With increasing participation in marathons and triathalon events, medical complications of endurance athletic events are being increasingly reported. Hyponatremia is not uncommon in this setting. We report a case of hyponatremia in a marathon runner that led to encephalopathy and death.
A 35 year-old 1st time marathoner collapsed at mile 21 of the 2002 Marine Corps Marathon in Washington, DC. She had complained to her family of headache and blurry vision around mile 19. She was treated in the field with 0.9% saline for presumed dehydration, but there was a 2-hour delay in transporting her. Within 30 minutes after arrival in the ER, her mental status deteriorated quickly. She also developed cardiac arrhythmias and her oxygenation worsened, requiring intubation and mechanical ventilation. Her initial CXR demonstrated pulmonary edema. By 2.5 hours after collapse, her right pupil was dilated and fixed. She was immediately sent for computed tomography (CT) of her brain; this demonstrated diffuse cerbral edema with mid-line shift, effacement of the gyri/sulci, and compression of the 4th ventricle. On transfer back from CT, her left pupil became dilated and fixed. She had no gag or corneal reflexes by this point. A ventriculostomy was performed, returning clear CSF with an elevated pressure. Her initial labs came back, demonstrating a serum sodium of 123 meq/L. She was begun on 3% saline for symptomatic hyponatremia, but the rate was decreased when her repeat labs demonstrated a serum sodium of 128 meq/L. Her urine output increased markedly, and her urine osmolarity was low. Within an hour, repeat labs demonstrated a serum sodium of 131 meq/L and the 3% saline was discontinued. She never regained any brain stem function, brain CT scans showed worsening edema and shift with impending herniation, and she failed an apnea test. She was declared brain dead within 24 hours of admission.DISCUSSION: Hyponatremia following endurance events is not uncommon. 9% of participants in the 1996 New Zealand Ironman sought medical care, as did 29% in the Hawaiian Ironman. In 1998, 605 athletes in the New Zealand Ironman were studied. 330 finished the race and 58 had a serum sodium level < 135 meq/L, but only 18 sought medical attention. Premenopausal women appear to be more commonly affected perhaps because estrogen influences osmoregulation via oxytocin, augmenting anti-diuretic hormone (ADH) secretion. Excessive fluid intake may contribute, but hyponatremia has resulted despite only modest fluid intake. Exercise leads to loss of water and salt via sweat, resulting in decreased plasma volume. Baroreceptor activity due to decreased plasma volume results in ADH release, and effects plasma volume via thirst and other mechanisms. Volume contraction stimulates the release of atrial naturietic factor (ANF); causing loss of free water and sodium in the urine. Intake of water or another hypotonic rehydration solution exacerbates the hyponatremia. Intestinal fluid absorption increases on cessation of activity, with redistribution of blood flow to the splanchnic circulation. Furthermore, free water clearance is limited by the maximum glomerular filtration rate. Carbohydrate loading, common before endurance events, may worsen the problem via increased free water production from glycogenolysis. The quick increase in serum sodium in our patient likely reflects diabetes insipidus following brain death.CONCLUSIONS: Exercise induced hyponatremia is more common than generally realized. Medical personnel staffing such events should be aware of this potentially fatal complication of endurance exercise and should be trained in its recognition and management. This may include weighing participants before the event, proper equipment for detecting hyponatremia, and appropriate fluid administration. Athletes should be educated about this entity and be made aware of the risks of overhydration and carbohydrate loading.
A.J. Wolff, None.