CHAPTER 28. Heat-Related Emergencies

Reneé Semonin Holleran

Competencies

1. Identify risk factors that contribute to heat-related illnesses.

2. Identify the different types of heat-related illnesses, including heat exhaustion and heatstroke.

3. Initiate the appropriate management of a heat-related illness in the transport environment.

Deaths attributed to heat-related illnesses have been reported for centuries. The Bible refers to persons who had heatstroke after working in hot fields 2000 years ago. In 24 bc, a Roman army was annihilated in the heat of the Arabian desert. The warriors of the Crusades were ultimately beaten in the Holy Land by heat and fever. ²⁰ Incarceration in the infamous “Black Hole of Calcutta” resulted in high numbers of heat-related deaths. ⁹ During the summers of 1980, 1983, 1988, and 1995, severe heat waves in the United States resulted in multiple deaths from heatstroke. ^4,⁶ Recent data related to heat illness have been obtained from pilgrims in Mecca, Saudi Arabia, in 1984 and 1985, ^20,³³ and military experience has provided extensive data on heat illness and the effect of heat on human physiology. ²² In Europe in the summer of 2003, 52,000 deaths were reported from heatstroke. ⁷

Heatstroke is a true medical emergency that requires rapid diagnosis and treatment. The longer the body remains hyperthermic, the greater the damage and consequent increase in morbidity and mortality. The transport team, with quick recognition and immediate treatment of the heat illness, can do much to combat permanent organ damage and the sequelae of hyperthermia. ^9,¹⁰

INCIDENCE AND CAUSATIVE FACTORS

The very young and the elderly are at greatest risk of affliction with heat-related illness. Moderate forms of heat-related illness can cause discomfort but are of relatively short duration, with rare sequelae. Heat exhaustion and heatstroke are the two serious pathologic states of heat illness.

Even in relatively mild weather, heat illness can affect persons with predisposing risk factors; it can also affect persons who are unconditioned or not acclimatized and then pushed rapidly beyond their tolerance or physical capability, as can happen in military “boot camp” and with novice joggers. Even well-conditioned athletes are subject to heat illness if they are not properly acclimatized. Heat illness is second only to head injuries as a cause of death of US athletes. ^4,^5,^8,^9,^20,^21,^23,^25,³⁰

The mortality and morbidity statistics for heat illness do not reflect the true impact of this illness on the civilian population. Civilian statistics can be inferred from military experience. Records show that heat exhaustion affects 280 of 100,000 military recruits who undergo basic training in South Carolina. ^21,²⁶

Many times, death from heatstroke goes unrecorded during heat waves. The patient often has an underlying cardiovascular, pulmonary, renal, or neurologic disease. During heat waves, deaths from myocardial infarction, pneumonia, kidney failure, and stroke climb sharply; these conditions are then recorded as the cause of death. The estimate of heat illness is postulated to be a dramatic underrepresentation of the true magnitude of this problem. ^7,³⁴

Infants have a relatively small surface area for dissipation of heat. Parents often prevent heat loss by wrapping infants in blankets and clothing that are too heavy for a hot environment. The thermoregulatory ability of children lags behind other body systems in maturity and functional ability. Therefore, children are more predisposed to heat illness, and recognition and diagnosis of heat pathology are often made more difficult. ^3,^9,³¹

Heat illness can develop in elderly persons under conditions that do not generally affect younger persons. As a person’s age increases, physiologic ability to regulate temperature decreases. Older persons often do not notice temperature changes less than 2.3°C, probably because of sensory afferent deterioration. ¹⁷ The elderly population generally has a higher rate of cardiovascular and pulmonary disease, diabetes, and neurologic pathology, and they often take multiple medications. All of these conditions contribute to the increased likelihood of heat illness in persons in this age group.

Obese individuals also have a higher risk of heat illness. Heat loss is inversely proportional to body size and body weight. Adipose tissue has less ability to lose heat compared with nonadipose tissue because of decreased vascularity. Fat serves as an insulator, which is not conducive to heat loss.

