Halting Heat Illness Before It Turns Deadly

Emerg Med 40(6):33, 2008

By Christopher B. Colwell, MD

Excessive heat kills more Americans than all other natural disasters combined, but recognizing and treating heat illness quickly can save lives. The author discusses how to diagnose, treat, and prevent this dangerous sequela of summer.

Evan S, age 17, a previously healthy high school senior, collapsed on the second day of football practice during a heat wave. On the way to the emergency department, despite the administration of 500 ml of normal saline solution by EMS, he became unresponsive and began having seizures. When he arrived at the hospital, the seizures had stopped but he was still unresponsive.

His vital signs were: pulse, 140; blood pressure, 100/60; respiratory rate, 24; rectal temperature, 107.6°F. His head was atraumatic but his pupils were 5 mm and fixed. His neck showed no jugular vein distension and his lungs were clear. Auscultation of the heart revealed a rapid rhythm with no murmurs. His abdomen was soft and nondistended. His extremities had no deformities; no cyanosis, erythema, or edema was evident, and his skin was warm. Rectal examination revealed poor tone with heme-negative brown stool. At this point, the presumptive diagnosis of heat stroke was made.

Evan was placed on a cardiac monitor and given oxygen by face mask, and an additional intravenous line was placed. Blood was drawn for laboratory studies, later revealing a sodium level of 124 mmol/L, a glucose level of 60 mg/dl, and a potassium level of 5.8 mmol/L. His creatinine kinase (CK) was 9582 U/L (normal is less than 150 U/L) and his liver function panel showed an aspartate aminotransferase (AST) of 6257 U/L (normal is less than 30 U/L), an alanine aminotransferase (ALT) of 7956 U/L (normal is less than 32 U/L), and a lactate dehydrogenase (LDH) of 4383 U/L (normal is less than 250 U/L). His serum creatinine was 2.8 mg/dl. His white blood cell count was 12,100/mm3 and his hemoglobin was 16.4 gm/dl.

Treatment was initiated immediately. Evan’s clothing was removed, he was sprayed with lukewarm tap water, and standing fans were placed at his bedside. He continued to be unresponsive, so he was intubated using rapid sequence technique and admitted to the intensive care unit.

After two days in the ICU, Evan began responding to commands and was extubated. He was discharged on hospital day 5 neurologically intact without any apparent sequelae. Unfortunately, when he returned to football practice just four days after being discharged, he collapsed again after 30 minutes. Although he remained conscious, he was brought back to the hospital and observed overnight before being discharged with instructions not to return to practice until cleared by a physician.

ELEVATED CORE BODY TEMPERATURE

Heat illness is a form of hyperthermia, which is defined as an elevated core body temperature from any cause. The most common cause is fever, which results from pyrogens, exogenous or endogenous substances that act on the hypothalamus and affect the set point or temperature the body will try to achieve. Fever is treated with antipyretics, such as acetaminophen or ibuprofen, which reset the hypothalamic set point. However, heat illness is different from fever and does not respond to antipyretics.

Because heat illness is generally underreported, the actual incidence is unknown. From 1999 to 2003, 3442 deaths from exposure to extreme heat were reported in the United States, resulting in an annual mean of 688 deaths. In the decade from 1992 to 2001, more Americans died from excessive heat than from all national disasters combined. For example, during a three-day heat wave in Chicago in 1995, there were 700 excess (avoidable) deaths, mostly in people who were poor, sick, or socially isolated. France had a historic heat wave in 2003, in which almost 15,000 excess deaths were recorded.

Death rates from other causes also go up during heat waves, although these deaths are not always attributed to the heat. Deaths from hurricanes, tornadoes, floods, and lightning get more newspaper headlines, but heat waves are more deadly than any of these calamities.

PATHOPHYSIOLOGY OF HEAT ILLNESS

Thermoregulation is a very efficient process that keeps the body within a narrow temperature range, which is important because many of our enzyme systems function only within this range. This process ensures that our internal temperature will change less than 1 degree even if the external temperature changes more than 20 degrees. 

Our bodies accomplish this feat by balancing heat production with heat loss. Because our body temperature is often higher than the outside temperature, we need to generate heat in order to live. We produce heat in many body organs, including the heart, liver, and brain; this is commonly referred to as the basal metabolic rate. Skeletal muscle is also able to generate heat.

We lose heat in essentially four ways: by conduction, convection, radiation, and evaporation. Conduction is the transfer of heat between objects in direct contact. The direction of heat flow is always from the higher to the lower temperature. The thermal conductivity of air is significantly lower than that of water, so water is able to move heat away from the body far more effectively than air. This is why an air temperature of 78°F feels warm but the same water temperature feels cool.

