Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
INTRODUCTION — The manifestations, evaluation, and management of heat stroke in children will be reviewed here. Other forms of heat illness in children and hyperthermia in the adult patient are discussed separately. (See "Heat illness (other than heat stroke) in children" and "Severe nonexertional hyperthermia (classic heat stroke) in adults" and "Malignant hyperthermia: Clinical diagnosis and management of acute crisis".)
HYPERTHERMIA DEFINITION — Hyperthermia is defined as elevation of core body temperature above the normal diurnal range of 36 to 37.5°C (96.8 to 99.5°F) due to failure of thermoregulation. Hyperthermia is not synonymous with the more common sign of fever, which is induced by cytokine activation during inflammation and regulated at the level of the hypothalamus. Heat-related illnesses range from minor syndromes to life-threatening processes. While there are many manifestations of heat-related illnesses, all heat-related illnesses result from excessive heat stress caused by an increased environmental heat burden, an inability of the body to dissipate endogenous heat, or a combination of these two factors. Heat stroke is the most severe heat-related illness and can rapidly lead to death without prompt treatment.
HEAT STROKE DEFINITION — Heat stroke is defined as a core temperature ≥40 to 41°C (104 to 105.8°F) accompanied by central nervous system dysfunction in patients with environmental heat exposure . While anhidrosis (lack of sweating) is frequently present, especially with classic heat stroke, this is not an absolute diagnostic criterion [1,2]. This condition represents a failure of the body's ability to maintain thermoregulatory homeostasis. Heat stroke is further classified as follows:
●Classic (nonexertional) heat stroke – Classic heat stroke arises from environmental exposure to heat and is more common in younger children who are unable to escape from hot environments and those with underlying chronic medical conditions that impair thermoregulation (table 1).
●Exertional heat stroke – Exertional heat stroke generally occurs in young, otherwise healthy individuals who engage in heavy exercise during periods of high ambient temperature and humidity. Typical patients are athletes and military recruits in basic training [3,4].
EPIDEMIOLOGY — Heat-related deaths occur with regularity in the United States. Between 2006 to 2010, 3340 deaths were attributed to heat . The highest rates of death from heat-related illness are in the elderly population and in adult patients with comorbid disease [6-10], but young children are also at risk . For example, young children, who cannot operate car door locks or who are restrained in car seats, may suffer morbidity or mortality when left unattended in vehicles, as temperatures inside a closed vehicle rapidly rise to dangerous levels even when ambient temperature is only moderately high [11-14]. Education of parents regarding the high risk of leaving young children unattended in cars appears warranted [11,12]. Key components of guidance include reinforcing the vulnerability of infants and young children to heat stress, the rapidity with which temperature may rise in a locked car, and the importance of keeping cars locked when not in use.
Among teenage athletes, heat illness is the third major cause of death behind traumatic and cardiac causes of death [15-18]. The highest rate of nonfatal heat illness in United States high school athletes is found among American football players who account for 4.5 episodes of heat illness and limitation of athletic activity per 100,000 athlete-exposures . American football also was the leading activity associated with an emergency department evaluation for heat illness in US patients ≤19 years [20,21]. Approximately two-thirds of these episodes occur in August, and increased body-mass index (ie, being overweight or obese) appears to pose a significant risk. Prescription amphetamines for ADHD and dietary supplements, including creatine, may also contribute to subclinical dehydration and heat stroke in selected athletes . Since creatine supplementation may increase serum creatinine concentrations, this supplement may act as a false indicator of renal dysfunction .
Heat illness in athletes is potentially preventable. Key components of a successful strategy include age-appropriate periods of acclimatization; emphasis on proper hydration before, during, and after organized sports activities; and awareness of ambient temperatures with limitation of activities when heat poses a significant risk (table 2). (See "Heat illness (other than heat stroke) in children", section on 'Prevention of heat illness'.)
Temperature homeostasis — Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body's heat load 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 to allow for reduction of body heat.
Evaporation is the principal mechanism of heat loss in a hot environment, but this becomes ineffective above a relative humidity of 75 percent . The other major methods of heat dissipation; radiation (emission of infrared electromagnetic energy), conduction (direct transfer of heat to an adjacent, cooler object), and convection (direct transfer of heat to convective air currents); cannot efficiently transfer heat when environmental temperature exceeds skin temperature (typically 35°C or 95°F).
Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia . Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to these effects, but all organs may be involved. As a result, these patients are at risk of multiorgan failure.
Pediatric considerations — Several key anatomic and physiologic differences exist between children and adults [26-28]; however, children do not appear to be at higher risk for heat illness when compared to adults [27,29].
●Heat production – Children produce more metabolic heat per kilogram of body weight because they have a higher basal metabolic rate than adults .
●Body surface area – Younger children have a higher surface area to mass ratio, resulting in a greater rate of heat absorption in hot environments . However, body composition (especially an increase in body fat) and lack of fitness are likely more important contributors to susceptibility to heat illness in older children and adolescents .
●Blood circulation – Children have a smaller absolute blood volume which limits the potential of blood borne heat transfer from the body core to the body surface where this heat can be dissipated . In addition, children have a lower cardiac output at a given metabolic rate than adults, further limiting heat dissipation during exercise .
●Sweat production – Children have a lower rate of sweating than adults as a result of a lower sweat rate per gland and begin sweating at a higher body temperature [26,31,32].
●Fluid replenishment – Children are more likely to inadequately replenish fluid losses during prolonged exercise [27,28,33,34].
●Acclimatization – Physiologic changes that result in increased heat tolerance include increased rate of sweating, a lower temperature threshold for sweating, reduced electrolyte losses in sweat, lower heart rate, increased aldosterone production with decreased urinary sodium, and lower core and skin temperatures [35,36]. Children achieve these adaptations to a hot environment more slowly than adults and typically require 10 to 14 days to achieve adequate acclimatization [26,28].