Dehydration occurs because of a decrease in body water. As heat illness progresses, the circulatory blood volume decreases. When heat illness is superimposed on preexisting dehydration, the body has a severely limited volume reserve. The more severe the dehydration, the faster the physiologic compensation is exhausted. Fluid intake is crucial for the prevention of heat illness.

An increased endogenous heat load limits the body’s ability to maintain normothermia in a hot environment. A classic endogenous heat source is fever. Fever is generally caused by pyrogens released from bacteria or viruses or by breakdown of cells caused by the infectious organism.

Two different mechanisms are involved in fever and heat illness. With fever, the thermal set point is elevated because of the induction of prostaglandin synthesis in the thermoregulatory center. Certain medications such as salicylates work well to inhibit the reactions that lead to elevation of the thermal set point and thus relieve hyperthermia caused by fever. With heat illness, the thermal set point remains normal. Hyperthermia occurs because of the body’s inability to dissipate heat; normal defense mechanisms designed to protect the set point are overwhelmed. The medications used for fever medication do not work well in this setting and should not be used. ^9.^10.^{and 11.}¹⁸

Hyperactive states demand more energy. The increasing energy demand is met by an increase in metabolic activity. Endogenous heat increases as a byproduct of the increased metabolic rate. Strenuous physical exercise and seizures are examples of hyperactive states. Drugs can also lead to a hyperactive state and increase endogenous heat production.

Muscular exertion increases endogenous heat because of increased metabolic demand. Skeletal muscle is one of the major sources of heat production in the body. Muscular exertion often occurs outdoors under conditions in which the ambient temperature exceeds body temperature and high humidity is present. Hyperthermia can occur in this setting. “Weekend warriors,” novice hard laborers, military inductees in physical training, football players who practice in the heat, and persons who use hot tubs unwisely can all predispose their bodies to heat illness.

Use of many prescription drugs and alcohol can also predispose a person to heat illness. Anticholinergic drugs reduce sweat gland secretions because of the blocking action of anticholinergics on transmission of sympathetic postganglionic nerve impulses to sweat glands. This cessation of sweating removes the body’s chief agent of heat dissipation. Use of tricyclic antidepressants, phenothiazines, butyrophenones, thiothixenes, diuretics, and beta-blockers predispose the patient to heat illness. ^9,^18,^21,³⁰

Other drugs associated with hyperthermia are glutethimide, those that induce hypersensitivity or idiosyncratic reactions (antibiotics, anticonvulsants, and hypertensives), and those that induce direct pyrogenic stimulation (bleomycin). ^6,^9,^18,^20,²²

Psychiatric patients often take anticholinergic drugs. Lithium and haloperidol have been reported to cause fatal hyperthermia. Haloperidol may reduce awareness or recognition of thirst. ¹⁶ Thioridazine (Mellaril) overdose is documented to cause hyperthermia. ^8,^13,¹⁶ The interaction of monoamine oxidase inhibitors with amphetamines, tricyclic antidepressants, or phenothiazines is a well-documented cause of hyperthermia. Psychiatric patients may lack the awareness or desire to care for themselves properly in hot environments.

Alcohol use is known to predispose most persons to heat illness. ^18,³⁰ The exact mechanisms of this phenomenon are complex. Alcohol is a vasodilator and may enhance external heat absorption. Use of alcohol interferes with the judgment and mental acuity necessary to care for oneself. Use of cocaine and lysergic acid diethylamide (LSD) has also been documented to cause fatal hyperthermia. ^8,¹⁴

One of the major organs that must be functional if heat is to be dissipated is the skin. Any pathologic process that disrupts skin integrity interrupts normal physiologic functions, or both conditions sharply limit heat dissipation. Sunburn and heat rash are relatively minor conditions that can have a drastic impact on physiologic compensation for heat stress. Major burns cause partial to total loss of skin function. Lack of ability to regulate body temperature is a complication of burn injury. Obviously, the burn victim may be a candidate for heat illness. ²²

