Exercise-associated Hyponatremia

aka  001

Reviewed and revised 17 May 2012

A 30 year-old female was BIBA following a seizure. She was running a marathon in hot weather. Nearing the end, after 5 hours running, she was seen to fall to the ground and had a generalised tonic-clonic seizure. On arrival in the ED she was confused and agitated. Her oral temperature is 36.6 C, her chest is clear with SaO2 98% on air, she appears to have bitten her tongue and she has oedematous ankles.

The following blood test results are available:


Q1. What is the diagnosis and what complications are present?

Exercise-associated hyponatremia complicated by encephalopathy (confusion and seizure). There is also evidence of seizure-induced or exercise-induced rhabdomyolysis and mild renal impairment.

EAH is defined as a serum sodium level below the normal reference range (135 mmol/l) in an individual engaged in prolonged physical activity (generally >4 hours), or within 24 hours of it ending.

Q2. What are the risk factors for this condition?

Risk factors for exercise-associated hyponatremia may include:

  • low body weight
  • prolonged exercise
  • slow speed of running associated with ease of drinking
  • access to fluids
  • NSAID use
  • female sex

Q3. What is the cause?

Exercise-associated hyponatremia is caused by the excessive intake of hypotonic fluid during prolonged exercise, resulting in dilutional hyponatremia with an increase in total body water.

Other factors may also play a role:

  • Inadequate antidiuretic hormone (ADH) suppression
    (due to factors such as exertion, nausea, vomiting, exertional hypovolemia, pain and thermal stress)
  • failure to mobilize osmotically inactive extracellular sodium stores
    (e.g. in bone)

Q4. Describe the spectrum of clinical manifestations of this condition.

Exercise-associated hyponatremia may have:

  • no symptoms
  • mild symptoms — e.g. bloating, weakness, dizziness, headache, nausea and/ or vomiting
  • severe symptoms — acute pulmonary oedema and/ or encephalopathy (confusion, seizures, coma)
  • Death can occur.

Q5. How would you manage this patient?

A reasonable management plan would include:

  • Resuscitation — attend to ABCDEFG (don’t ever forget glucose) and vital signs.
  • Secondary survey to check for evidence of injury secondary to fall/ seizure.
  • Supportive treatment and monitoring.
  • Fluid restriction to correct dilutional hyponatremia, but ensure adequate urine output to avoid renal failure secondary to rhabdomyolysis. Be aware that unabsorbed hypotonic fluids in the GI tract can lead to further dilutional hyponatremia.
  • Consider hypertonic saline (see Q6).
  • Referral to HDU/ ICU level care for ongoing monitoring in severe cases such as this.

Q6. Is the administration of hypertonic saline indicated? What are the indications?


Most authorities consider the following as indications for hypertonic saline in the treatment of exercise-associated hyponatremia:

  • severe hyponatremia (Na <120 mmol/L)
  • significantly symptomatic (e.g. vomiting, encephalopathy or acute pulmonary oedema)

Most authorities advocate 3% hypertonic saline given at 1 to 2 ml/kg/h.

  • This may be increased to 3-4 mL/kg/h if urine output is inadequate.
  • The infusion rate can be decreased following significant water diuresis.
  • Infusion should be stopped when the patient is asymptomatic with a normal level of consciousness.
  • Serum electrolytes need to be closely monitored (e.g. hourly initially).

There are no reports of cerebral pontine myelinoysis resulting from over-vigorous treatment of  exercise-associated hyponatremia (an acute process) with hypertonic saline.

Q7. How can this condition be prevented?

Don’t drink too much!

Athletes should drink only according to thirst (generally no more than 400 to 800 ml/h).

Some authorities recommend estimating sweat loss by serial weight measurements during prolonged exercise, but this is impractical in most situations. There is no good evidence for adding salt to fluids or for commercial sport drinks (which are generally hypotonic).

References and links


Journal Articles and Textbooks

  • O’Connor RE. Exercise-induced hyponatremia: causes, risks, prevention, and management. Cleve Clin J Med. 2006 Sep;73 Suppl 3:S13-8. Review. PubMed PMID: 16970148. (fulltext)
  • Rogers IR, Hew-Butler T. Exercise-associated hyponatremia: overzealous fluid consumption. Wilderness Environ Med. 2009 Summer;20(2):139-43. PMID: 19594207 (fulltext)
  • Rosner MH, Kirven J.  Exercise-associated hyponatremia. 2007 Jan;2(1):151-61. PMID:17699400 (fulltext)
  • Rothwell SP, Rosengren DJ. Severe exercise-associated hyponatremia on the Kokoda Trail, Papua New Guinea. Wilderness Environ Med. 2008 Spring;19(1):42-4. PMID 18333641

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  1. Glenn Rogers says

    This great piece has relevance to a practice of mine, which is to drink large amounts of water whenever it is available while on arduous backpacking trips. We don’t like to pack water (because it’s heavy!) and when we come across a stream we often drink a half liter or more beyond what our thirst dictates, reasoning that if we don’t run across more water for a long time we will be able to hold out better for having diluted the metabolic wastes in our bloodstream. I suppose I should reconsider this practice. Also, this relates to another question I’ve often wondered about: to what extent can a person improve their apparent eGFR by forcing fluids before they have their blood drawn? Often when one of my patients has an elevated creatinine that was unexpected, I will ask them to repeat the test after drinking a couple of extra glasses of water the day before (maybe they were just dehydrated.) Sometimes the second test is normal. But if a patient got overzealous and drank 4 or 8 extra glasses of water, could they thereby mask true CRF? Any thoughts you have will be greatly appreciated. Great site by the way--I just discovered it.

    Glenn Rogers, MD