Much of the risk for heat illness in children is attributable to general anatomic and physiologic characteristics, as well as environmental variables such as the ambient temperature and humidity levels. However, medical conditions may augment the susceptibility to heat illness in specific individuals (table 1).
Heat stress — Children sustain serious heat-related injury when the critical thermal maximum (CTM) is exceeded. The CTM is defined as the degree of elevated body temperature and duration of heat exposure that can be tolerated before cell damage occurs . Human thermal maximum is estimated as a core body temperature of 42°C (107.6°F) lasting between 45 minutes and 8 hours.
Physiologic heat stress causes cell injury through several proposed mechanisms:
●Production of acute-phase reactants (eg, cytokines) that initiate an inflammatory cascade [1,38]
●Direct injury to cells with denaturation of proteins 
●Direct injury to the vascular endothelium resulting in impaired microcirculation and disseminated intravascular coagulation [40,41]
●Intestinal ischemia and increased permeability followed by endotoxemia 
These pathophysiologic changes result in a systemic inflammatory response that results in multiple organ dysfunction and injury . The cascade of acute-phase reactants is countered, to some degree, by the production of heat shock proteins, which confer protection by preventing unfolding of denatured proteins and by impeding cytokine production .
CLINICAL FEATURES — The diagnostic criteria for patients with heatstroke are elevated core temperature (≥40°C [104°F]) and central nervous system (CNS) abnormalities following environmental heat exposure. There is some overlap of symptoms between heat exhaustion and heat stroke (table 3). While the distinction between heat exhaustion and heat stroke is sometimes unclear, children with elevated body temperature and CNS abnormalities should be treated as victims of heat stroke, given the significant morbidity and mortality associated with this condition. (See "Heat illness (other than heat stroke) in children", section on 'Heat exhaustion'.)
CNS symptoms may be subtle or deceptive and can be manifested as impaired judgment or inappropriate behavior. However, children commonly present with more significant neurologic symptoms such as seizures, delirium, hallucinations, ataxia, dysarthria, or coma.
Other typical clinical manifestations include tachycardia and tachypnea. The skin may be flushed and warm or diaphoretic. Vomiting and diarrhea are also common. In addition, those patients with coagulopathy may demonstrate purpura, hemoptysis, hematemesis, melena, or hematochezia.
Clinical assessment — The diagnosis of heat stroke is based upon a careful history and physical examination. The full differential diagnosis of hyperthermia should be considered in each patient. The context in which symptoms develop usually suggests the etiology (eg, evidence of heat stress in patients with heat stroke, serotonin syndrome in patients receiving serotonergic agents, sepsis among children with an infectious prodrome). (See 'Differential diagnosis' below.)
Core temperature measurement — Core body temperature should be determined in all patients and continuously monitored. Rectal temperature is the most commonly obtained core temperature measurement, although esophageal, central venous, pulmonary artery, or bladder probe temperature are potential alternatives. Oral, axillary, or tympanic membrane temperatures are unreliable in treating heat illness .
Laboratory findings — Patients with heat stroke have abnormal laboratory findings, reflecting the systemic inflammatory response and end-organ damage resulting from heat stress. Laboratory studies should include:
●Rapid blood glucose to identify hypoglycemia 
●Blood gas determination (venous or arterial) to evaluate for the presence and severity of metabolic acidosis (especially in patients with exertional heat stroke) and respiratory alkalosis 
●Complete blood count, prothrombin time (PT), partial thromboplastin time (PTT), and INR (International Normalized Ratio) to detect anemia and disseminated intravascular coagulation [40-42]
●Serum electrolytes to check for increased or decreased sodium and potassium levels 
●Liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) to assess for liver injury
●Blood urea nitrogen and/or serum creatinine to identify prerenal azotemia or renal failure resulting from myoglobinuria
●Serum creatine kinase (CK), ionized or total calcium, and phosphate to detect rhabdomyolysis and associated hypocalcemia and hyperphosphatemia
●Urine rapid dipstick and microscopic urinalysis to diagnose myoglobinuria, which should be suspected in a patient who has a brown urine supernatant that tests positive for hemoglobin, but does not have increased red blood cells seen on microscopic analysis (see "Clinical manifestations and diagnosis of rhabdomyolysis" and "Clinical features and diagnosis of heme pigment-induced acute kidney injury")
●Toxicologic screening for drugs of abuse or prescribed medications in those patients for whom an illicit drug or medication side effect is suspected
Ancillary studies — Additional studies may be indicated based on the patient's clinical presentation and response to treatment:
●Chest radiograph – A chest radiograph helps identify pulmonary edema in patients who develop persistent high output cardiac insufficiency and is useful in patients for whom pulmonary aspiration is a concern.
●Electrocardiogram – An electrocardiogram should be obtained in patients with electrolyte abnormalities (eg, hyperkalemia, hypokalemia, hypocalcemia) and/or rhabdomyolysis.
●Computed tomography – A computed tomography scan of the head should be obtained if a child has persistently altered mental status despite cooling or shows signs of increased intracranial pressure suggestive of cerebral edema or intracranial hemorrhage. (See "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)
DIFFERENTIAL DIAGNOSIS — Other medical conditions may coexist with or mimic heat stroke in children:
●Sepsis – Sepsis, especially in association with meningitis, can cause high fever and abnormal mental status. However, in most instances, the height of the fever does not exceed 41°C (105.8°F). Furthermore, a focus for infection (eg, pneumonia, cellulitis, meningitis) or an infectious prodrome (eg, upper respiratory infection, gastrointestinal complaints) is frequently present. (See "Approach to the ill-appearing infant (younger than 90 days of age)".)
●Central nervous system conditions – Central nervous system (CNS) pathology can result in an elevated body temperature and alteration in mental status. This can occur from acute or chronic injury isolated to the hypothalamus (eg, CNS infection, cerebrovascular accident, hemorrhage). However, traumatic brain injury involving any part of the brain can cause neurogenic fever . In addition, congenital anomalies of the brain may cause temperature dysregulation, including hyperthermia. In all of these conditions, the CNS abnormality precedes temperature elevation.
