Body temperature is maintained in a narrow range by an integrated system of internal and external processes. Internal thermal homeostasis is controlled by the hypothalamus, with the parasympathetic nervous system regulating sweat gland function and the sympathetic nervous system controlling changes in skin blood flow and vasodilatation (3) (Fig 57-1). As environmental temperatures rise, blood flow is diverted to the skin, and sweat production increases (3,4). The rate of sweat production is affected by, among other factors, the acclimatization of the athlete being challenged. In general, a sweat rate of 1 to 2 L per hour with a sodium content of 65 mEq per L is achieved in the nonacclimatized individual (3,5). With the physiological changes of heat adaptation, the sweat rate increases to 3 to 4 L per hour, and the sodium concentration drops to 5 mEq per L (5).

Available mechanisms of cooling include conduction, convection, radiation, and evaporation (Fig 57-2) (6). Conduction is the transference of heat from one body to another cooler one by direct contact. Air can act as an insulator to heat loss,
whereas water provides better conduction of heat, which is key in its use for immersion cooling.

Convection is transfer of heat to the surrounding circulating air. With elevated ambient temperatures, as when the air temperature is greater than the skin temperature, heat can actually be transferred to the skin.

Radiation is dispersal of heat in the form of infrared electromagnetic waves. These first three mechanisms are most useful for cooling when the ambient temperature is less than or equal to the skin temperature (3). In humans, by far the most important method of heat dissipation is evaporation (7). As sweat forms on the skin, surrounding warmer air evaporates the fluid, thus providing cooling. Evaporation of sweat is the primary means of cooling once the environmental temperature exceeds 68°F (20°C) (8,9). Each milliliter of evaporated sweat cools the body by 0.58 kcal (3); evaporative losses are influenced by wind current and clothing and, most importantly, by the relative humidity. Sweat that is not evaporated, as when there is elevated humidity, but instead rolls off and/or is absorbed by clothing does not provide the needed cooling.

The ability of the athlete to function in a hot environment is determined by many factors. Two of them, the physiological mechanisms available for cooling and acclimatization of the individual, have been mentioned. Also affecting thermoregulation of the athlete is the clothing worn, medications that are being used, and pre-existing medical illnesses. Recent National Collegiate Athletic Association (NCAA) guidelines support the gradual introduction of heavier uniform items such as full padding during the acclimatization process (10). Lighter clothing allows sweat to be wicked away from the body as it is more easily evaporated.

A large number of medications can decrease the ability of the athlete to regulate internal temperatures. These include antihistamines, anticholinergics, benzodiazepines, alpha-adrenergics, beta- and calcium blockers, neuroleptics, phenothiazines, diuretics, and tricyclic antidepressants (6,11). In addition, drugs such as alcohol, cocaine, amphetamines, and ecstasy can adversely affect thermoregulation (4,6). Performance-enhancing supplements (e.g., ephedra) have also been implicated as deleterious to maintaining normal core temperatures (1). All medications and supplements must be identified to allow effective counseling with regard to performance and safety concerns.

Many pre-existing medical conditions can contribute to an individual’s inability to adapt and function in a hot environment. These include alcoholism, anorexia, cardiac disease, cystic fibrosis, dehydration, diabetes insipidus, extremes of age, febrile illnesses, gastroenteritis, hypokalemia, obesity, poor conditioning, sleep deprivation, sunburn, and sweat gland dysfunction (3,4,6). Of note, anorexia (along with other eating disorders), dehydration, and gastroenteritis are conditions that are commonly observed in young populations. Coaches, athletic trainers, and physicians must be ready to identify those at risk. Furthermore, these multiple and diverse risk factors for heat illness highlight the importance of preparticipation screening as well as periodic medical updates to allow appropriate and individualized levels of play and/or activity in hot environments.

A history of previous heat injury has been listed as elevating the risk of subsequent heat illnesses. While it is true that activity modification is necessary as the athlete recovers from an illness, recent studies have not shown that an episode of heat injury universally predisposes to future episodes (12,13).

Gradual acclimatization to a warm, humid environment is an important process in preventing heat-related illnesses. Normally taking 10 to 14 days to accomplish, it is a series of gradual physiological adaptations to heat that occurs with regular exposure to and exercise in a hot environment (13,14). Physiological changes that improve tolerance to heat include an increase in blood volume, an increase in sweat rate with a faster onset of sweating, a wider distribution of areas producing sweat, and a decrease in the sweat sodium concentration (Fig 57-3).

