Endocrine Abstracts

Hyponatraemia is the most common electrolyte abnormality encountered in clinical practice and second most common endocrine referral. Acute severe hyponatremia is potentially life-threatening and must be treated promptly and aggressively. SIADH, Cortisol deficiency, Liver Disease, Heart disease, certain medications and excess alcohol intake can frequently lead to hyponatremia. We present a case of 41 year old male known to have alcoholic liver disease and depression who presented to Emergency department with hematemesis, epistaxis and drowsiness. Clinical history suggested increased alcohol intake, decreased oral fluid intake and recently increased dose of risperidone. On assessment, vital signs were normal with Fluctuating GCS, ascites on abdominal examination and clinically dehydrated with decreased urine output and dry mucous membrane. Investigations revealed low serum sodium of 99 mmol/l, normal potassium: 4.2 mmol/l, hemaglobulin: 89g/l, creatinine: 38, Albumin: 24g/dl, normal thyroid function test and blood glucose. Serum and urine osmolality”s and cortisol were not available in acute setting. Initially patient was fluid restricted to 750 ml/day in view of ascites on clinical examination. ICU and Endocrine review was also sought. Endocrine team deemed hyponatraemia multifactorial with decompensated liver disease, excess alcohol intake, dehydration and antidepressant as contributing causes and considering hypovolemia status advised albumin infusion with careful fluid replacement with 0.9% normal saline and close monitoring of serum sodium and withholding hypertonic saline with the review of reassessing after fluid replacement. Serum sodium improve to 113 mmol/l in 24 hours. Serum and urine osmolality”s done on 7th day of admission reveal serum 283mOsm/kg, urine osmolality: 315mOsm/kg, urine sodium<20mEq/l with serum sodium of 137 mmol/kg. Patient managed as decompensated liver disease under gastroenterology team. While commonly encountered metabolic abnormality, it can sometimes prove difficult to manage especially in acute settings when investigations are not available immediately. Although Current guidelines would support hypertonic saline in in the context of fluctuating GCS it”s usually not straightforward and whilst normal saline worked in this case, Central pontine demyelination risk is much higher particularly in patient with excess alcohol intake. Fluid assessment, treating underlying cause with careful fluid administration remains the mainstay of management.