Heat loss from the body occurs primarily through the evaporation of sweat. However, sweat trapped near the body in undergarments and below heavy clothing cannot evaporate because of lack of air circulation. Although adequate hydration ensures that you sweat enough, the mechanism is thwarted by saturated clothing. Differential humidity also plays a factor. In low humidity conditions, sweat evaporates readily. In people without adequate acclimatization, sweat production actually declines if the skin is wet, further blunting these cooling mechanisms. ³²

Patients with cystic fibrosis have a striking elevation of sweat electrolytes; the sodium and chloride content of their sweat is two to five times greater than that of healthy control subjects, and this occurs in 98% to 99% of affected children. These children are subject to massive sodium depletion in hot weather. Today, because of improved early diagnostic measures and treatment, many more patients with cystic fibrosis are living into early adulthood.

Lack of acclimatization predisposes a person to heat illness. On entering a warmer climate, exercise and general activity levels must be gradually increased. Persons vacationing in warm climates often overexert. Even well-conditioned athletes can be affected by heat-related illness if their training programs do not allow sufficient acclimatization before vigorous physical activity in hot humid weather.

Persons can become acclimated to a hot climate in 10 days with daily exposure to moderate work and heat. ^8,¹⁴ With a less zealous routine, acclimatization occurs in several weeks. The recognition of the principle of acclimatization has led to a reduction of the incidence rate of heat illness for those who are exposed to hot or high-risk environments. Acclimatization can occur at any age; however, its effectiveness can be limited by any of the aforementioned predisposing factors. Recent experience in the Middle East has shown that full acclimatization can take several months and requires deliberate planning and varied work/rest/heat exposure schedules that initially avoid any activity during normal (daytime) work hours. Two different combat brigades using the traditional and the extended acclimatization strategies had 10% heat casualties and 0%, respectively. ³²

The most important physiologic adaptations during the acclimatization period include retention of salt and water, expansion of extracellular fluid volumes, and slight hemodilution. ^8,¹⁵ Through these processes, sweating mechanisms improve. This improvement is characterized by early onset of sweating, an increase in the volume of sweat, and a lowering of electrolyte concentration in the sweat. ^10,^18,^31.^32.^{and 33.}

The increase in the volume of sweat accompanied by a lowering of the threshold for the onset of sweating results in better heat dissipation. An increase in aldosterone production lowers the sodium content of sweat. Combined with a 7% increase in total body water, the increase in aldosterone lowers sodium content of sweat from 100 mEq/L to 70 mEq/L. ¹ The chloride concentration in sweat falls from 40 or 45 mEq/L to as low as 15 or 20 mEq/L, and sweat volume rises from 1 to 3 L/h. ^9,¹⁴

After acclimatization, cardiovascular and metabolic proficiency is improved. Vasodilation occurs earlier and in greater magnitude. The heart rate is lower with a higher stroke volume, thus increasing cardiac output. Biochemical efficiency at the cellular level improves to the point that heat production for a given amount of work is less than in a person who is not acclimatized. Storage and utilization of glycogen are improved, which delays the onset of anaerobic metabolism with resultant lactic acidosis.

PATHOPHYSIOLOGIC FACTORS

Normal Thermogenesis

Human core temperature is closely regulated by a number of mechanisms to maintain a body core temperature of between 36°C and 38°C. Processes that alter temperature homeostasis result in pathologic changes at the cellular level. Rising body temperature, if unregulated, can exceed the critical thermal maximum and cause irreversible organ damage; death quickly ensues. The human thermal maximum is well documented to be 43 °C.

Body core temperature is a species-specific genetically determined set point that is regulated by the hypothalamus. Temperature regulation is quite precise, with response to temperature changes as small as 0.2°C (1.6°F). ³² A “thermostat” in the preoptic anterior portion of the hypothalamus receives information from various body thermoregulators. Peripheral and core temperature sensors in the skin, viscera, and nervous system tissues produce both thermal and endocrine signals. These signals are transmitted to the hypothalamus via neuronal and circulatory pathways. The thermostat then responds through a variety of negative feedback mechanisms to activate processes by which heat is lost or gained. These responses are mediated by means of the sympathetic nervous system.