●Status epilepticus – Status epilepticus from any cause can result in hyperthermia. The most common cause of status epilepticus in young children is prolonged febrile seizures or underlying epilepsy. Rhabdomyolysis is a common comorbidity. Clinical features may be indistinguishable from heat stroke. (See "Clinical features and complications of status epilepticus in children" and "Clinical features and evaluation of febrile seizures".)
●Toxic overdose – Drug-related causes of seizures and hyperthermia (eg, overdose of cocaine, methamphetamine, amphetamine, MDMA [ecstasy], salicylates, anticholinergic agents) are important considerations in the hyperthermic child. Therapeutic levels of prescribed amphetamines or anticholinergic agents may also impair thermoregulation. In addition, salicylate intoxication also causes uncoupling of oxidative phosphorylation with hyperthermia and multiple organ failure. A history of drug exposure, an elevated salicylate level, or a positive toxicology screen for drugs of abuse is typically present. (See "Cocaine: Acute intoxication" and "MDMA (ecstasy) intoxication" and "Methamphetamine: Acute intoxication" and "Anticholinergic poisoning" and "Salicylate poisoning in children and adolescents".)
●Serotonin syndrome – Hyperthermia commonly occurs in patients with serotonin syndrome, a potentially life-threatening condition associated with increased serotonergic activity in the central nervous system (CNS). Although classically described as the triad of mental status changes, autonomic hyperactivity, and neuromuscular abnormalities, serotonin syndrome is actually a spectrum of clinical findings ranging from benign to lethal. The recognition that the patient has been exposed to a serotonergic drug is essential to the diagnosis. (See "Serotonin syndrome (serotonin toxicity)".)
●Hemorrhagic shock and encephalopathy syndrome – Hemorrhagic shock and encephalopathy syndrome is a rare condition associated with hyperpyrexia, altered mental status, shock, disseminated intravascular coagulopathy, diarrhea, renal insufficiency, and liver failure, primarily in previously healthy infants under one year of age [45-47]. Although the etiology is unknown, this syndrome is very similar to heat stroke and is treated with supportive care and rapid cooling.
●Neuroleptic malignant syndrome – Neuroleptic malignant syndrome (NMS) is an idiosyncratic reaction to antipsychotic agents. In addition to hyperthermia, NMS is also characterized by "lead pipe" muscle rigidity, altered mental status, choreoathetosis, tremors, and evidence of autonomic dysfunction, such as diaphoresis, labile blood pressure, and arrhythmias. The history of antipsychotic drug exposure is a key component of the diagnosis. (See "Neuroleptic malignant syndrome".)
●Thyroid storm – Although most commonly seen in adults, children can, very rarely, manifest symptoms of thyroid storm including tachycardia, heart failure, and hyperpyrexia (temperature elevation up to 41.1ºC [106ºF]). Agitation, delirium, psychosis, stupor, or coma is usually associated with the diagnosis. Although thyroid storm can develop in patients with long-standing untreated hyperthyroidism, it is more often precipitated by an acute event such as thyroid or nonthyroidal surgery, trauma, infection, or an acute iodine load. (See "Thyroid storm".)
●Malignant hyperthermia – Malignant hyperthermia is a rare genetic disorder that manifests following exposure to certain agents, most commonly succinylcholine and halothane. Other potent inhalational anesthetics (eg, sevoflurane, desflurane, isoflurane) can also cause malignant hyperthermia. The onset of malignant hyperthermia is usually within one hour of the administration of general anesthesia, but rarely, may be delayed up to 10 hours after induction. (See "Malignant hyperthermia: Clinical diagnosis and management of acute crisis".)
PREHOSPITAL CARE — In general, children who have a loss of consciousness with exertion in warm weather should be treated as patients with heat stroke. However, the diagnosis of heat-related illness can be challenging in the prehospital environment. Core temperature measurement is generally not performed, and some cooling may have occurred prior to the arrival of prehospital personnel. Furthermore, the history in these patients is often unreliable, and mild environmental conditions may lead to a low level of suspicion for heat-related illnesses .
There are no studies that address the best method of prehospital cooling in the pediatric population. The following guidance for prehospital treatment is based on small trials and observational series performed in adult populations:
●Patients with severe heat-related illness require removal from the source of heat stress and rapid initiation of cooling, as the risk of morbidity and mortality for patients with heat-related illness is associated with the duration of hyperthermia [4,49].
●We suggest that children with heat stroke undergo treatment with either ice water immersion (if equipment and trained personnel are immediately available for initiation of this technique) or evaporative external cooling in the field [50,51]. Evaporative external cooling may be initiated if immersion cannot be performed. Prehospital cooling measure should be initiated prior to, or simultaneously with, activation of emergency medical services. The procedure for prehospital ice water immersion is described separately. (See "Exertional heat illness in adolescents and adults: Management and prevention", section on 'Cooling measures'.)
Evaporative cooling may be accomplished in the field by spraying patients with water or saline and fanning these patients, either manually or with ambulance fans or air-conditioners. Application of ice packs to the neck, axilla, and groin and administration of room temperature intravenous normal saline may complement evaporative cooling efforts. Interventions include the removal of clothing and external cooling techniques. The institution of prehospital cooling in children should not delay timely transportation to definitive care. (See 'Rapid cooling' below.)
Because significant cooling can occur during transport, the prehospital provider should relay the concern for heat-related illness to clinicians at the hospital.
Prehospital management for healthy adolescents and adults with exertional heat illness is discussed in detail separately. (See "Exertional heat illness in adolescents and adults: Management and prevention", section on 'Prehospital'.)