Convection involves the movement of heat from the body to the ambient (open) air. One way to think about convection is that when we heat the air around us, we create a blanket of warm air at the skin surface. Wind can take this blanket of warm air away, so we lose more heat attempting to create that warm blanket. This is basically what is meant by the wind-chill effect.

Radiation works in two ways: by radiating heat out of our bodies and radiating heat into them. When our blood vessels are maximally dilated, a large amount of blood flows to the periphery (close to the skin) and radiates heat out to the environment. When our blood vessels are maximally constricted, very little blood flows to the periphery and far less heat is lost. Heat also radiates into our bodies when we are exposed to direct sunlight. The amount of heat lost due to radiation depends on the temperature gradient between the body and the ambient air, since heat moves from warmer to cooler environments.

Evaporation is a very effective method of cooling our bodies on a warm day. When water changes state, a large amount of energy is either absorbed by our bodies or given off. The sweat that you see on your skin does not provide the same amount of heat loss as the sweat that evaporates into the air. The amount of heat loss due to evaporation depends on the moisture gradient. In an environment with 100% humidity, people do not lose heat by evaporation. They still perspire, but the sweat simply rolls off their bodies without cooling them. This is one reason people in humid environments are at a higher risk for heat illness.

Medical conditions that decrease cardiac reserve and reduce the ability to maximally vasodilate the peripheral vasculature (a process that requires an increase in cardiac output) will increase the risk for heat illness. Dehydration, systemic vasoconstriction, or medications that cause anhidrosis (such as anticholinergics or phenothiazines) can limit the ability to dissipate heat and increase the risk for heat-related illness.

Injury resulting from heat illness is very likely a combination of direct cytotoxicity and a systemic inflammatory response. Heat can be directly toxic to cells and can cause protein denaturation that disrupts critical cellular processes. Heat can also result in the release of inflammatory cytokines that damage the vascular endothelium, leading to increased vascular permeability and activation of the coagulation cascade. Endothelial cell injury and diffuse microvascular thrombosis are prominent features of heat stroke, so disseminated intravascular coagulation and alterations in the vascular endothelium may be important pathologic mechanisms in heat stroke.

Damage from heat is a function of temperature and duration. The exact temperature at which cellular damage begins to occur in humans (the critical thermal maximum) has not been clearly defined and may vary from patient to patient. There are reports of full neurologic recovery in patients who had rectal temperatures as high as 115.7°F.

WHO IS AT RISK?

Anyone with impaired heat loss is at risk for heat illness. This includes people who are unable to maximally vasodilate, such as those with impaired cardiac output (from congestive heart failure, for example) and peripheral vascular disease, those taking medications such as beta blockers, and those who are dehydrated. Other medications, such as anticholinergics, phenothiazines, lithium, tricyclic antidepressants, antihistamines, and antispasmodics, can also reduce sweating and disrupt hypothalamic function, increasing the risk for heat illness.

People with excessive heat production are also at risk for heat illness. Taking stimulants such as cocaine, amphetamines, and phencyclidine can increase muscular activity and endogenous heat load. Excessive heat production also occurs in people withdrawing from substances such as alcohol; people with fevers; people who are active in warm environments; and people with impaired judgment who may not know when to get out of the heat. Those with reduced mobility are also at risk because they may be unable to escape the heat. In both the Chicago heat wave of 1995 and the French heat wave of 2003, lack of mobility was strongly associated with death, especially for those confined to bed.

In addition, people of lower socioeconomic status are less likely to have air conditioners and are at higher risk for heat illness. Also, hyperthyroidism can markedly increase the metabolic rate and result in a rise in endogenous heat production. Finally, for reasons that are not clear, people with a history of heat illness are at a higher risk for further episodes.

HEAT EXHAUSTION AND HEAT STROKE

Heat illness may be thought of as a continuum from mild heat exhaustion to severe heat stroke. But for the purposes of this discussion, and because treatment is essentially the same for both conditions, all heat-related illnesses will be divided into either heat exhaustion or heat stroke.

Heat exhaustion. The most common heat-related illness, heat exhaustion is characterized by volume depletion. It encompasses all heat-related illnesses that do not involve altered mental status. Patients often complain of fatigue, dizziness, weakness, headache, and nausea (see box below). On physical examination, they may be sweating, have moderate elevations in core temperature (often less than 104° F), and have a normal mental status. They may be tachycardic and may have orthostatic hypotension and other clinical signs of dehydration.

Heat exhaustion includes heat edema, heat tetany (heat cramps), and heat syncope. Heat edema is the pooling of interstitial fluid in the extremities and generally presents as swelling in the hands and feet. It is self-limited and can be treated with elevation and occasionally the application of compressive stockings. Diuretics are not necessary and should be avoided as they may exacerbate dehydration and salt depletion.

