Summertime Emergencies: How to Stay Cool as Summer Heats Up
ABSTRACT: Intense exercise or increased muscular activity, febrile illness, and a variety of drugs may precipitate heat-related illness. Risk factors for heat-related edema, rash, cramps, tetany, syncope, exhaustion and stroke include very young or old age, tight clothing, dehydration, and cardiovascular disease. Heat edema usually requires no treatment. If heat rash develops, apply chlorhexidine lotion to remove desquamated skin. Rehydration is the recommended treatment for heat cramps, syncope, and exhaustion. Remove patients with heat tetany from the hot environment; increase the ventilatory rate or institute carbon dioxide rebreathing. Heat stroke can be life-threatening and requires cautious oxygen therapy and rapid cooling in addition to rehydration.
Key words: heat edema, heat rash, heat cramps, heat tetany, heat syncope, heat exhaustion, heat stroke
The adverse effects of heat on men and women have been vividly recorded throughout history and remain a serious health problem today. Approximately 175 heat-related deaths are reported each year in the United States.1
A dramatic rise in heat-related illnesses will inevitably accompany the dog days of summer. However, by emphasizing prevention, early recognition, and aggressive treatment of heat-related illnesses, we can significantly reduce their morbidity and mortality.
In this article, we discuss the risk factors, clinical presentation, and management of heat-related edema, rash, cramps, tetany, syncope, exhaustion, and heat stroke. We preface our treatment discussion with a brief outline of the body’s mechanisms for heat regulation and transfer and its physiologic responses to heat stress.
HEAT REGULATION AND TRANSFER
The body maintains a narrow core temperature range through the interactions of various heat-productive and heat-dispersive mechanisms. The primary form of heat production in the body is the basal metabolic rate. This is an expression of many biochemical reactions that occur at the cellular level and combine to produce a tremendous amount of heat, even when the body is at rest. Although basic metabolic rates vary, they average 50 to 60 kcal/h/m2. Without the mediation of any cooling mechanisms, this can result in the body temperature increasing by 1.1°C each hour.2 Any mechanism that increases the basic metabolic rate is a risk factor for heat illness.
The body uses four important mechanisms to disperse or dissipate heat:
•Conduction.
•Convection.
•Radiation.
•Evaporation.
Conduction is the transfer of heat from warmer to cooler objects by direct physical contact. Because air is a good insulator, in normal circumstances only 2% of body heat is lost by conduction.
In some circumstances, conduction can result in a tremendous amount of heat loss. For instance, because the conductivity of water is 32 times greater than the conductivity of air, heat loss during submersion in cold water can be very rapid.2
Convection is the loss of heat to the surrounding air. Heat loss through convection is highly dependent on environmental conditions, including air temperature and wind velocity. Tight-fitting clothing decreases heat loss through convection.
Radiation is the transfer of heat by electromagnetic waves. Normally, this is the primary way the body disperses heat; in cool temperatures, two thirds of heat loss occurs through radiation.
However, if environmental temperatures exceed skin temperature, radiation can be a source of significant heat gain. A person exposed to direct sunlight can gain up to 300 kcal of heat per hour.
Evaporation is the loss of heat because of the conversion of a liquid to a gas. The primary mechanism of heat loss through evaporation in the human body is sweating. Evaporation of sweat from the skin results in the heat loss of 58 kcal/mL.2 Heat loss through evaporation can be greatly impaired by dehydration, high ambient humidity, or factors that decrease the ability to sweat.
Conduction, convection, and radiation are considered dry, or sensible, heat exchange mechanisms. This means that heat transfer can occur in either direction and therefore the body can lose or gain heat through these mechanisms. Thus, on a hot day when the ambient temperature is greater than the skin temperature, these mechanisms may actually become a source of heat gain rather than heat loss.
In contrast, evaporation is a wet, or insensible, heat exchange mechanism by which heat transfer can occur only in one direction. Thus, heat can only be lost through evaporation, not gained. This becomes important on very warm days in which the ambient temperature is greater than the skin temperature, when evaporation becomes the only source of heat loss for the human body.