Stabilization — In addition to the careful assessment and support of airway, breathing, and circulation, the clinician should anticipate and aggressively manage hyperthermia, dehydration, rhabdomyolysis, disseminated intravascular coagulation, high output cardiac insufficiency, renal failure, and hepatic failure [52,53]. (See 'Rapid cooling' below and 'Treatment of end-organ dysfunction' below.)
Initial stabilization should focus on the following:
●Airway and breathing – Children with heat stroke frequently require basic or advanced airway management to maintain oxygenation and ventilation because of central nervous system effects (eg, coma, seizures). (See "Basic airway management in children" and "Emergency endotracheal intubation in children".)
●Circulation – All patients with heat stroke need circulatory access, ideally with two large bore intravenous catheters or a central venous catheter. Initial therapy, however, can begin with a single peripheral catheter of any gauge or an intraosseous needle. Fluid resuscitation depends on the type of heat stroke and should replenish intravascular volume while avoiding fluid overload. Children with classic (nonexertional) heat stroke tend to only be mildly to moderately hypovolemic while those with exertional heat stroke may be moderately to severely hypovolemic. Thus, an initial rapid intravenous infusion of 20 to 40 mL/kg of normal saline may be adequate fluid resuscitation for a patient with classic heat stroke while a child with exertional heat stroke may require 60 mL/kg of normal saline or more. Infusion of room temperature fluids assists with other methods of rapid cooling. (See "Hypovolemic shock in children: Initial evaluation and management".)
Patients who are unresponsive or minimally responsive to fluid resuscitation should undergo central venous pressure monitoring to guide additional therapy. Children with heat stroke may have decreased cardiac contractility and systemic vascular resistance as a byproduct of the heat stress and require initiation of vasopressor therapy to maintain adequate tissue perfusion. (See "Initial management of shock in children", section on 'Early goal-directed therapy'.)
●Disability – Altered mental status typically resolves once oxygenation, adequate tissue perfusion, and normothermia are achieved. Seizures should be treated with benzodiazepines (eg, lorazepam 0.1 mg/kg, intravenously).
Rapid cooling — Children with heat stroke need to be treated aggressively, since the extent of end-organ damage is related to the duration of hyperthermia. No trials have compared cooling methods in children with either classic (nonexertional) or exertional heat stroke. The following recommendations are based on small trials and observational series performed in adult populations. Most studies have evaluated the impact of various types of cooling on the lowering of core body temperature in patients with exertional heat stroke [42,54-58].
●External cooling – We suggest that children with heat stroke undergo treatment with evaporative cooling. Application of ice packs to the neck, axilla, and groin and administration of room temperature intravenous normal saline may complement evaporative cooling efforts. Cooling measures should be stopped in pediatric heat stroke victims once the core temperature reaches 38°C (100.4°F) to prevent overshoot hypothermia.
Although cold water immersion has been demonstrated to more rapidly cool core body temperature in young healthy adults with exercise-induced hyperthermia greater than 38.5°C (101.3°F), it is associated with significant discomfort, shivering, agitation, and combativeness in vulnerable populations, such as the elderly and, theoretically, may be more likely to cause overshoot hypothermia and bradycardia in children [42,53,55]. Cold water immersion also hampers efforts to maintain monitoring and ongoing resuscitation in these unstable patients [42,53].
In addition, no research has demonstrated superior outcomes for adult patients undergoing cold water immersion despite the more rapid drop in core body temperatures achieved with this method . Although a systematic review suggests that ice-water immersion of exercise-induced hyperthermia >38.5°C (101.3°F) has the fastest cooling rate and is efficacious for exertional heat stroke (core temperature ≥40°C [104°F]) , our view is that safety and efficacy for cold water immersion in exertional heat stroke is not established given that much of the data appears to be drawn from patients with heat exhaustion, not heat stroke.
Isopropyl alcohol baths may lead to dermal absorption with toxicity in children and should be avoided [59,60].
Cooling rates and practical considerations are summarized as follows:
•Evaporative cooling – Evaporative cooling is achieved by spraying patients with tepid water (to minimize shivering) while fanning with high-flow fans to maximize air circulation. Cooling rates approaching 0.15°C per minute (0.27°F per minute) have been achieved in adults . Both spray bottles and fans are usually available from hospital housekeeping services. Suspension of the patient on a mesh hammock during treatment enhances air circulation and may increase the rate of cooling. Alternatively, the patient may be placed on a cooling blanket to enhance conductive cooling. If tolerated, selective application of ice packs to the neck, axillae, and groin during evaporative cooling may be of additional benefit.
•Cold water immersion – Cold water immersion is another adjunctive cooling modality when evaporative cooling with or without selective ice application is not possible . It remains unclear whether the inherent impediments of immersion to safe monitoring and resuscitation in the hospital outweigh the putative benefits .
•Other methods – In adults, cooling methods such as cooling blankets alone, covering patients in ice, covering patients with a wet sheet while fanning, or selective application of ice packs to the neck, axillae, and groin have very low to negligible cooling effect . However, cooling blankets with ice packs have been an effective form of total body cooling in infants after cardiac arrest  and might achieve rapid cooling in a small infant. If used, neuromuscular blockade or sedation may be necessary to prevent shivering. (See 'Pharmacologic therapy' below.)
●Internal cooling – The most effective method of lowering the core body temperature quickly is the use of cardiopulmonary bypass; however, this highly specialized intervention is not rapidly available at most institutions. Newer, less invasive devices such as intravascular cooling catheters have been utilized to rapidly induce therapeutic hypothermia in order to treat or prevent neurologic injury in victims of cardiac arrest and may be useful in cooling efforts, although their effect has not been studied in heat stroke victims [62-64]. Similarly, intravenous (IV) infusion of chilled normal saline via peripheral lines has been advocated although little data exist regarding its efficacy.
