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Sports Medicine

Exercise-Associated Hyponatremia

Exercise-associated hyponatremia (EAH) is defined as a serum sodium level below 135 mmol/L that develops during or up to 24 hours after physical activity. This activity reviews the epidemiology, pathophysiology, evaluation, management, and prevention of exercise-associated hyponatremia (EAH) and the role of the interprofessional team and athletic event staff in recognizing, managing, and educating athletes with this condition. Objectives: Describe the epidemiology and pathophysiology of EAH. Out

v1 · Reviewed Nov 7, 2026 by Automated Clinical Reviewer (Strict Verbatim v1)
  • Prompt differentiation of EAH from other exertional illnesses is critical, as isotonic fluid administration that may be given for other exertional diagnoses can worsen EAH, resulting in life-threatening sequelae of hyponatremia.
  • Athletes, coaches, healthcare providers, and athletic event staff must be educated on EAH prevention strategies and presenting symptoms to decrease athletes’ risk of development and progression to hyponatremic encephalopathy, coma, or death.
  • Severe symptoms include vomiting, oliguria or anuria, altered mental status, collapse, seizure, coma, and death during sport or soon after.
  • Differentiating EAH from exercise heat illness and dehydration is critical, as isotonic fluid administration that would be given for the empiric treatment of either heat illness or dehydration could be life-threatening if the true diagnosis is EAH.
  • Patients with severe EAH may demonstrate altered sensorium ranging from inattentiveness to complete obtundation, loss of sweating, hypotension, and abnormal limb movements.
  • Initial evaluation of suspected EAH includes vital signs, determination of mental status via the Glasgow coma scale, and assessment of airway patency, adequate respiration, and intact circulation.
  • Accurate core temperature is key and should be taken rectally if possible to differentiate from heat illness.
  • The serum sodium should be determined if point-of-care (POC) serum sodium testing is available
  • A history supporting excessive hypotonic fluid intake and prolonged exertion should be taken if the patient can participate in an interview or a coach, teammate, partner, or another witness is available.
  • A serum sodium level of less than 135 mmol/L with accompanying excessive fluid intake history is diagnostic for EAH.
  • The serum glucose should also be determined if POC glucose testing is available, as hypoglycemia can present similarly.
  • On transfer to the hospital for advanced care, patients with suspected EAH should have immediate measurement of serum sodium and other electrolytes.
Glasgow Coma Scale
determination of mental status via the Glasgow coma scale
  • EAH is treated with fluid restriction or sodium replacement, depending upon severity.
  • If a patient does not demonstrate neurologic symptoms, EAH is considered mild, and the patient is eligible for oral fluid restriction.
  • Patients restrict their total fluid intake to induce osmotic ADH suppression and, therefore, free water excretion.
  • Patients may also be given concentrated oral sodium repletion, though this may be poorly tolerated due to taste or nausea and vomiting.
  • Proposed regimens include 100 ml of hypertonic saline, 3 or 4 broth bouillon cubes in 125 ml of water, or a serving of salted pretzels.
  • Oral hypertonic saline is as effective as IV hypertonic saline in mild EAH.
  • IV isotonic fluids of any type or volume are not recommended in mild EAH.
  • EAH is considered severe if a patient demonstrates neurologic symptoms (altered mental status, seizure, coma).
  • The patient should receive a bolus of 100 ml of IV hypertonic saline.
  • This can be repeated every 10 minutes for a total of 3 doses.
  • Athletes with severe hyponatremia or evidence of cerebral edema with neurologic symptoms should be treated with a bolus of hypertonic saline as described above, with a goal serum sodium increase of 4-5 mmol/L and reversal of neurologic symptoms.
  • EAH falls on the spectrum of exertional injuries. The differential diagnosis for exertional injuries includes heat exhaustion, heatstroke, exercise-associated collapse, and exertional collapse associated with sickle cell trait (ECAST).
  • Providers caring for athletes must also consider hypovolemia, hypoglycemia, sudden cardiac arrhythmia (Wolff-Parkinson-White syndrome, prolonged QT syndrome, channelopathy), hypertrophic cardiomyopathy, sudden cardiac death of unknown cause, seizure, vasovagal syncope, and malingering.
  • Noncardiogenic pulmonary edema may also develop secondary to osmotic dysregulation in EAH, leading to respiratory distress and the need for respiratory support.
  • Rapid correction of hyponatremia may result in central pontine demyelination, a catastrophic and permanent demyelinating event that presents with neurologic deficits despite correction of the serum sodium.
  • If EAH is diagnosed mistakenly in the presence of true dehydration or heat stroke, treatment with hypertonic fluids, fluid restriction, and lack of cooling may cause further harm to the patient.
  • The majority of athletes recover from acute mild EAH within hours in the emergency care setting and do not require hospital admission.
  • The duration of the emergency room stay after treatment with either oral or IV hypertonic saline solution has been reported between 50 and 79 minutes.
  • Severe EAH requires ward or ICU admission depending upon institutional criteria.
  • Patients who develop exercise-associated hyponatremia encephalopathy risk significant morbidity and mortality secondary to cerebral damage from cerebral edema; the exact mortality rate is unknown.
  • The major complications of EAH and its treatment include exercise-associated hyponatremic encephalopathy (EAHE), noncardiogenic pulmonary edema, central pontine myelinolysis, and improper treatment resulting from an alternate diagnosis.
  • If left untreated, mild EAH can progress to severe EAH with profoundly altered mental status, seizure, and coma—an end-stage finding due to cerebral edema termed EAHE.
  • The treatment for EAHE is a prompt correction of serum sodium with hypertonic saline and supportive care for its sequelae (respiratory support, seizure management).
  • EAH can be prevented by avoiding overhydration, ensuring adequate oral sodium intake, and educating athletes, event staff, and healthcare providers on the prevention strategies and presenting symptoms.
  • review
    Exercise-Associated Hyponatremia. StatPearls [Internet] — Emily Buck, Rebecca McAllister, Jeremy D. Schroeder — StatPearls Publishing, 2023

Decision support only. Verify against local protocols and current labeling. Source: www.ncbi.nlm.nih.gov