PHYSIOLOGIC RESPONSE TO HEAT EXPOSURE
When the body is exposed to heat, the anterior hypothalamus activates several changes in the cardiovascular, endocrine, and nervous systems to help dissipate it. One of the earliest responses is peripheral vasodilation, which results in increased blood flow to the skin.
The body’s ability to shunt blood to the skin to help dissipate heat is remarkable. Cutaneous blood flow can increase from 0.2 to 0.5 L/min in cool temperatures to 7 to 8 L/min in a very warm environment. As a result of this peripheral vasodilation, cardiac output rises dramatically, up to 3 L/min for each 1°C rise in core body termperature.3
Parasympathetic fibers then stimulate sweat glands to transfer heat to the environment through evaporation. The body’s ability to sweat is also remarkable, since sweating can occur at a rate of 2 L/h in extremely hot environments. As sweating continues and peripheral vascular resistance falls, blood flow to the kidneys decreases, resulting in an increase in aldosterone secretion.
Prolonged heat exposure places increasing stress on the cardiovascular system. Plasma volume decreases from sweating, and electrolyte abnormalities can occur. Dehydration impairs the ability to sweat and causes further stress on the cardiovascular system.
Unless specific steps are taken to reduce heat stress, the body’s mechanisms of heat dispersion can become overwhelmed and serious heat-related illness can occur. Cellular enzyme systems fail above 42°C (107.6°F), and increased cellular membrane permeability and denaturation of proteins result in organ failure.
RISK FACTORS
With an understanding of the mechanisms by which the body disperses heat, the risk factors for heat illness become clear (Table 1). The first set of risk factors involve those that cause increased heat exposure or heat production in the body.
Increased heat production. Physical activity results in increased heat production. Strenuous exercise can produce up to 900 kcal of heat per hour, resulting in a gain of 1°C in core body temperature every 5 minutes.4 Other forms of intense physical activity other than exercise can also cause significant heat production. Seizures, drug-withdrawal states, and combative behavior can all raise heat production substantially.
Certain occupations that involve strenuous activity in intense heat can predispose to heat illness. Miners, steel mill workers, military personnel, and athletes are particularly susceptible to heat-related illnesses because they frequently work in extremely warm environments.
Febrile illnesses markedly increase endogenous heat production and can predispose to heat-related illness. Fever can occur from infectious and noninfectious processes. Examples of noninfectious processes that can cause hyperthermia include hyperthyroidism, malignancies, collagen vascular diseases, and pheochromocytoma.
Some medications can lead to increased heat production. Examples include the sympathomimetics, tricyclic antidepressants, and phenothiazines, which increase heat production by stimulating the hypothalamus and increasing muscle activity.
Illicit use of drugs that increase the metabolic rate can also lead to increased endogenous heat production. Cocaine, amphetamines, PCP, and LSD can generate significant heat production by increasing muscle activity and the basic metabolic rate.
Decreased heat dispersal. A second set of risk factors hinder the body’s ability to disperse heat. Clothing can prevent heat dispersal if it is tight-fitting or multilayered. Clothing will prevent the body’s most effective method of dispersing heat—evaporation of sweat. It will also inhibit heat loss through convection.
Dehydration increases the tendency toward heat-related illness by reducing the ability to sweat and by imposing additional stress on the cardiovascular system. Persons in warm environments who are unable to obtain adequate amounts of water, such as athletes without access to fluids during practice, are susceptible to heat-related illnesses through dehydration.
Obesity increases the body’s insulation and decreases heat dispersion. Also, obese persons often have underlying cardiovascular disease and cannot raise their cardiac output sufficiently to compensate for their large body mass.
Cardiovascular diseases prevent the increase of cardiac output that is necessary to promote heat loss. Heat stress has been shown to increase morbidity and mortality in those with cardiovascular disease. Heat stress can cause myocardial infarction, congestive heart failure, and cardiac arrhythmias. For example, during the St Louis heat wave of 1980, the death rate from cardiovascular disease was 10 times higher than normal.5
Extremes of age are a strong risk factor for heat-related illnesses. Elderly people are often not able to disperse heat because of underlying cardiovascular disease and the use of various medications. Infants are thought to be susceptible to heat-related illness resulting from increased sweat loss and their increased ratio of body surface to body mass. They are also unable to voluntarily drink fluids to compensate for dehydration.
