Introduction
Background
Heat illness may be viewed as a continuum of illnesses relating to the body's inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (ie, prickly heat), heat cramps, and tetany, as well as heat syncope and heat exhaustion. Heatstroke is the most severe form of the heat-related illnesses and is defined as a body temperature higher than 41.1°C (106°F) associated with neurologic dysfunction.
Two forms of heatstroke exist. Exertional heatstroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment. Classic nonexertional heatstroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons. Classic NEHS occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years. Both types of heatstroke are associated with a high morbidity and mortality, especially when therapy is delayed.
With the influence of global warming, it is predicted that the incidence of heatstroke cases and fatalities will also become more prevalent. Because behavioral responses are important in the management of temperature elevations, heatstroke may be entirely preventable.
Pathophysiology
Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body's mechanisms of heat loss, the body temperature rises, and a major heat illness ensues. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death. The exact temperature at which cardiovascular collapse occurs varies among individuals because coexisting disease, drugs, and other factors may contribute to or delay organ dysfunction. Full recovery has been observed in patients with temperatures as high as 46°C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106°F or 41.1°C generally are catastrophic and require immediate aggressive therapy.
Heat may be acquired by a number of different mechanisms. At rest, basal metabolic processes produce approximately 100 kcal of heat per hour or 1 kcal/kg/h. These reactions can raise the body temperature by 1.1°C/h if the heat dissipating mechanisms are nonfunctional. Strenuous physical activity can increase heat production more than 10-fold to levels exceeding 1000 kcal/h. Similarly, fever, shivering, tremors, convulsions, thyrotoxicosis, sepsis, sympathomimetic drugs, and many other conditions can increase heat production, thereby increasing body temperature.
The body also can acquire heat from the environment through some of the same mechanisms involved in heat dissipation, including conduction, convection, and radiation. These mechanisms occur at the level of the skin and require a properly functioning skin surface, sweat glands, and autonomic nervous system, but they also may be manipulated by behavioral responses. Conduction refers to the transfer of heat between 2 surfaces with differing temperatures that are in direct contact. Convection refers to the transfer of heat between the body's surface and a gas or fluid with a differing temperature. Radiation refers to the transfer of heat in the form of electromagnetic waves between the body and its surroundings. The efficacy of radiation as a means of heat transfer depends on the angle of the sun, the season, and the presence of clouds, among other factors. For example, during summer, lying down in the sun can result in a heat gain of up to 150 kcal/h.
Under normal physiologic conditions, heat gain is counteracted by a commensurate heat loss. This is orchestrated by the hypothalamus, which functions as a thermostat, guiding the body through mechanisms of heat production or heat dissipation, thereby maintaining the body temperature at a constant physiologic range. In a simplified model, thermosensors located in the skin, muscles, and spinal cord send information regarding the core body temperature to the anterior hypothalamus, where the information is processed and appropriate physiologic and behavioral responses are generated. Physiologic responses to heat include an increase in the blood flow to the skin (as much as 8 L/min), which is the major heat-dissipating organ; dilatation of the peripheral venous system; and stimulation of the eccrine sweat glands to produce more sweat.
As the major heat-dissipating organ, the skin can transfer heat to the environment through conduction, convection, radiation, and evaporation. Radiation is the most important mechanism of heat transfer at rest in temperate climates, accounting for 65% of heat dissipation, and it can be modulated by clothing. At high ambient temperatures, conduction becomes the least important of the 4 mechanisms, while evaporation, which refers to the conversion of a liquid to a gaseous phase, becomes the most effective mechanism of heat loss.
The efficacy of evaporation as a mechanism of heat loss depends on the condition of the skin and sweat glands, the function of the lung, ambient temperature, humidity, air movement, and whether or not the person is acclimated to the high temperatures. For example, evaporation does not occur when the ambient humidity exceeds 75% and is less effective in individuals who are not acclimated. Nonacclimated individuals can only produce 1 L of sweat per hour, which only dispels 580 kcal of heat per hour, whereas acclimated individuals can produce 2-3 L of sweat per hour and can dissipate as much as 1740 kcal of heat per hour through evaporation. Acclimatization to hot environments usually occurs over 7-10 days and enables individuals to reduce the threshold at which sweating begins, increase sweat production, and increase the capacity of the sweat glands to reabsorb sweat sodium, thereby increasing the efficiency of heat dissipation.
