Endocrine Abstracts

A 30 year old lady attended the Accident and Emergency department (A&E) with vomiting, collapse and confusion several hours after completing her first London Marathon in 5 hours. During the race she kept herself hydrated with water and isotonic fluids and took non-steroidal anti-inflammatory drugs (NSAIDs). On arrival in A&E her Mini Mental Test Score was 0 and Glasgow Coma Scale (GCS) was 11. She was volume replete and haemodynamically stable but confused and restless. Neurological examination did not reveal any lateralising signs. Serum biochemistry showed a sodium of 122 mmol/L (135-145), potassium of 3.7 mmol/L (3.5-5.0), urea of 3.2 mmol/L (2.5-6.6) and creatinine of 59 micromoles/L (60-125). Serum osmolality was 255 mosmol/L (283-295); paired urine osmolality was 275 mosmol/L (100-1000) and urine sodium 54 mmol/L. TSH was 0.95 mU/L (0.35-5.50) and random cortisol 530 nmol/L. A diagnosis of exercise associated hyponatraemia was made. CT brain did not show unequivocal evidence of cerebral oedema. She responded well to intravenous hypertonic (1.8%) saline (HTS) at 75 ml/hour with her serum sodium rising to 130 mmol/L within 3 hours. When reviewed the following morning her GCS had risen to 14 ; by the afternoon she was alert and orientated and able to start eating and drinking normally. She was discharged the following day with a serum sodium of 138 mmol/L and osmolality of 287 mosmol/L. This case highlights the multifactorial aetiology of endurance exercise associated hyponatraemia, including the syndrome of inappropriate ADH secretion (SIADH) with NSAID potentiation, sodium wasting and excess hypotonic fluid intake, particularly in untrained athletes with slow race times. Severe cases respond well to treatment with HTS.