Heat Illness - Clinical Tree

Key Concepts

Classic heatstroke is generally diagnosed in older patients with comorbidities during heat waves, whereas exertional heatstroke is more common in young athletic patients or military personnel.
Heat exhaustion and heatstroke are a continuum of the same pathophysiologic process. Neurologic dysfunction is a hallmark of heatstroke, and cerebral edema is common.
In heat stroke, morbidity and mortality are directly related to the duration of core temperature elevation. Rapid cooling should be initiated without delay.
The evaporative technique and ice water immersion are the 2 forms of primary cooling measures. Other cooling measures are secondary and considered adjunct therapy.
Antipyretics are ineffective and should not be used to control environmental hyperthermia.
Heatstroke can cause right-sided cardiac dilation and elevated central venous pressure and clinically resemble pulmonary edema but may still require crystalloid resuscitation.

Foundations

Background and Importance

Humans have been plagued by heat illness throughout recorded history. Heat illness has the potential to affect all age groups and population types. Older adults and the poor (who often lack adequate air conditioning and nutrition) are susceptible to heat illness during environmental extremes and heat waves. Those with preexisting disease are also prone to heat illness. It is estimated that at least 10 times as many heat aggravated illnesses occur in patients with comorbid conditions such as coronary artery disease, cerebrovascular disease, and diabetes. Children are also susceptible to heat stressors because of their higher surface area-to mass ratios. They also have lower sweat rates per gland. Military personnel, athletes, including American football players, and those who occupationally exert themselves in heat, are also at risk.

For an accurate heat illness diagnosis, information about living conditions, occupation, access to water, strenuous physical activity, acclimatization, and current environmental temperatures need to be ascertained. Heat illness is often associated with military exercises, athletic events, occupation, and recreational activities. A recognition of the microclimates conducive to heat illness including military tanks, tents in the sun, engine rooms, mines, hot tubs, saunas, and automobile interiors, is also important. In the United States, nearly 40 children die each year from hyperthermia after being left alone in a motor vehicle.

Anatomy, Physiology, and Pathophysiology

Heat Production

Humans are essentially biochemical furnaces that burn food to fuel with a complex array of metabolic functions. These chemical reactions consume substrate, generate usable energy, and produce byproducts that must be eliminated for continued operation of the system. Water and carbon dioxide are produced and eliminated in large quantities, as well as urea, sulfates, phosphates, and other chemical byproducts. These reactions are exothermic and combine to produce a basal metabolic rate that amounts to approximately 100 kCal/h for a 70-kg person. In the absence of cooling mechanisms, this baseline metabolic activity would result in a 1.1°C (2°F) hourly rise in body temperature.

Heat production can be increased 20-fold by strenuous exertion. Rectal temperatures as high as 42°C (107.6°F) have been recorded in trained marathon runners, without ill effects. Metabolic factors (hyperthyroidism and sympathomimetic drug ingestion) can dramatically increase heat production. Environmental heat not only adds to the heat load but also interferes with its dissipation. The physics of heat transfer as it relates to human physiology involves four mechanisms—conduction, convection, radiation, and evaporation.

Conduction

This is the transfer of heat energy from warmer to cooler objects by direct physical contact. Air is a good insulator; therefore, only approximately 2% of the body heat loss is by conduction. In contrast, the thermal conductivity of water is at least 25 times that of air.

Convection

This is heat loss to air and water vapor molecules circulating around the body. As the ambient temperature rises, the amount of heat dissipated by convection becomes minimal. Once the air temperature exceeds the mean skin temperature, heat is gained by the body. Convective heat loss varies directly with wind velocity. Loose-fitting clothing maximizes convective, and also evaporative, heat loss.

Radiation

This is heat transfer by electromagnetic waves. Although radiation accounts for approximately 65% of heat loss in cool environments, it is a major source of heat gain in hot climates. Up to 300 kCal/h can be gained from radiation when someone is directly exposed to the hot summer sun.

Evaporation

Evaporation is the conversion of a liquid to the gaseous phase. Evaporation of 1 mL of sweat from the skin cools the body by 0.58 kCal. In humans, heat loss through sweat evaporation is the principal means of heat loss during exercise and the dominant means of dissipating heat via the skin when ambient air temperatures exceed skin temperature. Panting mammals such as dogs have an oropharyngeal countercurrent flow mechanism (carotid rete mirabile) that results in selective cooling of the brain. In humans, respiratory and countercurrent mechanisms are minimal sources of heat loss.