Heat cramps are painful muscle spasms occurring after vigorous exercise in the heat and are likely the result of dehydration. Treatment consists of rest, rehydration, and salt replacement.

Heat syncope generally results from volume depletion and peripheral vasodilation. It is distinguished from heat stroke by the rapid return of a normal level of consciousness and mental status.

Heat stroke. Any prolonged alteration in mental status should be considered heat stroke. This life-threatening illness has a mortality rate as high as 50% and is characterized by a rise in core body temperature above 104°F and central nervous system dysfunction. Patients may complain of fatigue, malaise, dizziness, weakness, headache, and nausea. Vomiting and diarrhea occur in up to two-thirds of patients.

The critical difference between heat exhaustion and heat stroke is sustained alteration in mental status. Although lack of sweating has been described as characteristic of heat stroke, sweating may actually occur. Delirium, seizures, or even coma may also develop. Patients are often tachycardic and hypotensive. Tachypnea is generally seen and can result in a respiratory alkalosis with concomitant metabolic acidosis. The brain is sensitive to heat, especially the cerebellum, so early signs may include an ataxic gait, confusion, and disorientation.

Heat stroke is usually described as either classic or exertional (see table above). Classic heat stroke occurs when the environmental heat load is very high, such as during a heat wave. It generally develops over several days and affects the elderly most often, particularly those with underlying illness, immobility, or lack of air conditioning. Exertional heat stroke is more likely to occur in younger, otherwise healthy people who are involved in strenuous activities in hot environments.

Many similarities exist between classic and exertional heat stroke, and treatment is often the same. Hyperkalemia from cellular damage, lactic acidosis, rhabdomyolysis, and renal failure tend to be more severe in exertional heat stroke than in classic heat stroke.

DIFFERENTIAL DIAGNOSIS

Fever due to other causes can be mistaken for heat illness. For example, fever due to sepsis can be very difficult to distinguish from classic heat stroke, and both conditions may need to be treated simultaneously until one is ruled out. Meningitis and encephalitis can present with fever and altered mental status, and the clinical symptoms of thyroid storm can also mimic heat stroke. Taking an overdose of certain medications, such as anticholinergics, can lead to signs and symptoms similar to heat stroke. Hypothalamic strokes, typhoid fever, cerebral malaria, delirium tremens, malignant hyperthermia, neuroleptic malignant syndrome, and serotonin syndrome can all present with a clinical picture very similar to heat stroke.

Fortunately, treatment for heat illness can begin immediately, even before a diagnosis is made, in any patient presenting with altered mental status and a temperature above 104°F. If the patient turns out to have another condition, treating heat stroke initially will not adversely affect the outcome of the other condition.

EVALUATING THE PATIENT

Evaluation of the patient with heat illness requires a thorough history when possible and a complete physical examination. Some degree of altered mental status will be present in heat stroke victims, so the history may need to be obtained from witnesses, bystanders, or prehospital medical personnel. When the patient is able to give a history, he typically complains of fatigue, headache, nausea, malaise, and other flu-like symptoms. As noted above, physical examination often reveals tachycardia, hyperventilation, and an elevation in temperature. Remember that sweating, which often occurs in heat exhaustion, may or may not be present in heat stroke. Once again, the hallmark of heat stroke is sustained alteration in mental status, not sweating. 

Laboratory studies are often interesting in patients with heat illness, particularly those with heat stroke, and many values will be severely elevated. Keep in mind that most patients with mild to moderate heat illness do not need laboratory studies. These studies are only necessary when the history and physical examination reveal a strong possibility of heat stroke.

Significant elevations in aspartate aminotransferase (AST), alanine aminotransferase (ALT), and serum bilirubin levels are often seen in patients with heat stroke. One study found lactic acid dehydrogenase (LDH) to be the most useful prognostic indicator, followed by creatine kinase (CK) and AST. Glucose and sodium levels may be the most important laboratory values to consider in patients with heat illness; a full electrolyte panel should usually be obtained. Although hypoglycemia is unusual, it may occur because glucose stores can be depleted from exertion or other heat stress. Hyponatremia is seen more in patients with exertional heat illness caused by the replacement of salty sweat with large amounts of free water. Patients having trouble with oral rehydration due to nausea and vomiting are more likely to be hyponatremic.

Either hyper- or hypokalemia may also be seen. A serum creatinine level will help determine current renal function and also serve as a baseline, because patients with significant muscle breakdown from the heat can spill significant levels of CK, leading to rhabdomyolysis and renal failure. Rhabdomyolysis commonly affects renal function, particularly in exertional heat stroke. Hypophosphatemia on hospital admission may predict the occurrence of acute liver failure during heat stroke, which may be more common than previously described.

