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The reluctance to accept the evidence may be because it conflicted with the prevalent message of the sports drink industry
Late on the afternoon of 1 June 1981, a 46 year old lady of 49 kg was admitted in a coma to a hospital in Durban, South Africa. Before dawn that day, she had begun the 90 km Comrades marathon foot race in the same city. But 20 km from the finish in Pietermaritzburg, she failed to recognise her husband who had come to assist her. He convinced her to stop running and drove her to the medical facility at the race finish. There she received 2 litres of fluid administered intravenously. This is the logical treatment for the “dehydration” that was then, and continues to be, the expected cause of all complications that occur during prolonged exercise.1 But the treatment did not help.2
Instead, in the car travelling back to Durban, she suffered a grand mal epileptic seizure and lapsed into coma. She was admitted to hospital where blood testing found her serum sodium concentration to be reduced to 115 mmol/l; a chest radiograph indicated the presence of pulmonary oedema, but there was no evidence of cardiac failure. Thus the diagnosis was exercise associated hyponatraemic encephalopathy (EAHE) with neurogenic (non-cardiac) pulmonary oedema, the first such known case. Treated intravenously with 0.9% (normal) saline, her condition improved only very gradually. Her serum sodium returned to the normal range on the fourth day in hospital, and she was discharged from hospital, fully recovered, two days later.
In 1985 her story and another three similar cases were reported in a paper entitled “Water intoxication: a possible complication of endurance exercise”.3 On the basis of the history, the clinical findings, and the estimated sodium and water balance during exercise in …
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