The spectrum of heat-related illness includes those that are relatively benign and self-limited and those that are potentially more serious and life-threatening. Benign and self-limiting heat-related illnesses include heat cramps, heat edema, and heat syncope. However, these can be an indication of a more serous condition. Heat edema is a mild form of heat-related illness, while heat cramps are painful spasms of skeletal muscles of the extremities and abdomen and may be a sign of impending heat exhaustion (1). The more serious conditions in the spectrum of heat-related illness include heat exhaustion and heatstroke. Heat exhaustion typically occurs at core body temperatures of 38.0°C to 40.5°C and has symptoms such as progressive lethargy, headache, nausea, vomiting, lightheadedness, and myalgias. Heatstroke is classically differentiated from heat exhaustion by the presence of both a core temperature greater than 40.5°C and an acute neurological or mental status change (2). The neurological manifestations of heatstroke include ataxia, psychosis or irrational behavior, seizures, opisthotonos, posturing, and coma (3).

All humans produce heat as a byproduct of metabolism and muscle activity. Recognition of hyperthermia requires a rectal measurement of temperature in order to adequately assess core body temperature, as oral, axillary, and otic temperatures tend to underestimate core body temperature (4).

There are four mechanisms of heat transfer in the body: evaporation, radiation, convection, and conduction (Fig. 130.1). Normally, body heat is transferred from the core to the skin via cutaneous blood flow, where heat can be lost through the four heat transfer mechanisms. Radiation, the transfer of heat into the environment by means of photons of light, accounts for 55% to 65% of heat loss. This method of heat transfer is dependent on a gradient of heat between two sources; in heat-related illness, this is a gradient between core and ambient temperatures as well as the amount of exposed body surface area. Since heat-related illness often occurs when ambient temperature is above body temperature, heat loss occurs more by evaporation of water from perspiration from the skin and the evaporative cooling from exhaled moisture than from radiation. Evaporation is an important mechanism of heat loss to the environment while preserving skin blood flow and thus is the major means of heat reduction in the hyperthermic patient.

Convection and conduction account for 15% of the body’s heat transfer. Convection can be defined, in the context of cooling a hyperthermic patient, as the transfer of heat by particles of air or water having contact with the patient, and it is often used in conjunction with evaporation. Conduction can be defined as the direct transfer of heat from one object to another, and it is the mechanism at work when a patient is immersed in ice water. Since evaporation of water allows for more loss of heat than conduction, it is understandable that some human studies have shown evaporation techniques to be more effective in lowering core body surface temperature than ice water immersion (5).

Often, heat-related illness occurs when the ambient temperature exceeds the core body temperature. Although children
have a greater ratio of body surface area to mass than adults, they often lack the understanding or ability to remove themselves from an overheated environment. Evaporation becomes the primary mechanism of heat transfer in these environments. However, in humid conditions, evaporative heat loss is rendered ineffective and results in a rising core temperature.

Children who are risk for heat-related illnesses include patients with cystic fibrosis, heart disease, eating disorders/malnutrition/obesity, diabetes (increased water loss), congenital absence of sweat glands, familial dysautonomia (temperature instability), and cerebral palsy (6,7,8,9). Dehydration in conjunction with electrolyte abnormalities and situations involving strenuous exercise, lack of fluid intake, and poor feeding contribute to hyperthermia. In addition, neonates and infants have a limited ability to perspire and therefore are significantly hampered in their ability to lose heat in hot, humid weather.

The pathophysiology of thermoregulation occurs centrally in the hypothalamus. Heat-sensitive areas in the hypothalamus respond to a rising core temperature through sympathetic tone and autonomic mechanisms that utilize cholinergic pathways to the sweat glands. As the temperature rises, cholinergic stimulation causes sweat to be released from the glands. It is important to recall that young children possess a limited number of sweat glands and thus are limited in their response to a rising core temperature in this way. Sympathetic tone changes in arterioles and subcutaneous arteriovenous anastomoses increases blood flow to the skin surface in response to overheating. Flow through the skin can comprise up to 30% of cardiac output and effectively transfer heat from the body core to the skin surface. Vasodilatation dissipates heat by convection, and sweat dissipates it by evaporation (10).

