exceeding sodium retention, resulting in dilutional hyponatremia. Severe hyponatremia in decompensated cirrhosis is associated with increased mortality, hepatic encephalopathy, refractory ascites, longer hospitalization, and worse transplant outcomes.
Case Description
A 35-year-old man with heavy alcohol use (12–15 beers daily) presented with progressive jaundice, abdominal distention, and bilateral leg edema. Imaging showed cirrhosis with portal hypertension, splenomegaly, large-volume ascites, and diffuse anasarca. Labs revealed serum sodium 107 mmol/L, serum osmolality 232 mOsm/kg, urine sodium <20 mmol/L, urine osmolality 442 mOsm/kg, and AST/ALT 90/40 U/L. Initial treatment included 1-liter fluid restriction and a 100 mL bolus of 3% hypertonic saline with minimal response. A second 100 mL bolus produced only modest improvement. By hospital day 3, after multidisciplinary discussion with hepatology, tolvaptan was started despite cirrhosis. He received tolvaptan 15 mg daily for two days. Serum sodium gradually improved to >125 mmol/L, allowing liver transplant listing.
Discussion
Tolvaptan is an oral selective vasopressin V2-receptor antagonist that promotes electrolyte-free water excretion and increases serum sodium without significant sodium loss. Although effective in euvolemic and hypervolemic hyponatremia, its use in cirrhosis remains controversial because of hepatotoxicity concerns, cost, transient response after discontinuation, and limited survival data.
This case highlights that carefully selected patients with advanced cirrhosis and severe dilutional hyponatremia may benefit from short-term inpatient tolvaptan when standard therapy fails or sodium correction is required to achieve transplant candidacy. In such cases, controlled short-term correction may outweigh theoretical hepatic risks when alternatives are limited.