TREATMENT OPTIONS

The treatment of victims of heat illness should focus on preventing heat stroke and lowering their temperature as quickly as possible. Immediate cooling is the cornerstone of treatment. How long the temperature is high is actually of more concern than how high the temperature gets. Patients should be removed from the hot environment immediately and placed in a cool, shaded area. All clothing should be removed and evaporative cooling initiated as soon as possible. You cannot cool a patient too rapidly.

Hydration should also be initiated early. At athletic events and in other situations when heat illness is detected early (in the heat exhaustion stage), oral hydration is very effective. In situations where nausea and vomiting or altered mental status do not permit oral rehydration, intravenous normal saline solution should be administered. Patients with significant volume depletion or electrolyte abnormalities generally require intravenous hydration as well. Room-temperature fluids stored in a climate-controlled environment will be cool enough and do not need to be cooled further.

What is the best method for cooling the patient? The advantages of various methods are still being debated. Evaporative cooling by spraying the patient with tepid water (59°F) and creating a breeze with fans provides cooling rates equivalent to any other method and is available in most health care settings. Spraying ice cold water can induce peripheral vasoconstriction and usually should not be done. While vasoconstriction may be beneficial in hypotensive patients, it can reduce the amount of heat lost by radiation. Cooling of the skin may cause shivering, even in patients with high core temperatures, and shivering may limit cooling by increasing metabolic heat production. When the evaporative cooling method described above is used, cooling rates can approach 0.56°F per minute.

Ice water immersion is another effective option that is advocated by some as the gold standard for treating heat stroke. However, randomized controlled trials have not shown that this technique is superior to evaporative cooling. What’s more, immersion of a patient with altered mental status presents monitoring difficulties and other management challenges, particularly for personnel not experienced in managing patients who are immersed. Other cooling modalities include ice packs to the neck, axillae, and groin, as well as cooling blankets and ice water lavages of the peritoneum, stomach, bladder, and rectum.

In extreme cases, cardiopulmonary bypass has been successful. As discussed earlier, the pathophysiologies of heat stroke and fever differ, so antipyretics are not indicated. Varieties of tachyarrhythmias are seen in heat stroke and generally resolve with cooling. Dantrolene has been advocated but is not effective in treating heat stroke.

The therapeutic interventions for heat exhaustion and heat stroke are summarized in the box below.

ACCLIMATIZATION PROCESS

The process of acclimatization (adaptation) to heat produces both short- and long-term changes in thermoregulatory responses involving sweating, skin circulation, and the thermoregulatory set point. Acclimatization to heat is possible but it must be done gradually, with moderate exercise for one to one-and-a-half hours a day, building up to more strenuous exercise over 8 to 10 days. (Acclimatization to cold is not possible.)

Although the process of acclimatization is not well understood, it appears to be mediated through the
renin-angiotensin system with increased production of aldosterone, which results in sodium conservation in both urine and sweat. Sweating is initiated at lower core temperatures, sweat becomes less salty, and the amount of sweat can more than double. Proteins also change during the process of acclimatization. Heat shock proteins increase and keep the body functioning as the temperature rises, preventing other proteins from denaturing and failing to work.

PREVENTING HEAT ILLNESS

Some simple precautions can help prevent heat illness. Children or pets should never be left alone in an enclosed vehicle, even for a short period of time. Even in relatively cool temperatures, the average rate of temperature elevations in a car is 3.2°F every five minutes, with 80% of the temperature rise occurring during the first 30 minutes. Cracking the windows open does not appear to decrease the rate of temperature elevations in a vehicle.

Fluid replacement is critical for people exerting themselves in a warm environment. It is best accomplished with electrolyte solutions, contained in most sports drinks. However, many commercial sports drinks contain more salt than is necessary, so diluting them with an equal volume of water is a good idea. To prevent hyponatremia, water should be used with caution unless sufficient salt intake can be ensured in other ways.  

It is important to recognize the early signs of heat stroke. Any athlete exerting himself in a warm environment who exhibits confusion, disorientation, or an unsteady gait should be removed from the environment immediately and treated with hydration and evaporative cooling. Even those who recover quickly should not return immediately to any exertional activity. Coaches and other people overseeing athletic events and practices should be knowledgeable about the early signs of heat illness and should advise event planners to limit strenuous activity in heat and humidity and allow for proper acclimatization.

During heat waves, special attention should be paid to the elderly; those confined to bed; those with cardiovascular disease, neurologic problems, or mental disorders; and those who do not have air conditioning. Increasing the frequency of showers or baths, using fans, or visiting air-conditioned areas are all prudent moves during hot weather.

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