This 35 year old athlete developed a generalized tonic-clonic convulsion following prolonged exertion. Was this a syncopal convulsion or a frank seizure ? While at first glance a syncopal episode seems to be more likely, a closer perusal of the history reveals several facts favoring a seizure. Syncopal convulsions rarely last more than 30 seconds, while tongue bites are generally uncommon. In addition, the drowsiness and confusion are suggestive of a postictal state. While a myriad of conditions may give rise to a seizure, the peculiar circumstances of presentation (including the fact that this individual was healthy enough to run for several hours continuously) significantly narrows down the differentials to heat stroke, hemorrhagic stroke, and acute metabolic disturbances such as hypoglycemia, lactic acidosis, or exercise associated hyponatremia. In addition, the possibility that this might be the first episode of new onset epilepsy should also be kept in mind. Note that rhabdomyolysis is another important cause of collapse following vigorous exercise. However, this does not usually result in convulsions. His normal core temperature and absence of a hyperdynamic state rule out heatstroke, the normal random plasma glucose excludes hypoglycemia, and the normal arterial blood gas assay rules out lactic acidosis. The absence of meningism and focal neurological signs are points against a hemorrhagic stroke - this is confirmed by the CT scan, which shows cerebral edema only. The serum electrolyte assay proves to be fruitful by demonstrating severe hyponatremia, establishing exercise induced hyponatremia as the probable diagnosis. Note that the cerebral edema and history of a seizure indicate that hyponatremic encephalopathy is present. While an EEG is recommended in all patients with new-onset seizures, this should only be performed emergently if nonconvulsive or subtle convulsive status epilepticus is suspected. In view of the life threatening hyponatremia, treatment with hypertonic saline should be commenced. Fluid restriction is also essential. DVT prophylaxis is indicated in all critically ill patients. IV 50% glucose is not indicated, as he is euglycemic.
Exercise associated hyponatremia (EAH) is defined as a serum sodium level of less than 135 mEq/L following high-intensity endurance activities such as marathons and triathlons. It is a potentially devastating condition that can occur in otherwise healthy, young individuals. Due to the increasing popularity of high intensity endurance activities, EAH has become the most common medical complication associated with ultra distance exercise. In several (small scale) studies conducted on endurance athletes, the incidence ranged from 13% to 29%, although the majority of individuals were asymptomatic or only mildly symptomatic. The hyponatremia of EAH appears to be mainly dilutional, with the main contributory mechanism being ingestion of hypotonic fluids (such as water or sports drinks) in excess of sweat, urinary and insensible losses. It should be particularly noted that many athletes drink an excess amount of water or sports drinks before and during the race in order to keep themselves hydrated, potentially overwhelming the renal excretory capacity. In addition, while over drinking appears to be the primary causative factor, there is also an important contribution of sodium loss from sweating. Risk factors for EAH include a low body weight, a slow running pace, race inexperience, use of NSAIDS, and extreme environmental conditions. In addition, female athletes are at a higher risk of developing EAH. The clinical manifestations of EAH are secondary to the hyponatremia. In this respect, the degree of symptomaticity is related not to the absolute level of serum sodium, but to the rate and extent of the drop in extracellular tonicity. The majority of patients are completely asymptomatic, or only mildly symptomatic, experiencing weakness, dizziness, headache, nausea or vomiting. In severe EAH, the acute severe hyponatremia results in cerebral edema, causing altered mental status, seizures, coma, and even death. In addition, these patients may also develop varying degrees of pulmonary edema. The management of EAH depends both upon the serum sodium level as well as the severity of symptoms. Asymptomatic patients usually requires only fluid restriction and observation until spontaneous diuresis occurs. In mildly symptomatic patients, oral rehydration with salty solutions is often the safest method of increasing the serum sodium level and improving symptoms. In patients with severe hyponatremia (< 120 mmol/l), pulmonary edema or encephalopathy, hypertonic (3%) saline should be administered, aiming to increase the serum sodium concentration by 2 mEq/L/hour until symptoms resolve. It is mandatory to manage these patients in a critical care setting. Note that over rapid correction of hyponatremia may result in central pontine myelinolysis. The best strategy for prevention of EAH is to educate athletes about the risks of fluid over consumption and the importance of maintaining the proper volume in order to ensure fluid balance during exercise. Generally, it has been suggested that fluid intake should be determined by thirst and that the maximum fluid intake should be between 400 and 800 mL/h. The main cause of death in these patients is severe cerebral edema causing brainstem herniation and mechanical compression of vital midbrain structures.