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[Case Report]

Seizure After Exercise in the Heat

Recognizing Life-Threatening Hyponatremia

Scott D. Flinn, MD; Ryan J. Sherer, MD


In Brief: A 20-year-old military recruit suffered a generalized tonic-clonic seizure following 9 hours of moderate activity in a hot, humid environment. He had drunk at least 5.8 L of plain water before the seizure, and laboratory studies revealed that his serum sodium concentration was 113 mmol/L. Overconsumption of fluids during exercise may precipitate acute hyponatremia, a potentially life-threatening medical condition. Prompt correction of serum sodium in acute exertional hyponatremia is important to reduce the risk of permanent neurologic sequelae or death. Recommendations for prevention include ingesting the correct amount of fluid for the activity (the most important method) and consuming adequate salt through diet or beverage.

Exercise-associated hyponatremia is a life-threatening condition that has been described in endurance athletes, Grand Canyon hikers, and military personnel over the past 15 years (1-6). Early hyponatremia symptoms are nonspecific and are similar to the spectrum seen in exertional heat illness (heat exhaustion and heatstroke) (3,5,6).

For this reason, early consideration of hyponatremia is critical for prompt diagnosis and appropriate treatment in an exercising individual who consumes fluids (see commentary "Hyponatremia in Distance Athletes: Pulling The IV on the 'Dehydration Myth'"). This case of a young man who presented with seizures as the first sign of the disorder illustrates the need to keep hyponatremia in the differential diagnosis of patients presenting with symptoms during endurance events.

Case Report

During a hot, midsummer day, a young male military recruit presented to the field aid station with a 1-week history of cough productive of yellow sputum. The trainee had been participating in 9 hours of moderate exertion consisting of hiking 10 km with an 18-kg pack, climbing obstacles, and crawling low over prescribed courses. During the hike he drank 2 to 3 L of water, and at presentation stated that he had drunk at least 5.8 L (6 canteens) of water during the previous 2 to 3 hours, and that he still felt thirsty.

He denied headache, fever, chills, hemoptysis, shortness of breath, and dyspnea on exertion. He had no history of trauma, or of gastrointestinal or genitourinary symptoms. His medical history was unremarkable.

Physical examination. Physical exam revealed a pulse of 88; blood pressure, 122/64 mm Hg; respirations, 12 per minute; and an oral temperature of 97.5°F (36.3°C). The patient was alert and oriented and not in any apparent distress. Postnasal drip was noted in the posterior pharynx. An occasional irregular heart beat without any murmur was detected. Auscultation of the lungs revealed bibasilar rales and wheezes. No signs of peripheral edema were present. The patient was then directed to the medical clinic from the field aid station for further evaluation and treatment of probable pneumonia.

While the patient was waiting for evaluation at the clinic, he slid to the floor and had a generalized tonic-clonic seizure that lasted approximately 2 minutes. After the seizure, he was oriented only to person and his location. He was given 4 L of oxygen via nasal cannula. Cardiac monitoring showed a normal sinus rhythm. Fingerstick glucose was 115 mg/dL. Blood samples were drawn and an intravenous (IV) line was started to infuse normal saline and to provide IV access for medication. Paramedics arrived and transported the patient to the hospital emergency department. While en route, the recruit had another generalized tonic-clonic seizure and was given 5 mg IV diazepam. He had no subsequent seizures.

Laboratory studies. Initial blood samples taken after the first seizure were evaluated on arrival in the emergency department and revealed a glucose level of 120 mg/dL and a sodium concentration of 113 mmol/L. Other blood chemistry measurements were within normal limits. Normal saline infusion was discontinued, 3% saline begun, and IV furosemide (40 mg) and IV ceftriaxone (2 g) were administered.

Other laboratory studies obtained in the emergency department revealed the following: white blood cell count, 12,300/mm3 with a differential of 82% neutrophils, 14% lymphocytes, and 4% monocytes; hemoglobin, 11.3 mg/dL; and hematocrit, 34.4%. Urinalysis showed a specific gravity of 1.030, trace blood, 30 mg/dL protein, 5 to 10 white blood cells per high power field, and 1 to 3 red blood cells per high power field.

Lumbar puncture revealed clear fluid with a normal opening pressure, no cells, negative Gram stain, glucose level of 79 mg/dL, and protein concentration of 37 mg/dL. Blood cultures were obtained and results showed no growth of bacteria and fungi. Electrocardiography showed a normal sinus rhythm without ectopy. A chest x-ray revealed a right lower lobe infiltrate.