Gastric, rectal, and/or bladder lavage with cold isotonic fluids (eg, normal saline that has been iced) have been proposed as additional means of invasive cooling [53,65-67]. However, it is not clear that these methods are any more effective than evaporative cooling or cold water immersion alone. For example, in canine studies, iced gastric lavage was inferior to evaporative cooling , while iced peritoneal lavage was equivalent . Thus, these methods are not routinely employed.
Duration of cooling — Decreases in core body temperature as measured by rectal temperature generally lag behind the actual drop in core temperature at the hypothalamus . For this reason, cooling measures are generally stopped in pediatric heat stroke victims once the core temperature reaches approximately 38°C (100.4°F) to prevent overshoot hypothermia [52,53]. The amount of time required to reach this endpoint depends on the patient's initial temperature and the mode of cooling. (See 'Rapid cooling' above.)
Pharmacologic therapy — Medications have a limited role in the management of heat stroke. However, pharmacologic measures taken to prevent shivering in heat stroke patients undergoing cooling may prevent increased endogenous heat production.
The majority of studies investigating the use of medications to treat shivering have been conducted in perioperative settings, and no controlled studies have been conducted in patients with heat illness . We suggest that patients with heat stroke receive benzodiazepines (eg, midazolam 0.05 to 0.1 mg/kg intravenously) to prevent shivering during cooling measures. Benzodiazepines have the added benefit of treating or preventing seizures. (See 'Stabilization' above.)
Although antipsychotic agents (eg, chlorpromazine) have been used in adults to prevent shivering, their alpha-1 blocking properties may exacerbate hypotension in heat stroke victims. They also have a greater propensity to cause dystonia in children. Thus, they should be avoided.
Dantrolene, a nonspecific skeletal muscle relaxant that acts by blocking the release of calcium from the sarcoplasmic reticulum, is used for the treatment of malignant hyperthermia and was once proposed as a treatment for hyperthermia from heat stroke. Although initial evidence suggested that dantrolene shortened cooling times in adults with heat stroke, additional small trials have not identified a consistent benefit [69-71]. Thus, dantrolene is not routinely used. Some experts advocate the use of dantrolene in patients who are not responsive or are poorly responsive to initial cooling efforts .
Antipyretic medications (eg, acetaminophen, ibuprofen) are ineffective for the treatment of hyperthermia in heat stroke victims and should not be used because they may exacerbate liver injury (acetaminophen) or compound coagulation disorders (nonsteroidal antiinflammatory agents, eg, ibuprofen).
Treatment of end-organ dysfunction — After stabilization and rapid cooling, the child with heat stroke remains at high risk for multiple organ failure, metabolic abnormalities, and disorders of coagulation. The clinician should carefully evaluate for the following abnormalities and treat accordingly:
●Rhabdomyolysis with hyperkalemia, hypocalcemia, and hyperphosphatemia (see "Prevention and treatment of heme pigment-induced acute kidney injury")
●Disseminated intravascular coagulation (see "Disseminated intravascular coagulation in infants and children", section on 'Treatment')
●Acute kidney injury (see "Prevention and management of acute kidney injury (acute renal failure) in children")
●Hyponatremic dehydration (see "Treatment of hypovolemia (dehydration) in children", section on 'Therapy according to serum sodium')
●Cardiogenic shock with low systemic vascular resistance (see "Initial management of shock in children", section on 'Early goal-directed therapy')
●Cardiogenic and noncardiogenic pulmonary edema (see "Noncardiogenic pulmonary edema", section on 'Permeability pulmonary edema due to ARDS')
●Liver failure - Treatment is supportive. Rarely, liver transplantation has been necessary in teenagers with heat stroke-associated liver failure [72-75] (see "Acute liver failure in adults: Management and prognosis")
●Cerebral edema (see "Elevated intracranial pressure (ICP) in children: Management", section on 'Ongoing Management' and "Elevated intracranial pressure (ICP) in children: Management", section on 'Treatment of elevated ICP')
Disposition — All children with heat stroke should be admitted to a pediatric critical care unit setting in order to maintain appropriate monitoring and to treat ongoing and delayed end-organ dysfunction. (See 'Treatment of end-organ dysfunction' above.)
If there is no pediatric critical care coverage at the admitting hospital, the child should be resuscitated and promptly transferred to an appropriate institution.
OUTCOMES — The prognosis in children with heat stroke is poorly characterized. Extrapolation from studies in adults suggests that morbidity or mortality are directly related to duration and degree of hyperthermia. Thus, heat stroke must be treated aggressively. In addition, prognosis depends on the patient population and type of heat stroke:
●Mortality – Mortality of up to 63 percent has been reported in elderly adults with classic heat stroke. In contrast, mortality is much lower (eg, 1 to 15 percent) in adolescents and young adults with exertional heat stroke . Additional poor prognostic indicators for mortality include the height of the initial core body temperature and the number of organ systems affected during the course of treatment. (See "Severe nonexertional hyperthermia (classic heat stroke) in adults".)
●Neurologic abnormalities – Permanent neurologic damage is more commonly seen in patients with core temperatures >42ºC (107.6ºF) and consist of spasticity, ataxia, dysarthria, poor coordination, impaired memory, and behavioral changes . Patients recovering from rapidly treated exertional or classic heat stroke with core body temperatures below this level may manifest some of these neurologic findings but typically recover fully [76,77].
Heat intolerance — Heat intolerance refers to a disorder in temperature homeostasis that is seen in heat stroke victims and that places them at greater risk for repeated heat illness. The clinician should anticipate some degree of heat intolerance in all children who recover from heat stroke. Children and their family should be counseled to avoid heat exposure until repeat evaluation establishes that they have fully recovered and a period of acclimatization has occurred [78-80]. Patients with severe heat stroke may have ongoing impaired physiologic response to exertion in hot environments .