Body heat production occurs because of two separate processes: endogenous metabolic processes and exogenous environmental exposure. Close regulation of body temperature is critical because the human body is dependent on relatively low temperature biochemical reactions at the microcellular level to sustain life.

Every body process produces exothermic heat. Normal basal cellular metabolism generates 50 to 60 kcal/h and causes a rise of 1°C/h if not dissipated by compensatory mechanisms. ¹⁰ Digestion of food is the source of body heat. Major heat-producing organs are the liver and skeletal muscle. Increasing bodywork raises body temperature. Maximal sustained exercise produces 600 to 900 kcal/h, which raises body core temperature 5°C/h without functional compensatory mechanisms. ²⁵

Exogenous (external) heat comes from the environment. Exposure to direct sunlight raises body core temperature 150 kcal/h. The amount of humidity present in the air directly affects the body’s ability to disperse heat. Humidity limits cooling via evaporation, which is caused by a lack of an evaporation gradient from skin surface to air.

Methods of Heat Loss

Thermoregulation by the hypothalamus maintains normothermia by balancing heat production and heat loss. When thermoregulation breaks down because of excess heat generation (endogenous), inability to dissipate heat (pathophysiologic), overwhelming environmental conditions (high ambient temperature with high humidity), or a combination of these factors, hyperthermia results. Under normal conditions, 90% of the heat produced by the body is lost to the environment via the skin surface by conduction, radiation, convection, and evaporation.

Environmental temperature obviously has a direct effect on the patient. The higher the temperature, the more external heat is present. When the environmental temperature is equal to or greater than the body’s temperature, passive heat loss through the means of conduction and radiation is decreased. Radiant heat loss occurs when the ambient temperature is lower than the body’s temperature; conversely, the body readily absorbs radiant heat from the environment.

When air or water moves across the body surface, heat is lost via convection. An increase in the amount of air moving over the skin (forced convection) increases the amount of heat loss. The drier the air, the better the skin surface-to-air gradient, and the more heat that is lost.

The primary mechanism for heat dissipation is the evaporation of sweat. Through vaporization from the body surface, loss of 1 mL of sweat reduces body heat load by 1.7 kcal. ^8,^14,^15,^18,^23,^26,²⁸ Under conditions of high ambient temperature and high ambient humidity, the skin is unable to provide effective cooling as the evaporation gradient is lost. At 75% humidity, evaporation decreases; at 90% to 95% humidity, evaporation ceases. ⁸

The average person can produce up to 1.5 L of sweat per hour. Through conditioning and acclimatization, sweat production increases. The well-trained athlete can produce up to 3 L/h. ^8,^21,²⁶

Insensible heat loss also occurs; heat is lost with passage of urine and feces, and the respiratory tract can dissipate heat via convection and evaporation.

Physiologic Compensation

Physiologic compensation begins in the hypothalamus. The exact chemical nature of thermoregulation is not yet fully understood. As endocrine and thermal sensors arrive from the heated periphery and core, the hypothalamic thermostat reduces bioamine concentrations. Final common pathway effectors probably include prostaglandins, central nervous system amines, and a host of other hypothesized candidates. ^10,³⁰

On reception of effector “messages” from the hypothalamus and peripheral thermoreceptors, the cardiovascular system responds with peripheral vasodilation. Vasodilation maximizes the cooling surface and greatly decreases peripheral vascular resistance. In this manner, the cardiovasculature conducts heat to the surface of the body, where it can be released to the environment. When skin vessels dilate, blood flow shunted through the area can exceed 4 L/min. ^9,¹⁸ With this increased flow, 97% of cooling occurs at the skin surface. ²³

Heat Pathophysiology

The initial response to heatstroke begins on a cellular level. Subcellular disruption directly causes cell destruction. Hypothermia also initiates apoptosis or programmed cellular destruction. The cells that produce the greatest number of apoptotic cells from hypothermia are the thymus, spleen, lymph nodes, and mucosa of the small intestine. ¹⁰

On exposure to heat, the body initiates compensation by decreasing peripheral vascular resistance, thus shunting blood to the periphery. This action causes an increase in stroke volume and cardiac output, which increases demand on the heart. The healthy cardiovascular system can sustain this hyperdynamic state for a limited time; however, it eventually taxes the myocardium.

