Article, Emergency Medicine

A near-fatal case of exercise-associated hyponatremia

Case Report

Contents lists available at ScienceDirect

American Journal of Emergency Medicine

journal homepage: locate/ ajem

A near-fatal case of exercise-associated hyponatremia

Abstract

A 42-year-old woman presented to our emergency department with headache, nausea, and confusion after completing an Ironman triathlon. She performed the race at a slow pace, in hot and dry weather. The first medical examination reported confusion with a Glasgow Coma Scale score of 13. A few minutes later, she presented with seizures. A cerebral computed tomographic (CT) scan showed major cerebral edema. blood analysis showed severe acute hypona- tremia (123 mEq/L) with hypotonicity (255 mEq/L). Her clinical condition quickly worsened, leading to a Glasgow Coma Scale score of 3 with fixed dilated pupils. After intubation and mechanical ventila- tion, she was transferred to the intensive care unit. A transcranial Doppler ultrasonography (TCD) showed Intracranial hypertension signs motivating emergency osmotherapy by infusion of 20% mannitol over 15 minutes. To guide the therapeutics, an intracranial pressure monitoring was inserted, showing a value of 30 mm Hg. A few minutes later, intracranial pressure increased to 68 mm Hg with a low cerebral perfusion pressure. Concomitantly, another TCD reported critical flows with poor cerebral perfusion. A second infusion of mannitol led to an ICP lowering and a decrease in pupil size after 10 minutes. During the next hours, the patient stayed stable without further intervention. Sixteen hours later, natremia was normal, mainly due to hyperdiuresis. On day 2, the tracheal tube was removed. A cerebral CT scan showed disappearance of cerebral edema. One month later, the patient had good recovery apart from some residual memory problems. Six months later, she was able to come back to work.

In June 2012, a 42-year-old woman presented to our emergency department with headache, nausea, and confusion after completing an Ironman triathlon. There was no notable illness on her medical history. She performed the race at a slow pace, in hot and dry weather. We had no information on a possible weight gain during the race and on the fluid consumption. The first medical examination reported confusion with a Glasgow Coma Scale score of 13. A few minutes later, she presented with seizures. A cerebral computed tomographic (CT) scan showed major cerebral edema. Blood analysis showed severe acute hyponatremia (123 mEq/L) with hypotonicity (255 mEq/L). Her clinical condition quickly worsened leading to a Glasgow Coma Scale score of 3 with fixed dilated pupils. After intubation and mechanical ventilation, she was transferred to the intensive care unit (ICU). A transcranial Doppler ultrasonography (TCD) (Fig. 1) showed intracranial hypertension signs motivating emergency osmotherapy by infusion of 20% mannitol over 15 minutes. To guide the therapeutics, an Intracranial pressure monitoring was inserted, showing a value of 30 mm Hg (normal, b 15 mm Hg). A few minutes later, ICP increased to 68 mm Hg with a low cerebral perfusion pressure. Concomitantly, another TCD reported

critical flows with poor cerebral perfusion (Fig. 2). A second infusion of mannitol led to an ICP lowering and a decrease in pupil size after 10 minutes. During the next hours, the patient stayed stable without further intervention. Sixteen hours later, natremia was normal, mainly due to hyperdiuresis. On day 2, the tracheal tube was removed. A cerebral CT scan showed disappearance of cerebral edema. One month later, the patient had good recovery apart from some residual memory problems. Six months later, she was able to come back to work.

Exercise-associated hyponatremia is defined by an acute sodium low value less than 135 mEq/L during or within the next 24 hours after a prolonged physical activity [1]. During the 2002 Boston Marathon, the reported incidence was 13% [2]. In collapsed runners, it is 6 times less frequent than hypernatremia [3]. Most of the time, patients are asymptomatic. In symptomatic patients, severity of signs is correlated to level of hyponatremia. Nonspecific neurologic symptoms are fatigability, confusion, seizures, and eventually, coma. Abdominal signs are frequent such as pain, nausea, and vomiting. Typical presentation is an afebrile patient with nonspecific neurologic and abdominal symptoms after a prolonged exercise. Most of the time, prognosis is good, but some deaths have been reported. The pathophysi- ology is mainly a dilutional hyponatremia due to an excessive fluid consumption compared with body fluid losses, with sodium depletion in sweat [4]. A nonmaximally suppressed arginine vasopressin secretion by painful conditions and inflammatory status during exercise can lead to a decreased free water clearance. Identified risk factors are female sex, nonsteroidal anti-inflammatory drug and diuretic use, cold or hot weather, duration and intensity of the physical activity, excessive fluid intake, and weight gain during the exercise. Usually, asymptom- atic hyponatremia does not require treatment, as spontaneous hyperdiuresis should correct the trouble. If patients exhibit hyponatremic encephalopathy, oral intake of concentrated broth or intravenous infusion of hypertonic fluid is recommended.

Fig. 1. Transcranial ultrasonography showing signs of intracranial hypertension on admission in ICU.

0735-6757/(C) 2014

Fig. 2. Poor cerebral perfusion with low diastolic flows a few minutes later.

Most severe cases require on field Bolus infusion of 3% sodium chloride [5]. Centropontine myelinolysis is a rare complication as almost all exercise-associated hyponatremias represent an acute disorder.

Exercise-associated hyponatremia is still an underdiagnosed complication of endurance sports. In the most severe cases, aggressive management allows complete Neurologic recovery.

Mathilde Severac Jean-Christophe Orban, MD, PhD Intensive Care Unit, Saint-Roch Hospital

Nice University Hospital

Nice, France E-mail address: [email protected]

Thibaut Leplatois, MD

Emergency Department, Saint-Roch Hospital

Nice University Hospital

Nice, France

Carole Ichai, MD, PhD

Intensive Care Unit, Saint-Roch Hospital

Nice University Hospital

Nice, France

http://dx.doi.org/10.1016/j.ajem.2013.12.041

References

  1. Hew-Butler T, Ayus JC, Kipps C, et al. Statement of the second international exercise-associated hyponatremia consensus development conference, New Zealand, 2007. Clin J Sport Med 2008;18:111-21.
  2. Almond CS, Shin AY, Fortescue EB, et al. Hyponatremia among runners in the Boston Marathon. N Engl J Med 2005;352:1550-6.
  3. Siegel AJ, d’Hemecourt P, Adner MM, et al. Exertional dysnatremia in collapsed marathon runners: a critical role for Point-of-care testing to guide-appropriate therapy. Am J Clin Pathol 2009:336-40.
  4. Noakes TD, Sharwood K, Speedy D, et al. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci U S A 2005;102: 18550-5.
  5. Rosner MH, Kirven J. Exercise-associated hyponatremia. Clin J Am Soc Nephrol 2007;2:151-61.

Leave a Reply

Your email address will not be published. Required fields are marked *