There is a common misconception that, as the athlete acclimates to elevated temperature, there is a concomitant decrease in hydration requirement. The converse is true; normal sweating rates may double, thus significantly increasing the required fluid intake to maintain euhydration.

The significance of adequate hydration cannot be overemphasized. It has been estimated that for each 1% decrease in body weight secondary to dehydration, the core temperature increases by 0.15 to 0.2°C (7,15). Increased sweat rates add to the dehydrated state with hemodynamic instability resulting. Results of a recent study of high school athletes showed that over 60% began summer practice sessions in a dehydrated state, based on a initial urine-specific gravity of greater than 1.020 (16). Thirst is not a reliable indicator of volume status because a level of 2% to 3% dehydration is necessary to initiate this response (7). This level of dehydration is not uncommon with normal practice conditions and has also been noted to impair athletic performance. With thirst as the sole prompter of fluid ingestion, an athlete will only ingest one third to two thirds of fluid loss as sweat (17).

Assessment of environmental conditions that increase risk of heat illnesses is another important step in injury prevention. A number of indices have been developed to attempt to define site-specific risk. One of the most widely known and used is the Wet Bulb Globe Temperature (WBGT) Index (13). Using three measurements to reflect dry temperature,
humidity, and radiant heat effects and weighting them for importance, the generated score is correlated to a certain degree of danger from heat exposure. In this way, activities can be modified to reduce potential harm (18). The National Weather Index is another tool to evaluate heat exposure but is not specific to the area of play (4). While a WBGT meter is expensive, a more affordable method uses a sling psychrometer, and a free program is available on the internet (19).

With heat cramps, affected individuals experience painful muscle contractions primarily in the arms, calves, and abdomen, with inadequate electrolyte intake being the probable etiology. Athletes complain of extremity cramping in the most worked muscle groups and often after the activity has stopped. Other symptoms include nausea, vomiting, fatigue, and lightheadedness. Risk factors for heat cramps include the use of diuretics (as caffeinated beverages), unacclimatized state, and inadequate sodium intake. A classic study of workers in several industrial settings demonstrated four characteristics of heat cramps that are still valid: (a) contractions occur after sustained heavy effort in a hot environment; (b) affected individuals sweated profusely; (c) fluid replacement consisted of large volumes of water; and (d) cooling seemed to precipitate the spasms because they began after cessation of work (23).

Clinically, patients may appear ill and uncomfortable secondary to the cramping, and sweating will be noted. If measured, the rectal temperature would be below 104°F. Treatment involves removal of the patient to a cool environment, encouraged oral hydration with electrolyte-containing solutions, and stretching/massage of affected muscle groups. If fluid replenishment cannot be accomplished orally secondary to vomiting, parenteral hydration can be initiated. An athlete can return to play if, after treatment, he can successfully participate at the level expected for the sport and position played (24).

Athletes with heat exhaustion present with symptoms of fatigue, inability to continue activity, mild confusion, nausea, vomiting, chills, piloerection, and profuse sweating. Heat syncope may occur, but there is no major neurological impairment. Hypotension, hyperventilation, and elevated rectal temperatures are objective evidence for heat exhaustion.

Physiologically, affected athletes may be either volume depleted or sodium depleted, although there is often an overlap between the two types of heat exhaustion (4). Water-depleted heat exhaustion is most often observed in elderly populations (as a result of medications that affect hydration status) and in active individuals who are inadequately hydrated for the activity level and the environmental conditions.

Sodium-depleted heat exhaustion, on the other hand, is seen in unacclimatized persons who have overhydrated, taking in sufficient free water, but have not accounted for sodium losses in sweat by altering intake. Acclimatization increases sweat rates but concomitantly decreases sodium content in sweat.

Treatment of heat exhaustion depends on the type and degree of impairment. For mild heat exhaustion, in which the patient is hemodynamically stable, removal to a cool environment, removal of excess equipment and clothing, and replenishment of fluids orally are usually sufficient. Electrolyte/salt replacement is provided as needed (4).

Patients with more severe manifestations (hypotension, cardiac arrhythmias, or deteriorating mental status) or those unresponsive to conservative measures must be transported to emergency medical facilities. Although intravenous hydration may be initiated prior to transport, the volume of saline administered must be modest until electrolyte concentrations can be accurately measured. Heat exhaustion patients who are hypernatremic will need cautious hydration to avoid the cerebral edema caused by too rapid a correction.