Children with exertional heat illness should only return to practice and competition when their temperature homeostasis is reestablished, generally after a minimum of one week of rest, full recovery from the initial insult based on repeat physical examination and laboratory testing (as needed to ensure all previously identified laboratory abnormalities have resolved), and a period of acclimatization [78,79]. Once these conditions are met, the child should gradually return to physical activity over two to four weeks . The decision to return to play must be individualized, taking into consideration predisposing conditions for heat illness (eg, age, obesity) .
PREVENTION — Recognition and treatment of milder forms of heat illness prevents progression to heat stroke. In addition, several precautions may be taken to help prevent heat stress. (See "Heat illness (other than heat stroke) in children", section on 'Prevention of heat illness'.)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topic (see "Patient education: Heat stroke (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Heat stroke is defined as an elevated core temperature ≥40 to 41°C (104 to 105.8°F) accompanied by central nervous system (CNS) dysfunction in children with environmental heat exposure. This condition represents a failure of the body's ability to maintain thermoregulatory homeostasis and is a true medical emergency. (See 'Heat stroke definition' above and 'Pathophysiology' above.)
●Rectal or other core body temperature measurement (eg, esophageal, bladder, or central venous temperature) is typically ≥40°C (104°F) in children with heat stroke. However, the clinician should consider the possibility that prehospital cooling efforts have potentially lowered core body temperature prior to hospital assessment when making the diagnosis. (See 'Core temperature measurement' above and 'Prehospital care' above.)
●CNS symptoms may be subtle and can manifest as impaired judgment or inappropriate behavior. However, children commonly present with more significant neurologic symptoms such as seizures, delirium, hallucinations, ataxia, dysarthria, or coma. Other common clinical features include tachycardia, tachypnea, and hypotension. The skin may be flushed and warm (classic nonexertional heat stroke) or diaphoretic (exertional heat stroke). Vomiting and diarrhea are also common. In addition, those patients with coagulopathy may demonstrate purpura, hemoptysis, hematemesis, melena, or hematochezia. (See 'Clinical features' above and 'Clinical assessment' above.)
●Children with heat stroke have abnormal laboratory findings, reflecting the systemic inflammatory response and end-organ damage resulting from heat stress. These patients warrant extensive studies to detect the presence of hypoglycemia, metabolic acidosis, anemia, disseminated intravascular coagulation, electrolyte disturbance, liver injury, prerenal azotemia, rhabdomyolysis, and exposure to illicit drugs or other toxins associated with hyperthermia. (See 'Laboratory findings' above.)
●The diagnosis of heat stroke is made on the basis of clinical findings. The full differential diagnosis of hyperthermia should be considered in each patient. In addition, there is some overlap of symptoms between heat exhaustion and heat stroke (table 3). While the distinction between heat exhaustion and heat stroke is sometimes unclear, children with elevated body temperature and CNS abnormalities should be treated as victims of heat stroke. (See 'Diagnostic evaluation' above and 'Differential diagnosis' above.)
●We suggest that children with heat stroke undergo treatment with either ice water immersion (if equipment and trained personnel are immediately available for initiation of this technique) or evaporative external cooling in the field. Prehospital cooling measure should be initiated prior to, or simultaneously with, activation of emergency medical services (Grade 2C). (See 'Prehospital care' above.)
●Children with heat stroke frequently require basic and/or advanced airway management to maintain oxygenation and ventilation because of central nervous system effects (eg, coma, seizures). (See 'Stabilization' above.)
●Fluid resuscitation depends on the type of heat stroke and should seek to replenish intravascular volume while avoiding fluid overload. Patients unresponsive or minimally responsive to fluid resuscitation should undergo central venous pressure monitoring to guide additional therapy. Children with heat stroke often have decreased cardiac contractility and systemic vascular resistance as a byproduct of the heat stress and require initiation of vasopressor therapy to maintain adequate tissue perfusion. (See 'Stabilization' above.)
●Children with heat stroke need to be treated aggressively, because the extent of end-organ damage is related to the duration of hyperthermia. We suggest that children with heat stroke undergo treatment with evaporative external cooling (Grade 2C). Application of ice packs to the neck, axilla, and groin and administration of room temperature intravenous normal saline may complement evaporative cooling efforts. Cooling measures should be stopped in pediatric heat stroke victims once the core temperature reaches 38ºC (100.4ºF) to prevent overshoot hypothermia. (See 'Rapid cooling' above and 'Duration of cooling' above and 'Pharmacologic therapy' above and 'Prehospital care' above.)
●In addition to rapid cooling and careful assessment and support of airway, breathing, and circulation, the clinician should anticipate and aggressively manage dehydration, rhabdomyolysis, disseminated intravascular coagulation, high output cardiac insufficiency, renal failure, and hepatic failure. (See 'Treatment of end-organ dysfunction' above.)
●All children with heat stroke should be admitted to a pediatric critical care unit setting in order to maintain appropriate monitoring and to treat ongoing and delayed end-organ dysfunction. If there is no pediatric critical care coverage at the admitting hospital, the child should be resuscitated and promptly transferred to an appropriate institution. (See 'Disposition' above.)
- Bouchama A, Knochel JP. Heat stroke. N Engl J Med 2002; 346:1978.
- Seeyave DM, Brown KM. Environmental emergencies, radiological emergencies, bites and stings. In: Fleisher & Ludwig's Textbook of Pediatric Emergency Medicine, 7th ed, Shaw KN, Bachur RG (Eds), Wolters Kluwer, Philadelphia 2016. p.718.
- Simon HB. Hyperthermia. N Engl J Med 1993; 329:483.
- Heled Y, Rav-Acha M, Shani Y, et al. The "golden hour" for heatstroke treatment. Mil Med 2004; 169:184.
- Berko J, Ingram DD, Saha S, Parker JD. Deaths attributed to heat, cold, and other weather events in the United States, 2006-2010. Natl Health Stat Report 2014; :1.
- Centers for Disease Control and Prevention (CDC). Heat-related mortality--Arizona, 1993-2002, and United States, 1979-2002. MMWR Morb Mortal Wkly Rep 2005; 54:628.
