Endocrine Abstracts

Case report: A 40-year old male with a background history of autism, severe learning difficulties and childhood Hirschsprung’s disease had been on long-term lithium carbonate therapy, without any history of polyuria or polydipsia. During admission he underwent a subtotal colectomy for malignant colonic polyps. Pre-operative serum urea and electrolytes, glucose and lithium levels were normal. Pre-operative fluid balance was normal. The post-operative period was turbulent; he required a repeat laparotomy to washout an intra-abdominal collection and was transferred to the intensive care unit. At this stage, urine output rose to six litres per day, serum sodium 165(135–145) mmol/l, serum potassium 2.9(3.5–5.0) mmol/l, urea 4.1(2.5–7.0) mmol/l and creatinine 129(50–130) umol/l. Further investigations revealed plasma osmolality of 341(288–298) mosmol, urine osmolality 141(250–750) mosmol and urine sodium of 7(50–125) mmol/l. Although nephrogenic diabetes insipidus was suspected, a water deprivation test was impossible because of his poor clinical state. Lithium was stopped and desmopressin was commenced at 750 mcg/day. Urine output increased to approximately 20 litres per day. Desmopressin was gradually titrated up to 3 mg. His serum sodium dropped to 140 mmol/l but urine output remained between 8 to 9 litres per day. He was commenced on amiloride (5 mg daily), indomethacin (50 mg tds) and hydrochlorothiazide (2.5 mg daily). His condition improved, serum sodium stayed at around 140 mmol/l and daily urine output decreased to 1.8 litres. Desmopressin and indomethacin were stopped. He was discharged on amiloride (5 mg daily) and bendrofluazide (2.5 mg daily).

Comments: Lithium is known to cause nephrogenic diabetes insipidus. In patients on lithium treatment post-operative precipitation of nephrogenic diabetes insipidus is not a common phenomenon, although it has been previously reported. Temporary cessation of lithium should be considered during hypovolaemic states.