A temperature above 40ºC (or 104ºF) is generally considered to be consistent with severe hyperthermia. The body’s heat production results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. The presence of heat stroke should raise suspicion of other concurrent multifactorial processes such as genetic predisposition, unaccustomed drug use or subclinical viral infection.
Above 42ºC (108ºF), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function. A cytokine-mediated systemic inflammatory response then develops, and production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ system failure and disseminated intravascular coagulation (DIC)(2,3,4).
Risk factors. Risk factors include strenuous exercise in high ambient temperatures, lack of acclimatization, poor physical fitness, obesity, dehydration, acute illness, and external load (such as wearing clothing, equipment and protective gear) (5). Additional risk factors predisposing an individual to heat intolerance are outlined below in Table 3.
Diagnosis: The diagnosis of heat stroke first begins with measuring a rectal temperature above 41 C (or 106ºF) and who either demonstrates altered mental status (collapsed with unconsciousness or reduced level of consciousness, such as stupor or coma) or a change in mental stimulation (irritability or convulsions). (6,7) Common symptoms suggesting abnormalities in the athlete’s central nervous system include dizziness, weakness, nausea, headache, confusion, disorientation, and irrational behavior (aggressive combativeness or drowsiness) progressing to coma.
Physical exam: Physical exam. Upon initial assessment of vital signs, hypotension and tachycardia are present secondary to an initially low peripheral vascular resistance in the setting of increased cardiac output. (8) The team provider should then conduct a focused physical exam that should at least include neurologic, psychiatric, cardiovascular and pulmonary assessments in the setting of impending decompensation.
Management: Primary management of heat stroke should aim to rapidly reduce rectal temperature. The quicker the rectal temperature is reduced, the better the prognosis. The athlete should be placed in a bath of ice water for 5-10 minutes, as the body temperature should stabilize to 38C (100F) during this time frame (9). The clinician should proceed with caution in avoiding hypothermia since rectal temperature will lag behind the patient’s core temperature. Often, shivering indicates the core temperature has decreased to 37C (99F). IV fluids (1-1.5L of 0.45% or 0.9% normal saline) may be given initially to correct the expected dehydration of the patient and to stabilize hyperkinetic circulation. The clinician should administer IV fluids with caution, as it may precipitate pulmonary edema in the setting of hyperthermia which impairs cardiac function. (10)
Indications for hospital admission: Decision for hospitalization for further observation should be made after the patient’s temperature has normalized to 38C (100F) and is usually made within an hour after targeted cooling treatment. Rectal temperature may begin to increase again after cooling and this may be missed if the patient is sent home without appropriate supervision. Malignant hyperthermia may be a concurrent process contributing to this increase of rectal temperature after exercise and the cooling process, and indicates continued heat-generating biochemical processes in the muscles (see below). (10)
Patient should be hospitalized:
2. Failure for patient to maintain a stable hemodynamic/cardiovascular status, such as persistent tachycardia and hypotension in the supine head-down position. This may be suggestive of impending cardiogenic shock and is an absolute indication for hospitalization.
3. Patients regaining consciousness quickly, with a stable cardiovascular status and whose rectal temperature do not increase within the first hour after the active cooling treatment generally do not need to be hospitalized, however the clinician should be prepared to use clinical gestalt for appropriate discharge management.
Complications. It remains unclear whether the hyperthermia of heatstroke directly causes these damages) or if these complications are just a component of another concurrent disease process, such as hyponatremia (11). Cardiovascular complications include: arrhythmias, myocardial infarction and pulmonary edema. Neurologic complications include: coma, convulsions and stroke. Gastrointestinal system complications include liver damage and gastric bleeding. A common hematologic complication which implies a poor prognosis is disseminated intravascular coagulation (DIC). Renal system include acute renal failure secondary to hypoperfusion due volume depletion. There are several other important complications that should not be missed, these are discussed below.
Rhabdomyolysis, which is the destruction of striated muscle cells, is a common complication causing brown-colored urine and is accompanied by muscle weakness, swelling and pain. Skin may appear discolored because of hemorrhaging of the muscle, causing a “doughy” feel of the muscles. Increased levels of myoglobin in urine cause brown discoloration with granular casts. Also elevated are the levels of CPK, potassium, uric acid and in severe cases, there may be findings of DIC which requires ICU evaluation.
Malignant hyperthermia, is a process usually activated by general anesthetic agents is hypothesized to be triggered by exercise. It is a biochemical process occurring in skeletal muscle that activates uncontrolled metabolism and hyperthermia leading to potentially fatal rhabdomyolysis. The process of malignant hyperthermia can only be reversed by dantrolene or less often by rapid whole-body cooling. (12)
Exercise-associated collapse (EAC). EAC is described as phenomena that occurs usually at the end of an endurance event, resulting in the inability to stand or walk without aid, in a conscious athlete. (13) According to a prospective study done by Robert WO, which looked at the medical encounters (injury and illness) of 81,277 entrants in the Twin Cities Marathon from 1982 athletes can experience post-race EAC which can be attributed to non–life-threatening neurocardiogenic syncope event (14). The EAC is multifactorial and may include various causes such as dehydration, heat stress and exercise associated cramps to name a few. (15)
The main mechanism of EAC is primarily believed to be due to transient postural hypotension, that results from impaired cardiac baroreceptors after completion of an exertional event. (16,18) Holtshauzen et al conducted a study that compared pre and post-race blood pressure changes in a group of 31 marathon runners competing in an 80-km event. They concluded in this study that 68% of the runners developed post-exercise postural hypotension, though asymptomatic. (17) As a clinician, the diagnosis of EAC is the result of a carefully conducted history and physical examination. The history of the event is critical to establishing the diagnosis, as previously discussed.