Heat Regulation

The regulation of body temperature involves three distinct functions—thermosensors, a central integrative area, and thermoregulatory effectors.

Thermosensors

Temperature-sensitive structures are located peripherally in the skin and centrally in the body. However, skin temperature changes correlate poorly with changes in the rate of heat loss. Thermosensitive neurons, located in the preoptic anterior hypothalamus, are activated when the temperature of the blood circulating through that area exceeds a set point ( Fig. 129.1 ).

Fig. 129.1, Preoptic Anterior Hypothalamus.

The skin temperature affects heat loss when a person resting in a warm environment initiates sweating, even though the core temperature remains constant. In contrast, changes in core temperature are more dominant than skin temperature changes in producing heat-dissipating responses.

Central integrative area

The central nervous system (CNS) interprets information received from the thermosensors to instruct thermoregulatory effectors properly. The concept of a central thermostat where an alteration shifts effector thresholds in the same direction fits a variety of clinical situations. For example, fever, the circadian rhythm of temperature variation, and the difference in rectal temperature after ovulation can be explained by variation of a thermal set point.

Thermoregulatory effectors

Sweating and peripheral vasodilation are the major mechanisms whereby heat loss can be accelerated. In a warm environment, evaporation of sweat from the skin is the most important mechanism of heat dissipation. Heat loss from the skin by convection and radiation is maximized by increased skin blood flow to facilitate sweating.

Humans possess apocrine and eccrine sweat glands. Apocrine glands are concentrated in the axillae and produce milky sweat, rich in carbohydrate and protein. They are adrenergically innervated and respond to emotional stress as well as to heat. Most glands producing so-called thermal sweat are eccrine glands. These are cholinergically innervated and distributed over the entire body, with the largest number on the palms and soles. Eccrine sweat is colorless, odorless, and devoid of protein. Individuals exercising in hot environments commonly lose 1 or 2 L/h of sweat. A loss of up to 4 L/h is possible with strenuous exercise.

Cooling is best achieved by evaporation from the body surface; sweat that drips from the skin does not cool the body. Each liter of completely evaporated sweat dissipates 580 kCal of heat. The ability of the environment to evaporate sweat is termed atmospheric cooling power and varies primarily with humidity, but also with wind velocity. As humidity approaches 100%, evaporative heat loss ceases.

The vascular response to heat stress is cutaneous vasodilation and compensatory vasoconstriction of the splanchnic and renal beds. These vascular changes are under neurogenic control and allow heat to be dissipated quickly and efficiently, but they place a tremendous burden on the cardiovascular system. To maintain blood pressure, cardiac output increases dramatically. For this reason, saunas and hot tubs may be dangerous for patients with cardiac disease. Cardiovascular and baroreceptor reflexes also affect skin blood flow. Reduced forearm sweating and vasodilation have been observed in severely dehydrated subjects exercising in a warm environment.

Acclimatization

Acclimatization is the constellation of physiologic adaptations that occur in a normal person as the result of repeated exposures to heat stress. Daily exposure to work and heat for 100 min/day results in near-maximal acclimatization within 7 to 14 days. This is characterized by an earlier onset of sweating (at a lower core temperature), increased sweat volume, and lowered sweat sodium concentration. Acclimatization is hastened by modest salt deprivation and delayed by high dietary salt intake.

The cardiovascular system plays a major role in acclimatization and endurance training, largely resulting from an expansion of plasma volume. Heart rate is lower and associated with a higher stroke volume. Other physiologic changes include earlier release of aldosterone, although acclimatized individuals generate lower plasma levels of aldosterone during exercise heat stress. Total body potassium depletion of up to 20% (500 mEq) by the second week of acclimatization can occur as a result of sweat and urine losses, coupled with inadequate repletion.

Although many similarities exist among thermoregulatory responses to heat and exercise, the well-conditioned athlete is not necessarily heat-acclimatized. For heat and exercise-induced adaptive responses to be maintained, heat exposure needs to continue intermittently, at least on 4-day intervals. Plasma volume decreases considerably within 1 week in the absence of heat stress.