When heat gain exceeds heat loss, the body temperature rises. Classic heatstroke occurs in individuals who lack the capacity to modulate the environment (eg, infants, elderly individuals, individuals who are chronically ill). Furthermore, elderly persons and patients with diminished cardiovascular reserves are unable to generate and cope with the physiologic responses to heat stress and, therefore, are at risk of heatstroke. Patients with skin diseases and those taking medications that interfere with sweating also are at increased risk for heatstroke because they are unable to dissipate heat adequately. Additionally, the redistribution of blood flow to the periphery, coupled with the loss of fluids and electrolytes in sweat, place a tremendous burden on the heart, which ultimately may fail to maintain an adequate cardiac output, leading to additional morbidity and mortality.
Factors that interfere with heat dissipation include an inadequate intravascular volume, cardiovascular dysfunction, and abnormal skin. Additionally, high ambient temperatures, high ambient humidity, and many drugs can interfere with heat dissipation, resulting in a major heat illness. Similarly, hypothalamic dysfunction may alter temperature regulation and may result in an unchecked rise in temperature and heat illness.
On a cellular level, many theories have been hypothesized and clinically scrutinized. Generally speaking, heat directly influences the body on a cellular level by interfering with cellular processes along with denaturing proteins and cellular membranes. In turn, an array of inflammatory cytokines and heat shock proteins (HSPs) (HSP-70 in particular, which allows the cell to endure the stress of its environment), are produced. If the stress continues, the cell will succumb to the stress (apoptosis) and die. Certain preexisting factors, such as age, genetic makeup, and the nonacclimatized individual, may allow progression from heat stress to heatstroke, multiorgan-dysfunction syndrome (MODS), and ultimately death. Progression to heatstroke may occur through thermoregulatory failure, an amplified acute-phase response, and alterations in the expression of HSPs.
Frequency
United States
According to the National Centers for Health Statistics (NCHS), 7046 deaths were attributed to excessive heat exposure from 1979-1997, or an average of 371 deaths occurred per year. Heatstroke and deaths from excessive heat exposure are more common during summers with prolonged heat waves. For example, during the heat wave of 1980 (a record year for heat), 1700 deaths were attributed to heat, compared to only 148 deaths attributed to heat the previous year. Persons older than 65 years accounted for at least 44% of cases. The numbers published by the NCHS are believed to grossly underestimate the true incidence of heat-related deaths because death rates from other causes (eg, cardiovascular disease, respiratory disease) also increase during the summer, and especially during heat waves.
International
Heatstroke is uncommon in subtropical climates. The condition is recognized increasingly in countries that experience heat waves rarely (eg, Japan), and it commonly affects people who undertake a pilgrimage to Mecca, especially when the pilgrims arrive from a cold environment. In 1998, one of the worst heat waves to strike India in 50 years resulted in more than 2600 deaths in 10 weeks. Unofficial reports described the number of deaths as almost double that figure.
Mortality/Morbidity
Morbidity and mortality from heatstroke are related to the duration of the temperature elevation. When therapy is delayed, the mortality rate may be as high as 80%; however, with early diagnosis and immediate cooling, the mortality rate can be reduced to 10%. Mortality is highest among the elderly population, patients with preexisting disease, those confined to a bed, and those who are socially isolated.
Race
With the same risk factors and under the same environmental conditions, heatstroke affects all races equally. However, because of differences in social advantages, the annual death rate due to environmental conditions is more than 3 times higher in blacks than in whites.
Sex
With the same risk factors and under the same environmental conditions, heatstroke affects both genders equally. However, because of gender differences in the workforce, the annual death rate due to environmental conditions is 2 times higher in men than in women.
Age
Infants, children, and elderly persons have a higher incidence of heatstroke than young, healthy adults.
- Infants and children are at risk for heat illness due to inefficient sweating, a higher metabolic rate, and their inability to care for themselves and control their environment.
- Elderly persons also are at increased risk for heat-related illnesses because of their limited cardiovascular reserves, preexisting illness, and use of many medications that may affect their volume status or sweating ability. In addition, elderly people who are unable to care for themselves are at increased risk for heatstroke, presumably because of their inability to control their environment.
- EHS is the second most common cause of death among high school athletes, surpassed only by spinal cord injury. Lack of acclimatization is a major risk factor for EHS in young adults.
Clinical
History
Heatstroke is defined typically as hyperthermia exceeding 41°C and anhidrosis associated with an altered sensorium. However, when a patient is allowed to cool down prior to measurement of the temperature (as may occur during transportation in a cool ambulance or evaluation in an emergency department), the measured temperature may be much lower than 41°C, making the temperature criterion relative. Similarly, some patients may retain the ability to sweat, removing anhidrosis as a criterion for the diagnosis of heatstroke. Therefore, strict adherence to the definition is not advised because it may result in dangerous delays in diagnosis and therapy.
