Hyponatraemia Induced by Terlipressin in Patients Diagnosed with Decompensated Liver Cirrhosis and Acute Variceal Bleeding
Mahmoud Elshehawy, Richel Merin Panicker, Alaa Amr Abdelgawad, Patrick Anthony Ball, Hana Morrissey

TL;DR
A patient with liver cirrhosis developed dangerous low sodium levels after terlipressin treatment, highlighting the need for careful monitoring.
Contribution
This case emphasizes the risk of terlipressin-induced hyponatraemia in cirrhotic patients and provides practical management recommendations.
Findings
A 39-year-old cirrhotic patient developed severe hyponatraemia within 48 hours of terlipressin therapy.
Discontinuation of terlipressin and fluid restriction led to gradual sodium normalization and symptom resolution.
The case underscores the importance of early fluid balance monitoring and individualized risk assessment in such patients.
Abstract
Background: Hyponatraemia is a rare but potentially life-threatening complication of terlipressin therapy. Case history: In the current case, a 39-year-old female with decompensated liver cirrhosis (Child-Pugh C) and acute variceal bleeding experienced a precipitous decline in serum sodium—from 136 mmol/L to 115 mmol/L—within 48 h of initiating terlipressin therapy. This was accompanied by marked fluid retention, reduced urine output, and symptoms of confusion and agitation. Laboratory tests confirmed dilutional hyponatraemia, characterized by urinary sodium <20 mmol/L and urine osmolality <100 mOsm/kg, indicating excessive free water reabsorption. Outcomes: The prompt discontinuation of terlipressin, fluid restriction and the cautious administration of hypertonic sodium chloride solution (2.7% NaCl) achieved a gradual normalization of sodium levels and resolution of symptoms. Fluid…
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Taxonomy
TopicsElectrolyte and hormonal disorders · Liver Disease and Transplantation · Diet and metabolism studies