- Centers for Disease Control and Prevention (CDC). Heat-related deaths--Chicago, Illinois, 1996-2001, and United States, 1979-1999. MMWR Morb Mortal Wkly Rep 2003; 52:610.
- Centers for Disease Control and Prevention (CDC). Heat-related deaths--four states, July-August 2001, and United States, 1979-1999. MMWR Morb Mortal Wkly Rep 2002; 51:567.
- Centers for Disease Control and Prevention (CDC). Heat-related deaths--United States, 1999-2003. MMWR Morb Mortal Wkly Rep 2006; 55:796.
- Dhainaut JF, Claessens YE, Ginsburg C, Riou B. Unprecedented heat-related deaths during the 2003 heat wave in Paris: consequences on emergency departments. Crit Care 2004; 8:1.
- McLaren C, Null J, Quinn J. Heat stress from enclosed vehicles: moderate ambient temperatures cause significant temperature rise in enclosed vehicles. Pediatrics 2005; 116:e109.
- Guard A, Gallagher SS. Heat related deaths to young children in parked cars: an analysis of 171 fatalities in the United States, 1995-2002. Inj Prev 2005; 11:33.
- King K, Negus K, Vance JC. Heat stress in motor vehicles: a problem in infancy. Pediatrics 1981; 68:579.
- Roberts KB, Roberts EC. The automobile and heat stress. Pediatrics 1976; 58:101.
- Coris EE, Ramirez AM, Van Durme DJ. Heat illness in athletes: the dangerous combination of heat, humidity and exercise. Sports Med 2004; 34:9.
- Rice SG, American Academy of Pediatrics Council on Sports Medicine and Fitness. Medical conditions affecting sports participation. Pediatrics 2008; 121:841.
- Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980-2006. Circulation 2009; 119:1085.
- Van Camp SP, Bloor CM, Mueller FO, et al. Nontraumatic sports death in high school and college athletes. Med Sci Sports Exerc 1995; 27:641.
- Centers for Disease Control and Prevention (CDC). Heat illness among high school athletes --- United States, 2005-2009. MMWR Morb Mortal Wkly Rep 2010; 59:1009.
- Centers for Disease Control and Prevention (CDC). Nonfatal sports and recreation heat illness treated in hospital emergency departments--United States, 2001-2009. MMWR Morb Mortal Wkly Rep 2011; 60:977.
- Nelson NG, Collins CL, Comstock RD, McKenzie LB. Exertional heat-related injuries treated in emergency departments in the U.S., 1997-2006. Am J Prev Med 2011; 40:54.
- Bailes JE, Cantu RC, Day AL. The neurosurgeon in sport: awareness of the risks of heatstroke and dietary supplements. Neurosurgery 2002; 51:283.
- Yoshizumi WM, Tsourounis C. Effects of creatine supplementation on renal function. J Herb Pharmacother 2004; 4:1.
- Khosla R, Guntupalli KK. Heat-related illnesses. Crit Care Clin 1999; 15:251.
- Bross MH, Nash BT Jr, Carlton FB Jr. Heat emergencies. Am Fam Physician 1994; 50:389.
- Bytomski JR, Squire DL. Heat illness in children. Curr Sports Med Rep 2003; 2:320.
- Council on Sports Medicine and Fitness and Council on School Health, Bergeron MF, Devore C, et al. Policy statement—Climatic heat stress and exercising children and adolescents. Pediatrics 2011; 128:e741.
- Naughton GA, Carlson JS. Reducing the risk of heat-related decrements to physical activity in young people. J Sci Med Sport 2008; 11:58.
- Rowland T. Thermoregulation during exercise in the heat in children: old concepts revisited. J Appl Physiol (1985) 2008; 105:718.
- Falk B. Effects of thermal stress during rest and exercise in the paediatric population. Sports Med 1998; 25:221.
- Falk B, Bar-Or O, Calvert R, MacDougall JD. Sweat gland response to exercise in the heat among pre-, mid-, and late-pubertal boys. Med Sci Sports Exerc 1992; 24:313.
- Wagner JA, Robinson S, Tzankoff SP, Marino RP. Heat tolerance and acclimatization to work in the heat in relation to age. J Appl Physiol 1972; 33:616.
- Bar-Or O, Dotan R, Inbar O, et al. Voluntary hypohydration in 10- to 12-year-old boys. J Appl Physiol Respir Environ Exerc Physiol 1980; 48:104.
- Bar-Or O, Wilk B. Water and electrolyte replenishment in the exercising child. Int J Sport Nutr 1996; 6:93.
- Seto CK, Way D, O'Connor N. Environmental illness in athletes. Clin Sports Med 2005; 24:695.
- Nielsen B, Hales JR, Strange S, et al. Human circulatory and thermoregulatory adaptations with heat acclimation and exercise in a hot, dry environment. J Physiol 1993; 460:467.
- Bynum GD, Pandolf KB, Schuette WH, et al. Induced hyperthermia in sedated humans and the concept of critical thermal maximum. Am J Physiol 1978; 235:R228.
- Leon LR. Heat stroke and cytokines. Prog Brain Res 2007; 162:481.
- Lim CL, Mackinnon LT. The roles of exercise-induced immune system disturbances in the pathology of heat stroke : the dual pathway model of heat stroke. Sports Med 2006; 36:39.
- Mustafa KY, Omer O, Khogali M, et al. Blood coagulation and fibrinolysis in heat stroke. Br J Haematol 1985; 61:517.
- Bouchama A, Bridey F, Hammami MM, et al. Activation of coagulation and fibrinolysis in heatstroke. Thromb Haemost 1996; 76:909.
- Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care 2007; 11:R54.
- Bouchama A, De Vol EB. Acid-base alterations in heatstroke. Intensive Care Med 2001; 27:680.
- Thompson HJ, Pinto-Martin J, Bullock MR. Neurogenic fever after traumatic brain injury: an epidemiological study. J Neurol Neurosurg Psychiatry 2003; 74:614.
