A 38-year-old woman is brought to the emergency department after a witnessed seizure. Earlier that day, she participated in a high-altitude marathon. She had no symptoms before the race, but toward the end she began to feel severely nauseated. Following the race, she vomited twice and then had a generalized tonic-clonic seizure. She reported no headache. The patient has no significant medical history. Her trainer insists that she had hydrated aggressively before, during, and after the race. He is quite certain that the only medicine she had taken in the past 24 hours was ibuprofen for aches and pains. In the emergency department, she is afebrile, blood pressure is 110/70 mm Hg, pulse is 100/min, and respirations are 18/min. Pulse oximetry is 98% on room air. Pupils are equal and reactive to light. The neck is supple. The patient is quite confused and does not fully cooperate with a neurological examination, but withdraws all 4 extremities to noxious stimuli. Laboratory results are as follows:
| Hemoglobin | 15.5 g/dL |
| Sodium | 116 mEq/L |
| Blood urea nitrogen | 18 mg/dL |
| Creatinine | 1.0 mg/dL |
| Glucose | 72 mg/dL |
Which of the following is the most likely cause of this patient's current condition?
Stimuli for secretion of antidiuretic hormone | |
Osmotic |
|
Nonosmotic |
|
This patient has exercise-associated hyponatremia (EAH), which is a recognized phenomenon that may occur in individuals participating in prolonged exercise (eg, marathons, triathlons). Depending on the degree of hyponatremia, patients may be asymptomatic or mildly symptomatic (eg, lethargy, nausea) or may demonstrate severe symptoms (eg, seizures, profound confusion) that, when present, are indicative of life-threatening hyponatremia.
The largest contributing factor to EAH is the ingestion of large amounts of hypotonic fluid (eg, water, some sports drinks) during and immediately following prolonged exercise. In addition, many individuals with EAH demonstrate temporary inability to excrete appropriately dilute urine (urine osmolality inappropriately remains >100 mOsm/kg H2O), which is consistent with syndrome of inappropriate antidiuretic hormone (SIADH). In these individuals, excessive ADH secretion is triggered by nonosmotic stimuli (eg, exertion, pain, hypoglycemia, nausea) that occur during intense exercise.
Additional risk factors for the development of EAH include female sex, low body weight, and extended duration of exertion. To lower the risk of EAH, individuals participating in prolonged exercise are advised to avoid a "drink-as-much-as-possible" approach and, rather, drink when thirsty.
(Choice A) Hypoxemia caused by rapid ascension to high altitude may lead to high-altitude cerebral edema (HACE). Seizures may occur, but HACE is rare and is usually accompanied by severe headache and concomitant pulmonary edema. Absence of headache and respiratory difficulty in this patient make HACE very unlikely.
(Choice B) Sweat is hypotonic compared to blood. Therefore, a larger amount of fluid than salt is lost to perspiration, which drives the serum sodium concentration toward hypernatremia. Excessive perspiration can indirectly lead to hyponatremia through hypovolemia-induced release of ADH and increased water retention, but this process plays a minor role in the development of EAH.
(Choice D) Nonsteroidal anti-inflammatory drugs (NSAIDs) increase ADH activity, and their use during prolonged exercise may increase the risk of developing EAH. However, NSAID use plays a minor role overall in the development of EAH.
(Choice E) Severe uncorrected hypovolemia may cause hyponatremia but should present with tachycardia and hypotension. This patient's normal blood pressure, mild tachycardia, and reported history of ongoing fluid intake make severe hypovolemia unlikely.
Educational objective:
Exercise-associated hyponatremia occurs due to a combination of excessive fluid intake and nonosmotically mediated release of inappropriately high levels of antidiuretic hormone. In severe cases, patients may experience seizures, profound confusion, and even death.