Skin disorders can inhibit sweating and predispose to heat illness. Cystic fibrosis, congenital anhidrosis, scleroderma, psoriasis, and even extensive sunburns are examples of skin disorders that can inhibit sweating.
Finally, many medications can hinder the body’s ability to disperse heat. Any medication that has anticholinergic activity (eg, antihistamines and tricyclic antidepressants) will impair the sweating response.
Cardiovascular drugs, such as beta-blockers and calcium channel blockers, inhibit the rise in cardiac output needed to disperse heat. Diuretics obviously predispose to dehydration and impair the sweating mechanism. Sympathomimetics inhibit peripheral vasodilation in addition to raising endogenous heat production.
HEAT EDEMA
Presentation and diagnosis. Transient swelling of the hands, feet, and ankles during the first few days of heat exposure is characteristic. Heat edema is generally secondary to increased aldosterone secretion, which enhances water retention. When combined with peripheral vasodilation and venous stasis, the excess fluid accumulates in the dependent areas of the extremities.
A thorough history and physical examination can usually help you establish the diagnosis and rule out a more serious cause for the edema (eg, congestive heart failure or hepatic disease). Extensive diagnostic testing is generally unnecessary.
Treatment. Heat edema resolves within several days after the patient becomes acclimated to the warmer environment. No treatment is required, although wearing support stockings and elevating the legs help minimize the edema. Diuretics should be avoided (Table 2).
HEAT RASH
Presentation. Known also as “prickly heat,” this maculopapular, pruritic rash is accompanied by acute inflammation and blocked sweat ducts. The sweat ducts become dilated and eventually rupture, producing small, pruritic vesicles on an erythematous base. Heat rash frequently affects areas of heavy sweating that are covered by tight clothing.
Continued heat exposure can result in deeper blockage of the sweat ducts and recurrent rupture into the dermis. This can lead to the development of chronic dermatitis or a secondary bacterial infection.
Treatment. Prevention is the best therapy (Box); advise patients to wear loose-fitting clothing in the heat. However, once heat rash has developed, initial treatment involves application of chlorhexidine lotion to remove any desquamated skin (talcum powder is not effective). Treat associated pruritus with topical or systemic antihistamines.
Vesicles may subsequently form in the deeper layers of the dermis, and secondary Staphylococcus aureus infection may be common.
HEAT CRAMPS
Presentation. These painful, often severe, involuntary spasms of the large-muscle groups used in strenuous exercise tend to occur after intense exertion. Heat cramps usually develop in persons who perform heavy exercise in the heat, sweat profusely, and replenish lost fluids with unsalted water. This triad is believed to lead to hyponatremia, which induces cramping in stressed muscles. Patients who suffer from heat cramps generally have hypochloremic hyponatremia and low urinary levels of sodium and chloride.
Treatment. Rehydration with salt-containing fluids provides rapid relief. Patients with mild cramps can be given oral 0.2% salt solution, while those with severe cramps require intravenous isotonic fluids. Interestingly, mandated consumption of salt-containing liquids has eliminated heat cramps among workers at several steel mills. Encourage patients who are predisposed to heat cramps to maintain adequate hydration with salt solutions. The many sports drinks on the market are a good source and are readily accessible. We do not recommend that patients use salt tablets for two reasons:
• They provide inadequate fluid/volume replacement.
• They are gastric irritants that may cause nausea and vomiting.
HEAT TETANY
Presentation. Severe carpopedal spasm, paresthesias, and tetany may occur in previously asymptomatic persons who have experienced a short period of intense heat stress. Heat stress induces hyperventilation, which leads to respiratory alkalosis and subsequent symptoms. In general, heat cramps do not precipitate heat tetany.
Treatment. Recommended therapy consists of removing the patient from the hot environment and either decreasing the ventilatory rate or instituting carbon dioxide rebreathing.
HEAT SYNCOPE
Presentation. Heat exposure may produce postural hypotension, which can precipitate a near-syncopal or syncopal episode. The following heat-related features are believed to be responsible:
• Intense sweating, which leads to dehydration.