The purpose of this response is to cool the body. Heat is lost from the skin surface via evaporation of sweat. In severe heat stress, the body loses as much as 1.5 L/h, and even 3 L/h in extreme cases. ^9,³⁰ Over time, the circulating blood volume is reduced.

The cardiac output continues to drop as a result of the ensuing hypovolemia. Homeostasis becomes compromised. An altered hemodynamic state may develop that mimics high-output failure, such as that seen in sepsis. This results in hyperdynamic failure. In persons with heatstroke, structural damage to the heart is common, although not extensive. Rarely, acute transmural myocardial infarction or widespread myocardial damage may occur. ^9,³⁰

Cardiac dysrhythmia and myocardial damage may occur because of subendocardial hemorrhage, rupture of muscle fibers, necrosis, and infarction. This pathology is second to increased cardiac workload and thereby increases myocardial oxygen demand. Not enough oxygen is available because of disruption of oxidative phosphorylation and a resulting shock state. Hypotension is usually a sign of severe or premorbid heat illness. ^9,³⁰

The respiratory system initially responds with an increase in respiratory rate and depth to meet increased oxygen demand. This hyperventilation results in an initial heat loss from an increased volume of air moved over and through the respiratory tract. This evaporative loss decreases with increased respiratory fatigue. A high ambient humidity also limits this evaporative loss. An initial respiratory alkalosis develops as a result of the hyperventilation, with concurrent hypocarbia and the traditional muscle tetany. This tetany is the pathophysiologic basis for the ill-defined syndrome of heat tetany.

Ataxia, dysmetria, and dysarthria may be seen early in the onset of heatstroke because the Purkinje’s cells of the cerebellum are particularly sensitive to the toxic effects of high temperature. Because these changes are seen in other neurologic events, such as stroke, heatstroke may not be recognized initially. Cerebral edema combined with associated diffuse petechial hemorrhages is often found in fatal cases.

When the hyperthermic insult is associated with status epilepticus and profound hypotension, the energy requirements of the brain increase. This in turn contributes to the spiraling core temperature, increasing up to four times the metabolic rate of the brain. The cerebral vessels dilate maximally, and thus, the blood flow is dependent on mean arterial pressure. The added effects of dehydration (hypovolemic source) produce a pathophysiologic state conducive to brain death and damage.

Kidney function is altered from the loss of sodium and water in sweat. The kidneys retain sodium, and thus, they retain water and excrete potassium. Renal dysfunction occurs because of hypovolemia and hypoperfusion. Urinary output drops, and acute renal tubular necrosis may ensue. If sodium losses are of sufficient severity, signs of hyponatremia may appear. A risk hypokalemia may develop because of the excretion of potassium in the urine.

The liver, which is particularly sensitive to temperature damage, is affected in nearly every case. ^10,¹³ Liver function decreases by 20%. This decrease in function theoretically should aid in heat reduction because the liver is one of the major heat-producing organs. Prothrombin times become prolonged. ^2,²⁸ Reduced hepatic perfusion caused by shunting of blood to the periphery leads to hypoglycemia in 20% of patients with exertional heatstroke. ^4,¹⁹ Interestingly, the pancreas is the only organ not damaged by the toxic effects of heat stress. ⁹

During heat stress, the gastrointestinal tract undergoes direct thermotoxicity and relative hypoperfusion because of the shunt of blood to the periphery. Ischemic intestinal ulceration can also occur, which may lead to frank gastrointestinal bleeding. ⁹

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