Predisposing Factors

Advanced age, psychiatric conditions, chronic disease, obesity, and certain medications increase the risk for classic heatstroke during periods of high heat and humidity. Adequate fluid intake is essential. Older adults often overdress during hot weather conditions. Heat loss is maximized by light, loose-fitting garments.

Exertional heatstroke is most likely to occur in young healthy people involved in strenuous physical activity, especially if they have not acclimatized to environmental factors that overwhelm heat-dissipating mechanisms. For example, wrestlers frequently fast, restrict food and fluid intake, and exercise vigorously wearing vapor-impermeable clothing in an effort to maintain or drop their current weight class. Pre-existing illness may not increase the risk of exertional heat stroke. Fluid intake is the most critical variable. Dehydration can be minimized by education on work-rest cycles and fluid consumption, and through provision of cool flavored fluids.

The goal is to maximize voluntary fluid intake and gastric emptying so that fluid can rapidly enter the small intestine, where it is absorbed. Gastric emptying is accelerated to 25 mL/min by large fluid volumes (500 to 600 mL) and cool temperatures (10°C to 15.8°C [50°F to 60.4°F]). High osmolality inhibits gastric emptying; osmolality of less than 200 mOsm/L is optimal. Most commercially available electrolyte solutions contain excessive sugar. Hydration can be monitored by measurement of body weight before and after training or athletic competition. An athlete with a loss of 2% to 3% body weight (1.5 to 2 L in a 70-kg man) should drink extra fluid and be permitted to compete only when his or her body weight is within 0.5 to 1 kg (1 or 2 pounds) of the starting weight on the previous day. A weight loss of 5% or 6% represents a moderately severe deficit and usually is associated with intense thirst, scant dark-colored urine, tachycardia, and increase in rectal temperature of approximately 2°C (3.6°F). These athletes should be restricted to light workouts after hydration until they return to normal weight. A loss of 7% or more of body weight represents severe water depletion; participation in sports should not be permitted until the athlete is evaluated by a physician or sports trainer. The administration of salt tablets during strenuous exercise can cause delayed gastric emptying, osmotic fluid shifts into the gut, gastric mucosal damage, and hypernatremic dehydration. A 6-g sodium diet is sufficient for successful adaptation for work in the heat, with sweat losses averaging 7 L/day. Excessively high salt intake in relation to salt losses in sweat during initial heat exposure can impair acclimatization because of the inhibition of aldosterone secretion. Excessive salt ingestion can also exacerbate potassium depletion.

Evaporative cooling can be lost when clothing inhibits air convection and evaporation. Water evaporated from clothing is much less efficient for body cooling than water evaporated from the skin. Loose-fitting clothing or ventilated fishnet jerseys allow efficient evaporation. Light-colored clothing reflects rather than absorbs light.

The heat dissipation mechanisms of the body are analogous to the cooling system of an automobile ( Fig. 129.2 ). Coolant (blood) is circulated by a pump (heart) from the hot inner core to a radiator (skin surface cooled by the evaporation of sweat). Temperature is sensed by a thermostat (CNS), which alters coolant flow by a system of pipes, valves, and reservoirs (vasculature). Failure of any of these components can result in overheating.

Fig. 129.2, Predisposing factors for heat illness, an automotive analogy.

Effective circulation requires an intact pump and adequate coolant levels. β-adrenergic blocking agents or calcium channel blockers may prevent an increase in cardiac output sufficient to produce the necessary peripheral vasodilation to dissipate heat. Dehydration caused by gastroenteritis, diuretics, or inadequate fluid intake predisposes to heat illness. Individuals working in the heat seldom voluntarily drink as much fluid as they lose and replace only approximately two-thirds of net water loss (so-called voluntary dehydration). Dehydration alone increases body temperature at rest by increasing the work of the sodium-potassium adenosine triphosphatase pump, which accounts for 25% to 45% of the basal metabolic rate. This is particularly true in cases of hypernatremic dehydration. The pipes and valves of the coolant system may be abnormal in diabetic or older patients with extensive atherosclerosis.