Core body temperature increases occur secondary to any combination of excess metabolic heat production, excessive environmental heat, and altered heat dissipation. In hyperthermia, the central hypothalamic set point is normal but overwhelmed, as peripheral mechanisms are unable to maintain the body’s temperature at that set point. Fever is differentiated from hyperthermia, despite their clinical similarities, in that during fever cytokines and other biochemical reactants cause the central hypothalamic set point to be elevated. Therefore, it is necessary to emphasize that drugs with antipyretic effects are not beneficial in treating hyperthermia, as their mechanism of action is to lower the central set point that has been elevated (10).

Patients presenting with heat-related illness require cooling management. Risk factors for hyperthermia based on a patient’s medical history, age, and the preceding environment will help in determining appropriate management. Infants, because of factors such as limited sweat glands and the inability to remove themselves from a potentially harmful situation, are at high risk in hot environments, as when they are left inside a closed automobile. Children and adolescents who are subjected to strenuous activity in a hot and humid environment increase their risk of heat illness. A preadolescent’s or poorly trained athlete’s ability to transport muscle-generated heat and to produce sweat is less than the ability of an older child or better trained athlete. Examples of common settings for heat-related illnesses in the pediatric population
include summer football camp, cross-country running, and marching in a band (8,9,10,11,12,13).

Characteristics of the clinical presentation of hyperthermia will determine the extent of treatment. Patients with severe presenting signs of heat illness such as heat exhaustion and heatstroke require aggressive treatment if heat illness is suspected. Recall that the clinical presentation of heatstroke includes an acute change in neurological or mental status and requires immediate intervention. In these patients with potentially life-threatening hyperthermia, rapid cooling measures are initiated before lab studies are obtained or a differential diagnosis is entertained. Treating these patients can be life-saving, and monitoring the temperature will ensure that cooling will not harm patients who are hyperthermic from other causes.

When a heatstroke victim presents to the emergency department, the clinician should begin treatment with attention to both immediate temperature reduction and the resuscitation basics of airway, breathing, and circulation. The patient should be attached to a cardiac a monitor with water-resistant leads and should be placed on a bed with a grated bottom or netting to allow for maximal heat transfer. A hyperthermic patient should receive supplemental oxygen and have two large-bore intravenous catheters placed. Hydration, electrolyte balance, and coagulation status must be determined expeditiously. Typical laboratory tests in severe cases might include complete blood count, prothrombin and partial thromboplastin times, serum electrolytes, blood urea nitrogen, creatinine, creatine phosphokinase, calcium, phosphorus, urinalysis with urine myoglobin, and arterial blood gas analysis. For patients requiring intravascular volume support, up to 20 mL/kg of lactated Ringer solution or normal saline is infused rapidly. Further cardiovascular support may be provided as needed, with inotropes such as low-dose dopamine and/or dobutamine, which enhance myocardial contractility while maintaining peripheral vasodilation. Subsequent fluid therapy (or initial treatment for more stable patients) is begun with 5% dextrose in 0.2% saline at an appropriate maintenance rate. Patients with hyperthermia are not often severely dehydrated and thus may not require large volumes of intravenous fluid. However, the clinician should monitor and support the cardiovascular system to maintain perfusion. The patient’s clothing should be removed, and a rectal temperature probe should be placed for continuous core temperature monitoring. Of note, glass thermometers are not appropriate for continuous monitoring because of the potential for breakage and injury to the patient. The clinician should consider drawing blood for evaluation of basic chemistries and electrolyte disturbances, renal function, and acid-base status. In addition, insertion of a Foley catheter for urinalysis and to measure urine output may be beneficial in the resuscitation of these patients. Finally, continued monitoring via placement of an arterial line should be considered.