It is imperative to begin the treatment of heat exhaustion as soon as it is identified because this condition can progress to heat stroke, which is a medical emergency. Because heat exhaustion and heat stroke symptoms are so similar and assessment of core temperatures may not be possible on the field, efforts should be directed at cooling the patient immediately as if the patient has heat stroke. If in doubt, transport to the emergency department is the most prudent action.

The athlete must be hydrated and asymptomatic before being allowed to return to the field, preferably after being cleared by a physician. In general, delaying return to play to the following day is preferable to allow recovery. Practices that may have contributed to the heat exhaustion episode, such as poor diet, insufficient fluids, and so on, should be examined, and corrective actions should be taken to prevent repeat occurrences. If the primary deficiency is one of not
being acclimated, a practice and activity schedule should be engineered to ensure heat tolerance while maintaining conditioning (24).

Heat stroke, a medical emergency, is a failure of internal and external thermoregulatory mechanisms to control the cumulative effects of exogenous heat on endogenous systems, with a subsequent loss of homeostasis and damage to multiple organ systems (3,13,25,26). The mortality of this illness depends primarily on the degree of heat experienced and the duration of the temperature elevation. This again emphasizes the importance of early recognition and treatment. Typically, onset is acute, and a high index of suspicion concerning nonspecific presenting symptoms is needed.

Two types of heat stroke are recognized and they differ in important aspects. The better known classic heat stroke occurs most often in the summer and usually during heat waves, which are defined as 3 or more days of air temperatures exceeding 90°F (27). The target populations are the elderly and those with chronic medical conditions and persons who are unable to seek cooler environments usually because of infirmities or financial constraints (Table 57-1). The heat insult occurs over several days and results in hyperthermia, central nervous system (CNS) dysfunction, and anhidrosis. This last characteristic is a major distinction from exertional heat stroke, in which sweating, often profuse, continues. Between 1979 and 1999, 8,015 deaths were reported as heat related in the United States, with almost 50% occurring in the age group over 65 years old (27). Again, comorbidities contribute to the mortality of classic heat stroke. It is likely that the true incidence of this disease is higher because the resulting organ system failures (e.g., cardiovascular, renal, CNS) may be identified as the cause of death instead of the initiating heat injury.

Exertional heat stroke is defined by a core temperature greater than 104°F and severe CNS disturbances (see Table 57-1). Affected individuals are usually younger, more physically fit, and involved in physically challenging activities. For the 20% who have a prodromal syndrome, presentation may be similar to that of heat exhaustion (13). Symptoms may include dizziness, nausea and vomiting, frontal headache, confusion, drowsiness, disorientation, muscle twitching, ataxia, and psychiatric symptoms. More often, however, collapse is acute. Patients may experience syncope, seizures, and coma. Objectively, tachypnea, tachycardia, hypotension, and cardiac arrhythmias may be noted in addition to the elevated rectal temperatures. In the field, where a rectal probe may not be available, a presumptive diagnosis of exertional heat stroke may be made when the patient is hot, environmental conditions are conducive to heat injury, and there are signs of moderate to severe CNS dysfunction.

Immediate recognition of heat stroke is critical because no inherent internal thermoregulatory mechanism is adequate to combat the widespread effects. Although CNS involvement is the hallmark, other systems are also damaged, including the cardiovascular, integument, renal, splanchnic, and hepatic systems. The clinical picture has been likened to sepsis. A current theory for the global abnormalities seen postulates that, as skin blood flow increases to dissipate an ever increasing heat load, splanchnic circulatory support erodes to the point that gram-negative proteins are able to cross the blood–tissue barrier and cause decreased vascular resistance (28). It should be no surprise, given our unfolding knowledge that the inflammatory system involvement comprises multiple processes, that the current heat stress model attributes at least some of the tissue effects to circulating cytokines such as interleukin C. These modulators effect further changes, which serve to worsen the clinical situation.

With the normal shunting of blood from central to peripheral circulation exacerbated by pre-existing dehydration, the patient will demonstrate hemodynamic compromise via an elevated heart rate, a decreased blood pressure,
and CNS compromise. It is not hard to appreciate, then, that the dehydrated or insufficiently hydrated athlete would be more susceptible to heat injury.