Radiator function depends on the skin and sweat glands. Occlusive, vapor-impermeable clothing hinders evaporative and convective cooling. Anticholinergic medications and stimulant drugs of abuse interfere with sweating and contribute to heat illness. Various skin diseases, including miliaria (prickly heat rash), extensive burns, scleroderma, ectodermal dysplasia, and cystic fibrosis, are risk factors. Anhidrosis can also be secondary to central or peripheral nervous system disorders.

Increased heat production causing heat illness most often accompanies exercise in a hot humid environment. When heat and humidity are extreme, exertion is not necessary to produce heat-related problems. Several indices help objectify heat strain. These indices can be divided into two categories, heat scales based on meteorologic parameters and those that combine environmental and physiologic parameters.

The wet bulb globe temperature heat index is an excellent meteorologic measure of environmental heat stress ( Box 129.1 ). It measures the effects of temperature, humidity, and radiant thermal energy from the sun. When climatic conditions exceed 25°C (77°F) wet bulb, even healthy people are at high risk during exercise. Above 28°C (82.4°F), exercise and strenuous work should be avoided or limited to extremely short periods of time.

BOX 129.1

Wet Bulb Globe Temperature

WBGT = 0.7 T_{n} + 0.2 T_{g} + T_{a}

$WBGT = 0.7 T_{n} + 0.2 T_{g} + T_{a}$

T _n = “Natural” wet bulb temperature—the temperature achieved by a thermometer covered with a moistened white wick and left exposed to the ambient environment
T _g = Globe temperature—the temperature inside a blackened hollow copper sphere exposed to the ambient environment
T _a = Ambient temperature

These measurements can be done manually or calculated automatically with the help of computer algorithms.

Fever Versus Hyperthermia

It is diagnostically and therapeutically important to identify patients suffering from a febrile response rather than heat illness. Fever does not cause primary pathologic or physiologic damage to humans and does not require primary emphasis in the therapeutic regimen, which is directed at the underlying disease state. If temperature-related physiologic changes such as febrile seizures and tachycardia compromise a patient with marginal cardiac reserve, the temperature should be artificially regulated with antipyretics. In contrast, antipyretics are not effective against heat illness and are not recommended to control environmental hyperthermia.

Minor Heat Illnesses

Miliaria Rubra

Miliaria rubra, also known as prickly heat, lichen tropicus, and heat rash, is an acute inflammatory disorder of the skin that occurs in hot and humid climates. It is the result of the blockage of sweat gland pores by macerated stratum corneum and secondary staphylococcal infection. The acute phase is characterized by vesicles in the malpighian layer of the skin, caused by dilation and rupture of the obstructed sweat gland ducts.

Clinical Features

Miliaria produces intensely pruritic vesicles on an erythematous base. The rash is confined to clothed areas, and the affected area is often completely anhidrotic. During the next week, a keratin plug develops and fills these vesicles, causing a deeper obstruction of the sweat gland duct. The obstructed duct then ruptures a second time, producing a deeper vesicle within the dermis. This is known as the profunda stage, and it can persist for weeks. Profunda vesicles are not pruritic and closely resemble the white papules of piloerection. Chronic dermatitis is a common complication ( Fig. 129.3 ).

Differential Diagnoses

Alternative diagnoses include contact dermatitis, cellulitis, and allergic reactions. A heat exposure history and distribution of the rash will solidify the diagnosis.

Diagnostic Testing

Laboratory data is not indicated with miliaria.

Management and Disposition

Miliaria rubra can be prevented by wearing light, loose-fitting, clean clothing and avoiding situations that produce continuous sweating. Avoid routine use of talcum or baby powder. Gentle exfoliation may help to remove debris that occlude the eccrine sweat ducts. However, soap may cause additional skin irritation. Topical corticosteroids, such as hydrocortisone 2.5% or triamcinolone 0.1% twice a day for one to two weeks, may decrease pruritus and inflammation but is not required for the resolution of miliaria. Patients can be discharged with dermatologic or primary care follow-up.

Heat Cramps

Heat cramps are brief, intermittent, and often severe muscle cramps occurring typically in muscles that are fatigued by heavy work or prolonged exercise. Heat cramps appear to be related to a salt deficiency. They usually occur during the first days of work in a hot environment and develop in persons who produce large amounts of thermal sweat and subsequently drink copious amounts of hypotonic fluid.

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