Treatment. On transfer to the intensive care unit (ICU), the patient's mental status returned to normal. Initially, 500 mL of normal saline had been infused. In calculating the required sodium dosage to elevate the plasma sodium, the desired dosage for this patient (72 kg) was determined to be 10 mmol/L * 43.2 L = 432 mmol = 840 mL 3% sodium chloride. During the next 9 hours, 900 mL of 3% sodium chloride was infused (539 mmol total of sodium ions from normal and 3% saline), and his plasma sodium rose to 123 mmol/L. Unfortunately, urine electrolytes were not assessed. The IV fluids were then switched to half-normal saline, and the plasma sodium normalized over the next 18 hours.

During the first 14 hours after admission to the ICU, the patient's total urine output exceeded total fluid input by 6.55 L, indicating profound overhydration. On hospital day 2, he was transferred to the ward, and discharged on day 5 with oral antibiotics and returned to complete recruit training. Discharge diagnosis was severe hyponatremia, seizures secondary to hyponatremia, and right lower-lobe pneumonia.


This case of symptomatic hyponatremia occurred during the first 9 hours of a training day that included a 10-km hike starting at 4:00 am. The day was extremely hot and humid (95°F [35°C] and 88% humidity). During the period that this incident occurred, drill leaders strongly encouraged recruits to drink plain water to prevent exertional heat injury. The recruits were also calorie restricted during this exercise, a fact that limited their salt intake. Additionally, this trainee, as is the case with other athletes, was highly motivated to complete the event and may have minimized any symptoms he was experiencing before his seizure. Rales and wheezes heard by physicians were thought to be due to pneumonia rather than fluid overload since the recruit did not have swollen hands or other signs of peripheral edema. Patient history revealed excessive plain water intake, sodium loss from sweat, and no sodium replacement.

Heat injury. Exertional heat illness is a spectrum of physiologic injury to organ systems that ranges from mild (heat exhaustion) to severe (heatstroke). Patients with heat exhaustion exhibit mild changes in mental status and function. Those with heat injury show evidence of organ injury such as elevated liver enzymes, and heatstroke patients manifest obvious mental status changes and more severe organ injury, for example renal insufficiency. Heatstroke can occur at core temperatures as low as 102°F to 103°F (38.9°C-39.4°C), but temperatures as high as 106°F to 107°F (41.1°C-41.7°C) may not produce heatstroke. The degree of end-organ injury should be used to classify exertional heat illness, rather than the core temperature alone.

Acute exertional hyponatremia. Acute exertional hyponatremia has been reported in endurance events lasting more than 4 hours, including marathons, military training, triathlons, and hikes (1-6). Although the symptoms overlap those of heat injury, hyponatremia is distinguishable by the serum sodium level. Four possible factors contribute to hyponatremia: overconsumption and retention of fluids, loss of sodium in the sweat, decreased sodium intake, and third spacing of salt into the unabsorbed water in the gut (2,5,7). The rapid intake of large quantities of fluids appears to be the major cause and results in a lowering of plasma sodium concentrations to dangerous levels. It appears that the kidneys preferentially try to maintain the intravascular volume and retain free water despite decreasing plasma sodium levels, though the mechanism for this phenomenon is unclear (2,5,7,8). Investigators (1,2,5) have reported cases in which patients appear hypovolemic, euvolemic, or hypervolemic, and a disorder at the renal tubular level has been suggested as the cause for some patients.

Because heat injury and acute exertional hyponatremia often present with headache, nausea, emesis, and mental confusion, symptom nonspecificity can result in delay of diagnosis (3,5,6). As hyponatremia worsens, seizures, coma, and death may ensue. Occasionally, seizures may be the first sign of hyponatremia.

Salt loss. Sweat loss is unlikely a major contributor to onset. If one considers a modest sweat rate of 1.0 L/hr for 9 hours, a sweat sodium concentration of one quarter that of normal saline (about 40 mmol/L), and an extracellular fluid compartment (ECF) of 13 L with no total body compensation, there would be a drop in serum sodium to 112 mmol/L by the end of that time. (The calculation: Assume 13 L ECF at 140 mmol/L; 1,820 mmol of sodium in ECF - 360 mmol lost in sweat = 1,460 mmol/13 L = 112 mmol/L.) This calculation would predict that almost every athlete who exercised would become profoundly hyponatremic.