- Gefen R, Eshel G, Abu-Kishk I, et al. Hemorrhagic shock and encephalopathy syndrome: clinical course and neurological outcome. J Child Neurol 2008; 23:589.
- Levin M, Pincott JR, Hjelm M, et al. Hemorrhagic shock and encephalopathy: clinical, pathologic, and biochemical features. J Pediatr 1989; 114:194.
- Rinka H, Yoshida T, Kubota T, et al. Hemorrhagic shock and encephalopathy syndrome--the markers for an early HSES diagnosis. BMC Pediatr 2008; 8:43.
- Shapiro Y, Seidman DS. Field and clinical observations of exertional heat stroke patients. Med Sci Sports Exerc 1990; 22:6.
- Vicario SJ, Okabajue R, Haltom T. Rapid cooling in classic heatstroke: effect on mortality rates. Am J Emerg Med 1986; 4:394.
- Lipman GS, Eifling KP, Ellis MA, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of heat-related illness. Wilderness Environ Med 2013; 24:351.
- Pryor RR, Roth RN, Suyama J, Hostler D. Exertional heat illness: emerging concepts and advances in prehospital care. Prehosp Disaster Med 2015; 30:297.
- Jardine DS. Heat illness and heat stroke. Pediatr Rev 2007; 28:249.
- Glazer JL. Management of heatstroke and heat exhaustion. Am Fam Physician 2005; 71:2133.
- Smith JE. Cooling methods used in the treatment of exertional heat illness. Br J Sports Med 2005; 39:503.
- McDermott BP, Casa DJ, Ganio MS, et al. Acute whole-body cooling for exercise-induced hyperthermia: a systematic review. J Athl Train 2009; 44:84.
- Gaffin SL, Gardner JW, Flinn SD. Cooling methods for heatstroke victims. Ann Intern Med 2000; 132:678.
- Clements JM, Casa DJ, Knight J, et al. Ice-Water Immersion and Cold-Water Immersion Provide Similar Cooling Rates in Runners With Exercise-Induced Hyperthermia. J Athl Train 2002; 37:146.
- Proulx CI, Ducharme MB, Kenny GP. Effect of water temperature on cooling efficiency during hyperthermia in humans. J Appl Physiol (1985) 2003; 94:1317.
- McFadden SW, Haddow JE. Coma produced by topical application of isopropanol. Pediatrics 1969; 43:622.
- Arditi M, Killner MS. Coma following use of rubbing alcohol for fever control. Am J Dis Child 1987; 141:237.
- Hutchison JS, Doherty DR, Orlowski JP, Kissoon N. Hypothermia therapy for cardiac arrest in pediatric patients. Pediatr Clin North Am 2008; 55:529.
- Polderman KH, Herold I. Therapeutic hypothermia and controlled normothermia in the intensive care unit: practical considerations, side effects, and cooling methods. Crit Care Med 2009; 37:1101.
- Broessner G, Beer R, Franz G, et al. Case report: severe heat stroke with multiple organ dysfunction - a novel intravascular treatment approach. Crit Care 2005; 9:R498.
- Mégarbane B, Résière D, Delahaye A, Baud FJ. Endovascular hypothermia for heat stroke: a case report. Intensive Care Med 2004; 30:170.
- Syverud SA, Barker WJ, Amsterdam JT, et al. Iced gastric lavage for treatment of heatstroke: efficacy in a canine model. Ann Emerg Med 1985; 14:424.
- White JD, Riccobene E, Nucci R, et al. Evaporation versus iced gastric lavage treatment of heatstroke: comparative efficacy in a canine model. Crit Care Med 1987; 15:748.
- White JD, Kamath R, Nucci R, et al. Evaporation versus iced peritoneal lavage treatment of heatstroke: comparative efficacy in a canine model. Am J Emerg Med 1993; 11:1.
- WYNDHAM CH, STRYDOM NB, COOKE HM, et al. Methods of cooling subjects with hyperpyrexia. J Appl Physiol 1959; 14:771.
- Bouchama A, Cafege A, Devol EB, et al. Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Crit Care Med 1991; 19:176.
- Channa AB, Seraj MA, Saddique AA, et al. Is dantrolene effective in heat stroke patients? Crit Care Med 1990; 18:290.
- Hadad E, Cohen-Sivan Y, Heled Y, Epstein Y. Clinical review: Treatment of heat stroke: should dantrolene be considered? Crit Care 2005; 9:86.
- Berger J, Hart J, Millis M, Baker AL. Fulminant hepatic failure from heat stroke requiring liver transplantation. J Clin Gastroenterol 2000; 30:429.
- Hadad E, Ben-Ari Z, Heled Y, et al. Liver transplantation in exertional heat stroke: a medical dilemma. Intensive Care Med 2004; 30:1474.
- Pastor MA, Pérez-Aguilar F, Ortiz V, et al. [Acute hepatitis due to heatstroke]. Gastroenterol Hepatol 1999; 22:398.
- Takahashi K, Chin K, Ogawa K, et al. Living donor liver transplantation with noninvasive ventilation for exertional heat stroke and severe rhabdomyolysis. Liver Transpl 2005; 11:570.
- American College of Sports Medicine, Armstrong LE, Casa DJ, et al. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med Sci Sports Exerc 2007; 39:556.
- Royburt M, Epstein Y, Solomon Z, Shemer J. Long-term psychological and physiological effects of heat stroke. Physiol Behav 1993; 54:265.
- Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior exertional heatstroke patients. Med Sci Sports Exerc 1990; 22:36.
- Epstein Y. Heat intolerance: predisposing factor or residual injury? Med Sci Sports Exerc 1990; 22:29.
- Shapiro Y, Magazanik A, Udassin R, et al. Heat intolerance in former heatstroke patients. Ann Intern Med 1979; 90:913.