Clinically, 2 forms of heatstroke are differentiated. Classic heatstroke, which occurs during environmental heat waves, is more common in very young persons and in the elderly population and should be suspected in children, elderly persons, and individuals who are chronically ill who present with an altered sensorium. Classic heatstroke occurs because of failure of the body's heat dissipating mechanisms.
On the other hand, EHS affects young, healthy individuals who engage in strenuous physical activity, and EHS should be suspected in all individuals with bizarre irrational behavior or a history of syncope during strenuous exercise. EHS results from increased heat production, which overwhelms the body's ability to dissipate heat.
- Exertional heatstroke
- EHS is characterized by hyperthermia, diaphoresis, and an altered sensorium, which may manifest suddenly during extreme physical exertion in a hot environment.
- A number of symptoms (eg, abdominal and muscular cramping, nausea, vomiting, diarrhea, headache, dizziness, dyspnea, weakness) commonly precede the heatstroke and may remain unrecognized. Syncope and loss of consciousness also are observed commonly before the development of EHS.
- EHS commonly is observed in young, healthy individuals (eg, athletes, firefighters, military personnel) who, while engaging in strenuous physical activity, overwhelm their thermoregulatory system and become hyperthermic. Because their ability to sweat remains intact, patients with EHS are able to cool down after cessation of physical activity and may present for medical attention with temperatures well below 41°C.
- Risk factors that increase the likelihood of heat-related illnesses include a preceding viral infection, dehydration, fatigue, obesity, lack of sleep, poor physical fitness, and lack of acclimatization. Although lack of acclimatization is a risk factor for heatstroke, EHS also can occur in acclimatized individuals who are subjected to moderately intense exercise.
- EHS also may occur because of increased motor activity due to drug use, such as cocaine and amphetamines, and as a complication of status epilepticus.
- Nonexertional heatstroke
- Classic NEHS is characterized by hyperthermia, anhidrosis, and an altered sensorium, which develop suddenly after a period of prolonged elevations in ambient temperatures (ie, heat waves). Core body temperatures greater than 41°C are diagnostic, although heatstroke may occur with lower core body temperatures.
- Numerous CNS symptoms, ranging from minor irritability to delusions, irrational behavior, hallucinations, and coma have been described.
- Anhidrosis due to cessation of sweating is a late occurrence in heatstroke and may not be present when patients are examined.
- Other CNS symptoms include hallucinations, seizures, cranial nerve abnormalities, cerebellar dysfunction, and opisthotonos.
- Patients with NEHS initially may exhibit a hyperdynamic circulatory state, but, in severe cases, hypodynamic states may be noted.
- Classic heatstroke most commonly occurs during episodes of prolonged elevations in ambient temperatures. It affects people who are unable to control their environment and water intake (eg, infants, elderly persons, individuals who are chronically ill), people with reduced cardiovascular reserve (eg, elderly persons, patients with chronic cardiovascular illnesses), and people with impaired sweating (eg, patients with skin disease, patients ingesting anticholinergic and psychiatric drugs). In addition, infants have an immature thermoregulatory system, and elderly persons have impaired perception of changes in body and ambient temperatures and a decreased capacity to sweat.
Physical
- Vital signs
- Temperature: Typically, the patient's temperature exceeds 41°C, but, in the presence of sweating, evaporating mechanisms, and the initiation of cooling methods, body temperatures lower than 41°C are common.
- Pulse: Tachycardia to rates exceeding 130 beats per minute is common.
- Blood pressure: Patients commonly are normotensive, with a wide pulse pressure; however, hypotension is common and is due to a number of factors, including vasodilation of the cutaneous vessels, pooling of the blood in the venous system, and dehydration. Hypotension also may be due to myocardial damage and may signal cardiovascular collapse.
- Central nervous system
- Symptoms of CNS dysfunction are present universally in persons with heatstroke. Symptoms may range from irritability to coma.
- Patients may present with delirium, confusion, delusions, convulsions, hallucinations, ataxia, tremors, dysarthria, and other cerebellar findings, as well as cranial nerve abnormalities and tonic and dystonic contractions of the muscles.
- Patients also may exhibit decerebrate posturing, decorticate posturing, or they may be limp.
- Coma also may be caused by electrolyte abnormalities, hypoglycemia, hepatic encephalopathy, uremic encephalopathy, and acute structural abnormalities, such as intracerebral hemorrhage due to trauma or coagulation disorders.
- Cerebral edema and herniation also may occur during the course of heatstroke.
- Eyes
- Examination of the eyes may reveal nystagmus and oculogyric episodes due to cerebellar injury.
- The pupils may be fixed, dilated, pinpoint, or normal.
- Cardiovascular
- Heat stress places a tremendous burden on the heart. Patients with preexisting myocardial dysfunction do not tolerate heat stress for prolonged periods.
