Endocrine Abstracts

Cranial diabetes insipidus in critically ill patient increases the complexity of fluid management. Well patients with cranial diabetes insipidus can drink enough fluid to replace their urine losses driven by their thirst mechanisms. In critically ill patients the thirst response cannot be relied upon. When fluid input is not adequate it results in hypernatremia. Here dextrose, water or hypo-tonic intravenous fluid is used. Complications related to this are high glucose levels, fluid overload and quick correction of hypernatremia. Treatment with desmopressin cause low urine output and anti-diuresis. Frequent monitoring serum sodium, urine osmolality and volume is very important. 39-year-old lady admitted to critical care with major haemorrhage following liver biopsy. Background Germinoma age 15, had a combination of chemotherapy and radiotherapy) craniospinal irradiation) which has left her with pan hypopituitarism with Diabetes insipidus. She takes Desmopressin 100micrograms in afternoon and 200 μg in the evening On admission she had hypotension, low urine output and positive fluid balance while on desmopressin normal dose. The fluid balance further increased and on fifth day, and one desmopressin dose was omitted and evening dose halved to facilitate diuresis. She also had hyponatremia at this stage. Next day, sodium normalised and had negative fluid balance and desmopressin was restarted. On day 7 of admission, she was still in negative fluid balance, but was clinically noted to be overloaded. Her sodium was normal, and frusemide was given for fluid overload. She then had large diuresis and hypernatremia. She was also started on NG feeds mixed in sterile water. As the urine output increased, she was given additional NG water with frequent sodium monitoring. Hydrocortisone was reduced to facilitate free water clearance. She continued to be in negative fluid balance with Na 158 mEq/l and 10% dextrose boluses were given. More strict fluid replacement strategy was employed with NG water and 10% dextrose replaced hourly by monitoring urine output. Sodium normalised and urine output in normal range and desmopressin continued at admission doses on discharge. This case outlines the intricacies in fluid management in CDI patients. The scope for improvement in this specific case is aggressive rationalisation of desmopressin doses, strict monitoring of urine osmolality or urine specific gravity, accurate recording of fluid intake and output and fluid replacement to match urinary losses. This might have to be done every hour.