• Peripheral vasodilation and reduced venous blood return.
• Decreased vasomotor control.
Treatment and prevention. Management consists of rehydrating the recumbent patient with oral fluids (eg, commercially available sports, or electrolyte-rehydration, drinks) or isotonic intravenous fluids. Use the history and physical examination to identify any underlying neurologic, cardiovascular, or metabolic abnormalities that may account for the episode. In addition, evaluate the patient for injuries that may have resulted from an associated fall.
Warn patients who experience heat syncope to avoid standing in the heat for prolonged periods, and advise them to move to a cooler environment and lie down when they recognize presyncopal symptoms. Wearing support stockings and engaging in deep knee-bending movements can help promote venous blood return.
HEAT EXHAUSTION
Presentation. Many experts consider this condition to be a forerunner of heat stroke. Heat exhaustion may resemble heat stroke; however, neurologic function is intact.
Heat exhaustion is marked by excessive dehydration and electrolyte depletion. Symptoms may include headache, nausea and vomiting, dizziness, tachycardia, malaise, and myalgia. Temperature may be normal, but it is usually elevated (although rarely above 40°C [104°F]).6
Laboratory test results almost always show dehydration, as indicated by elevated hematocrit and hemoglobin values. (Typically, sufficient time will not have elapsed for a high blood urea nitrogen level to have developed.) Various electrolyte abnormalities may be present, depending on whether the patient has been drinking plain water or salt-containing liquids to replenish lost fluids. Mildly to moderately elevated liver enzyme levels are commonly seen.
Treatment. Definitive therapy consists of removing patients from the heat and replenishing their fluids. Although mild episodes can be treated with oral fluids, most patients require intravenous fluid replacement. Use isotonic fluids initially; the salt content can be adjusted as necessary once electrolyte levels are known.
Volume replacement and a few hours of observation are sufficient for most patients, unless marked laboratory abnormalities (eg, hypokalemia, hyponatremia, hypocalcemia, and/or hypoglycemia) are found. Patients who remain stable during observation can be discharged; instruct them to rest, drink plenty of fluids for the next 2 to 3 hours, and avoid the heat for several days. Patients who are elderly, have unstable vital signs after 2 hours of treatment, or who have cardiovascular disease may need to be hospitalized for extended observation.
HEAT STROKE
This life-threatening medical emergency occurs when the thermoregulatory mechanisms of the body are overwhelmed and fail.
Presentation. Heat stroke is classically defined as the triad of hyperpyrexia, central nervous system (CNS) dysfunction, and anhidrosis. However, lack of sweating is no longer considered necessary for diagnosis.
In the early stages, patients may in fact sweat markedly. Nonetheless, most eventually lose their ability to sweat and display classic dry, hot skin.
Neurologic symptoms may include hallucinations, irritability, combativeness, hemiplegia, seizures, and coma. In general, temperature is significantly elevated (usually above 41°C [105.8F]); however, mildly elevated temperature does not preclude the possibility of heat stroke.
“Classic” heat stroke. This occurs during a period of sustained high temperature and humidity (ie, a heat wave). Epidemics are common, and sweating is absent in 84% to 100% of those affected. Typical victims are persons who are elderly, who are chronically ill, and/or who have little access to air-conditioning. It is not unusual for these persons to be taking prescribed medications (eg, diuretics, anticholinergics, antipsychotics, and/or antihypertensives) that interfere with the ability to dissipate heat.
“Exertional” heat stroke. In contrast, so-called exertional heat stroke is not necessarily linked with heat waves. It usually develops in young, healthy persons whose mechanisms of heat dispersal are overwhelmed by endogenous heat production. Athletes and military personnel are frequently affected.
In contrast with classic heat stroke, marked sweating, rhabdomyolysis, acute renal failure, severe hepatic damage, and disseminated intravascular coagulopathy (DIC) are characteristic.2 The distinction between classic and exertional heat stroke is academic, however, since both forms are treated in the same manner.
Multisystem effects. Widespread organ system injury may ensue. CNS effects can be extensive, since the CNS is very sensitive to heat.
