Endocrine Abstracts

Case History: An 83-year-old male patient was admitted with coffee ground vomiting. He had no associated melaena, abdominal pain or previous episodes of vomiting. He was on apixaban and bisoprolol for his hypertension and atrial fibrillation. He did not smoke and only drank alcohol occasionally. The patient underwent endoscopy and was found to have variceal bleeding and had band ligation. He was started on terlipressin and pantoprazole. He was referred to endocrine for ongoing persistent hyponatraemia (122 mmol/mol) with fluctuating confusion.

Investigations: His sodium level on admission was 136 mmol/mol. When examined, he was alert and oriented, and did not appear to be confused. He was euvolaemic on examination with BP of 126/81 mmHg and no postural drop. He was eating and drinking well. He was passing sufficient amount of urine (0.5 ml/kg/hour). He had no ascites or peripheral oedema. He had a normal chest X-ray. Hypothyroidism and adrenal insufficiency were excluded. His paired serum osmolality and urine osmolality were 248 mOsml/kg and 540 mOsmol/Kk respectively. His urinary sodium was 70 mmol/l.

Results and Treatment: In this instant, medications were the first potential reason causing his hyponatraemia. We replaced his IV pantoprazole with oral famotidine after discussing with his endoscopist. Fluid restriction to 1.5l was advised. However, his hyponatraemia continued to worsen (114 mmol/mol) (Table 1). Due to his recent variceal bleeding, terlipressin was not discontinued initially. Terlipressin can be given up to 5 days after oesophageal bleeding. However, in view of his persistent hyponatraemia, it was stopped after discussing with his team. Consequently, this led to a gradual improvement in his sodium levels to 132 mmol/mol.Table 1.

Conclusions and points for discussion: Apart from V1 receptors, Terlipressin has substantial affinity for V2 receptors which can lead to increased water reabsorption in the renal collecting tubules leading to dilutional hyponatraemia. I think this case would have been particularly challenging if the patient already had underlying hypervolaemic hyponatraemia because of decompensated liver cirrhosis and in addition required terlipressin treatment for his variceal bleeding. As a result of this, monitoring of sodium is required when patients are treated with terlipressin.