Conversely, if we allow for equilibration and total body distribution of the salt throughout with a total body fluid of 43.2 L, no hyponatremia would be seen. (The calculation: Total body sodium = 6,048 mmol - 360 mmol [sweat loss] = 5,688 mmol/43.2 L = 132 mmol/L.) Neither of these situations applies, so it would appear the salt loss from sweat has little effect on hyponatremia onset. There is a redistribution of sodium and fluids throughout the body, and it is interesting that the sodium level in this case (113 mmol/L) is exactly that predicted by Noakes (2) and Irving et al (7) for a patient with a 6-L fluid overload.

Chronic salt deprivation may lead to decreased total body sodium and may predispose athletes for hyponatremia when they overhydrate. Also, loss of sodium into the unabsorbed water in the gut may likewise exacerbate the problem.

Appropriate treatment. The athlete who collapses following prolonged physical activity may have exertion-associated collapse that requires no treatment other than continued ambulation and oral hydration. However, prompt identification of a casualty and initiation of treatment in the field is required for patients who exhibit signs and symptoms of exertional heat illness and/or hyponatremia. Prompt correction of serum sodium is important to reduce the risk of permanent neurologic sequelae or death.

At our facility, we initially treat potential exertional heat illness and hyponatremic cases alike (figure 1: not shown). A core temperature is taken, and if the patient is hyperthermic, field-cooling techniques are implemented. If the patient has altered mental status and is unable to take fluids orally, we begin IV normal saline (250 mL bolus). A hand-held portable analyzer (I-stat; I-stat Corporation, Princeton, New Jersey) is used to provide blood chemistry values in 2 to 3 minutes. If the plasma sodium level is very low (<125 mmol/L), the patient is transferred to the hospital, sodium is gradually replaced via IV fluids, and free water is eliminated by loop diuretics.

Correcting sodium levels. Correction can be achieved by administration of normal saline (0.9% sodium chloride) to increase plasma sodium concentrations at a rate of 1 to 2 mmol/L/hr. Free water intake should be restricted. Rarely, hypertonic (3%) sodium chloride is needed, and care must be taken not to correct levels too rapidly. Rapid correction has caused central pontine myelinolysis in patients with long-standing hyponatremia (8). Addition of a loop diuretic such as furosemide can aid in elimination of free water. In all cases, close monitoring of plasma sodium levels and neurologic symptoms is important. Measurements of urinary electrolytes are also helpful to determine kidney function in these patients.

Prevention. Prevention of hyponatremia is also important. Consumption of the proper amount of fluids is the best means of prevention. Also, for endurance events a salt-containing beverage may help to slow hyponatremia onset. In our setting, the trainees are calorie restricted, so in order to provide some sodium with the water ingested, a salt-enhanced water (0.06% sodium chloride) was developed with help from researchers at the US Army Research Institute of Environmental Medicine. This level was the highest concentration of salt palatable in water without adding glucose or flavoring. Additional salt packets are also given. Hydration guidelines now reflect adequate amounts of fluid needed to prevent exertional heat injury without increasing risk of hyponatremia (9). In nonmilitary training environments, athletes should be encouraged to consume proper amounts of electrolyte-containing beverages during endurance events. Too much fluid can hurt.

Wrapping Up

Physicians serving endurance events should be aware that acute exertional hyponatremia and heat illness may initially present with similar signs and symptoms. If an IV must be started, consider using normal saline as the IV fluid. Hand-held analyzers are now available that allow rapid field determination of blood chemistry values. Participants should consume electrolyte-containing beverages as part of their fluid replacement during the event.


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  6. Garigan TP, Ristedt DE: Death from hyponatremia as a result of acute water intoxication in an Army basic trainee. Milit Med 1999;164(3):234-238
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  8. Levinsky NG: Fluid and electrolytes, in Wilson JD, Braunwald E, Isselbacher KJ, et al (eds) Harrison's Principles of Internal Medicine, ed 12. New York City, McGraw-Hill, 1991, pp 278-284
  9. Latzka WA, Montain SJ: Water and electrolyte requirements for exercise. Clin Sports Med 1999;18(3):513-524

The views expressed in this article are those of the authors and do not represent an official position of the United States Navy.

Dr Flinn is the senior medical officer and director of the sports medicine department at the Branch Medical Clinic, Parris Island, South Carolina. Dr Sherer is a resident in family practice at Memorial Health University in Savannah, Georgia. Address correspondence to Scott D. Flinn, MD, Sports Medicine Dept, Branch Medical Clinic Parris Island, Bldg 669, Parris Island, SC 29905; e-mail to [email protected].