Treatment of EAC is primarily directed towards reversing the postural hypotension in the setting of attenuated baroreflex response. Therefore, it is targeted towards correcting volume status and positional intervention. In a randomized control trial conducted by Anley et al., who compared the use of oral hydration and Trendelenburg versus IV fluids in restoring normal hemodynamics, It was determined that IV fluids did not decrease the time to discharge among athletes being treated with EAH. Therefore it can be concluded that it can be effective to use oral hydration and Trendelenburg as the first line of treatment in EAC. (17)
EAC is ultimately a diagnosis of exclusion and should only be considered once other life-threatening causes have been excluded by the absence of neurological, biochemical or thermal abnormalities. Asplund et al proposed an algorithm for the treatment of EAC once potential life-threatening etiologies that cause collapse, such as cardiac arrest, exertional heat stroke or exercise-associated hyponatremia to name a few has been excluded. See Figure 1 (18)
Risk factors include dehydration, lack of heat acclimatization, loss of sodium and/or potassium (or insufficient intake of these electrolytes prior to and during intense activity), extreme environmental conditions, baseline (pre-activity) fatigue and neurogenic fatigue. (19, 20, 21, 22, 23) . In addition, a study football athlete by Horswill et al., suggests that individuals whose sweat possess high salt concentrations may be more prone to cramps and were coined “salty sweaters” (24). Another study by Stofan et al., observed football players with a history of muscle cramps found that they have larger acute sodium and fluid losses (in sweat) compared to teammates who had never had muscle cramps (25).
Diagnostic studies are usually unnecessary. Clinical criteria for establishing the diagnosis of muscle cramps generally include intense muscle pain (not associated with acute muscle strain or other injury) and spasm, and persistent contractions of the muscles primarily involved in the prolonged exercise. No signs of more severe illness, such as exertional hyponatremia or exertional heat stroke, should be present. EAMC is a well-documented phenomenon in endurance athletes, however, the risk factors are not fully characterized. There are conflicting data in the literature on the effects of hydration and serum electrolyte replacement in the prevention and treatment of EAMC (26).
In an effort to prevent injuries that occur due to dehydration or sweat loss, athletes may overhydrate, especially during endurance events such as ultra-distance events. Over-drinking also known as water intoxication occurs when athletes drink at rate that exceed their sweat loss.. Hyponatremia results in part when athletes ingest excessive amount of fluids low in sodium and in excess of sweat and urine losses. (27,28) Hyponatremia is defined as plasma sodium <135 mmol x L. It is a potentially serious complication of ultra-endurance sports. Although dehydration still remains the more typical fluid condition experienced by athletes, hyponatremia should be on the differential.
Athletes who are found to be hyponatremic may describe the sensation of feeling bloated and/or puffy although many athletes can be asymptomatic. (29) (30) On physical exam, the complaint of feeling bloated can be demonstrated by the presence of swollen hands and feet, which may be noticeable when their ring or bracelets fit tighter. Athletes may also present with nausea, vomiting, disorientation, and altered mental status. (31) EAH can also present in more serious manifestations such as cerebral edema, non cardiogenic pulmonary edema and death. (32,33). A cohort study by Almond et al., of the 2002 Boston Marathon participants was completed to identify risk factors associated with hyponatremia. The results of the study showed risk factors associated with hyponatremia included weight gain while running, length of race and the extremes of body mass indices. (31)
The therapy of choice for the treatment of is dependent on the severity of symptoms and the degree of hyponatremia as demonstrated by laboratory values. As a clinician there should always be a high level of suspicion of EAH symptoms at endurance events. Mild levels of hyponatremia which is defined as serum Na 130-135, requires fluid restriction and observation. (34) More severe cases of EAH requiring hypertonic saline should be transported to a medical center where serum sodium can be monitored closely. Ayus et al showed in a case study that athletes treated with hypertonic saline for EAH, cerebral edema and noncardiogenic pulmonary edema made full recovery. (35)
Stephen Henry DO MS, M.SC., CAQSM
Thomas M Best, MD, PHD, FACSM, CAQSM
Naima Stennett MD MS PGY 2
6. Maughan RJ. Thermoregulation in marathon competition at low ambient temperature. Int J Sports Med 1985;6(1):15-19.
7. Noakes TD, Myburgh KH, Duplessis J et al. Metabolic rate, not percent dehydration, predicts rectal temperature in marathon runners. Med Sci Sports Exerc 1991;23(4):443-9
8. O’Donnell TF Jr, Clowes GH Jr. The circulatory requirements of heat stroke. Surg Forum 1971;22:12-14