The cardiovascular system generally is hyperdynamic, manifested by increased heart rate, cardiac index, and central venous dilation. Heart failure, pulmonary edema, myocardial infarction, hypotension, and cardiovascular collapse may develop. The presence of hypotension and decreased cardiac output and index indicates a poor prognosis.
Hepatic damage almost always occurs. Liver transaminase levels can be markedly elevated, peaking within 48 to 72 hours. Jaundice sometimes develops after 24 to 48 hours. However, most survivors of heat stroke suffer no permanent liver dysfunction.
Coagulopathy, as indicated by reduced levels of platelets, fibrinogen, and clotting factors, is common; it suggests a poor prognosis and greater risk of death.4 Pulmonary symptoms nearly always include hyperventilation and respiratory alkalosis; pulmonary edema sometimes occurs.
Renal function abnormalities are common and are likely to be a consequence of hypovolemia and hypoperfusion. However, DIC and direct glomerular damage from heat may also contribute to renal dysfunction. Acute renal failure is seen in 25% to 30% of patients with exertional heat stroke. Rhabdomyolysis may impart a “machine oil” appearance to the urine.2 Although acute renal failure may necessitate dialysis, most patients recover full renal function.
Diagnosis. The key to prompt diagnosis is maintaining a high index of suspicion, since numerous conditions can lead to hyperpyrexia and neurologic dysfunction (Table 3). Although you may not be able to confirm the diagnosis until other entities are ruled out, immediate treatment is mandatory whenever you suspect heat stroke. Further testing to investigate alternative causes can be carried out during therapy.
Treatment. Initial management of both classic and exertional heat stroke includes immediate assessment of airway, breathing, and circulation (the “ABCs”). Oxygen therapy (10 L/min) is indicated, and immediate intubation may sometimes be needed to remedy respiratory distress or to secure control of the airway. Cardiac monitoring is also necessary.
Administration of intravenous isotonic fluids is mandatory, but avoid rapid fluid replacement, since it may worsen pulmonary edema. Do not give potassium until the urinary output is ensured.
Order laboratory tests when rehydration is started. Include a complete blood cell count; screens for electrolytes (including calcium); blood urea nitrogen, creatinine, and hepatic enzyme levels; measurements of arterial blood gases, prothrombin, and partial thromboplastin times, and fibrinogen and fibrin degradation products. A quick bedside check of the blood glucose level for all patients is advisable. Use a Foley catheter to monitor urinary output and order an ECG and chest films.
Rapid cooling is the crux of the therapy. Evaporative cooling is the easiest and quickest method of reducing body temperature7; other techniques include cold water submersion, complete body ice packing, strategic ice packing at the axilla and groin, and cold gastric and peritoneal lavage.
One effective method to induce evaporative cooling is to place fans around the undressed patient who has been sprayed with tepid water. Avoid cold water, since it causes peripheral vasoconstriction and diminishes heat loss.4 Likewise, do not cover the patient with sheets. Ice packs can be placed in the axillary and groin regions. When possible, insert a nasogastric tube and perform cold gastric lavage.
Immersion cooling involves setting the unclothed patient in a tub of cold water deep enough to cover the trunk and extremities. Cardiac monitoring is difficult when using this procedure, however, and defibrillation cannot be performed while the patient is submerged.7
Of note, cold peritoneal lavage is the most rapid cooling technique. However, it is highly invasive and not always available, and studies in humans are somewhat limited.
Whichever cooling method you choose, monitor your patient’s temperature frequently (every 5 minutes) with a rectal probe or esophageal thermometer until his or her temperature reaches 39°C (102.2°F). Additional cooling beyond this point may lead to hypothermia.
A common detrimental effect of rapid cooling by any route is shivering, which increases endogenous heat production. Intravenous diazepam (5 to 10 mg) or chlorpromazine (10 to 25 mg) can abolish shivering reflexes, although the latter’s anticholinergic effects impair heat loss.4
Note that neither aspirin nor acetaminophen is useful for lowering the temperature in patients with heat stroke. Avoid both medications, since they may worsen hepatic damage.
Finally, close supportive care must continue during cooling. Persistent hypotension or hemodynamic instability may necessitate hemodynamic monitoring via Swan-Ganz catheterization. ■
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