Guidelines Released for Exercise-Associated Hyponatremia

Diana Phillips

July 03, 2015

The treatment of athletes showing signs of acute hyponatremia should be guided by the severity of neurological symptoms on presentation, rather than by laboratory measures of blood sodium levels, experts recommend.

Acute, severely symptomatic exercise-associated hyponatremia (EAH) is a rapidly progressing emergency caused by overhydration. Untreated, the dangerous fluid imbalance can cause brain herniation, noncardiogenic pulmonary edema, and death, according to a statement developed at this year's Third International Exercise-Associated Hyponatremia Consensus Development Conference.

Although rapid determination of blood sodium level is critical in confirming clinical suspicion of EAH, it may not always be available, note Tamara Hew-Butler, DPM, PhD, from Oakland University in Rochester, Michigan, and colleagues in the statement, published in the July issue of the Clinical Journal of Sport Medicine. Further, treatment should be based on the degree of neurological impairment, and not just blood sodium levels, "as brain edema is dependent upon both the magnitude and rate of fall of [sodium levels in the blood,] not just the lowest level reached," they write.

"Any athlete with EAH associated with signs or symptoms of encephalopathy should be immediately treated with an [intravenous (IV)] bolus or infusion of [hypertonic saline (HTS)] to acutely reduce brain edema, with additional IV boluses administered until there is clinical improvement," the authors state. They note that "the dose and route of HTS administration should be based upon the severity of clinical symptoms and the available HTS formulations."

The goal of the IV HTS therapy is to stabilize the athlete for transfer to an advanced medical care facility. "Ideally, the athlete should be transported with knowledgeable event medical personnel able to maintain the same level of care en route and to ensure that the treatment is not interrupted for evaluation such as computerized tomography (CT) imaging of the brain or treatments that may worsen hyponatremia, such as administration of hypotonic fluids, lactated Ringer's, or isotonic (normal) saline," the authors stress.

Whether at the athletic event site or at presentation or transfer to a medical facility, diagnostic testing "should not delay potentially life-saving therapy with HTS," the authors write.

The use of IV HTS as the definitive treatment for acute hyponatremic encephalopathy is well validated, the authors write, noting that the IV HTS bolus is able to increase serum sodium levels 2 to 5 mmol/L, which decreases intracranial pressure and reduces symptoms. Importantly, if the diagnosis of EAH is not confirmed, "the administration of HTS in small boluses is not associated with any negative consequences and serves as an excellent volume expander," they write.

The updated consensus statement also addresses EAH risk factors and prevention. The risk factors for developing asymptomatic and symptomatic EAH include:

  • overdrinking water, sports drinks, and other hypotonic beverages;

  • weight gain during exercise;

  • exercise duration of more than 4 hours;

  • event inexperience or inadequate training;

  • slow performance pace;

  • high or low body mass index; and

  • readily available fluids.

To prevent EAH, the authors recommend that endurance athletes be advised to drink when thirsty. "[U]sing the innate thirst mechanism to guide fluid consumption is a strategy that should limit drinking in excess and developing hyponatremia while providing sufficient fluid to prevent excessive dehydration," they write.

Broad educational programs with consistent messages that stress the importance of appropriate hydration practices, the recognition of EAH, and appropriate therapy are warranted, the authors conclude.

One coauthor reported receiving research funding and consulting fees from the food and beverage industry and is currently chair of the Science Advisory Board of the European Hydration Institute. The remaining authors have disclosed no relevant financial relationships.

Clin J Sport Med. 2015;25:303-320. Full text


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