- Patients commonly exhibit a hyperdynamic state, with tachycardia, low systemic vascular resistance, and a high cardiac index.
- A hypodynamic state, with a high systemic vascular resistance and a low cardiac index, may occur in patients with preexisting cardiovascular disease and low intravascular volume. A hypodynamic state also may signal cardiovascular collapse.
- The central venous pressure generally is within the reference range or elevated unless the patient is severely volume depleted.
- High-output cardiac failure and low-output cardiac failure may occur.
- Pulmonary
- Patients with heatstroke commonly exhibit tachypnea and hyperventilation caused by direct CNS stimulation, acidosis, or hypoxia.
- Hypoxia and cyanosis may be due to a number of processes, including atelectasis, pulmonary infarction, aspiration pneumonia, and pulmonary edema.
- Gastrointestinal hemorrhage occurs frequently in patients with heatstroke.
- Hepatic
- Patients commonly exhibit evidence of hepatic injury, including jaundice and elevated liver enzymes.
- Rarely, fulminant hepatic failure occurs, accompanied by encephalopathy, hypoglycemia, and disseminated intravascular coagulation (DIC) and bleeding.
- Musculoskeletal
- Muscle tenderness and cramping are common; rhabdomyolysis is a common complication of EHS.
- The patient's muscles may be rigid or limp.
- Renal
- Acute renal failure (ARF) is a common complication of heatstroke and may be due to hypovolemia, low cardiac output, and myoglobinuria (due to rhabdomyolysis).
- Patients may exhibit oliguria and a change in the color of urine.
Causes
- Increased heat production
- Increased metabolism
- Infections
- Sepsis
- Encephalitis
- Stimulant drugs
- Thyroid storm
- Drug withdrawal
- Increased muscular activity
- Exercise
- Convulsions
- Tetanus
- Strychnine poisoning
- Sympathomimetics
- Drug withdrawal
- Thyroid storm
- Moderate physical exercise, convulsions, and shivering can double heat production and result in temperature elevations that generally are self-limited and resolve with discontinuation of the activity.
- Strenuous exercise and status epilepticus can increase heat production 10-fold and, when uninterrupted, can overwhelm the body's heat-dissipating mechanisms, leading to dangerous rises in body temperature.
- Stimulant drugs, including cocaine and amphetamines, can generate excessive amounts of heat by increasing metabolism and motor activity through the stimulatory effects of dopamine, serotonin, and norepinephrine. The development of heatstroke in individuals intoxicated with stimulants is multifactorial and may involve a complex interaction between dopamine and serotonin in the hypothalamus and the brain stem.
- Neuroleptic agents also may elevate body temperature by increasing muscle activity, but, occasionally, these agents may cause neuroleptic malignant syndrome (NMS). NMS is an idiosyncratic reaction characterized by hyperthermia, altered mental status, muscle rigidity, and autonomic instability and appears to be due to excessive contraction of muscles.
- Certain drugs, such as inhaled volatile anesthetics and succinylcholine, may result in malignant hyperthermia. In contrast to heatstroke, malignant hyperthermia is believed to be induced by a decreased ability of the sarcoplasmic reticulum to retain calcium, resulting in sustained muscle contraction.
- Increased metabolism
- Decreased heat loss
- Reduced sweating
- Dermatologic diseases
- Drugs
- Burns
- Reduced CNS responses
- Advanced age
- Toddlers and infants
- Alcohol
- Barbiturates
- Other sedatives
- Reduced cardiovascular reserve
- Elderly persons
- Beta-blockers
- Calcium channel blockers
- Diuretics
- Cardiovascular drugs - Interfere with the cardiovascular responses to heat and, therefore, can interfere with heat loss
- Drugs
- Anticholinergics
- Neuroleptics
- Antihistamines
- Exogenous factors
- High ambient temperatures
- High ambient humidity
- Reduced sweating
- Reduced ability to acclimatize
- Children and toddlers
- Elderly persons
- Diuretic use
- Hypokalemia
- Reduced behavioral responsiveness: Infants, patients who are bedridden, and patients who are chronically ill are at risk for heatstroke because they are unable to control their environment and water intake.
More on Heatstroke |
 Overview: Heatstroke |
| Differential Diagnoses & Workup: Heatstroke |
| Treatment & Medication: Heatstroke |
| Follow-up: Heatstroke |
| References |
| Next Page » |
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Further Reading
Keywords
heatstroke, heat stroke, hyperthermia, heat-related diseases, exertional heatstroke, EHS, heat exhaustion, heat illness, heat rash, heat edema, heat cramps, nonexertional heatstroke, hyperthermia
