Heatstroke—Predictable, preventable, treatable

Heatstroke can have devastating, even life-threatening consequences if not recognized quickly and treated effectively. With early recognition and proper care, the prognosis is very good.

Tom P. Moreau, MS, PA-C; Michael Deeter, MMS, PA

Tom Moreau is Assistant Professor in the Physician Assistant Program, Midwestern University, Glendale, Ariz. Michael Deeter is a recent graduate of the Midwestern University PA program. The authors have indicated no relationships to disclose relating to the content of this article.

   If you prefer to view this article in PDF form, click here.

It’s hot and it’s going to get hotter. Climate records show that 15 of the past 20 years have been the warmest on record.¹ Since the late 19th century, there has been a worldwide inoculation of greenhouse gases leading to accelerated global warming.^1,2 An increased number of heat waves, defined as air temperatures of 32.2°C (90°F) or higher for three or more consecutive days, is likely to accompany this trend. As a result, the Intergovernmental Panel on Climate Change predicts significant increases in heat-related mortality for urban areas of North America in the future.^3-5

In the United States, heat-related deaths average approximately 400 per year and are the most frequent environmentally related cause of death.⁵ Over the past decade, cities throughout the world have experienced epidemic death rates during heat waves.^3,5,6 This is true even though the pathophysiology of heatstroke (HS) is well understood and strategies for its treatment and prevention are well known.⁷

HS occurs when homeostatic thermoregulatory mechanisms fail, causing an elevation in core body temperature to higher than 40°C (104°F), CNS dysfunction such as confusion or seizures, and organ damage and death if not treated aggressively.^7-9 Risk factors for HS include prolonged exposure to high environmental temperatures, lack of acclimatization to warm environments, poor physical condition, and wearing excessive clothing in high temperatures.^7,9-11 People with preexisting cardiac, vascular, or respiratory disease; obesity; or alcoholism are at high risk for HS.^9,11 Numerous medications are also associated with an increased risk for HS (see Table 1).^9,11 Anhydrosis is no longer considered an essential element for the diagnosis of HS because some persons who develop HS while exercising continue to perspire.⁹ 

Classic and exertional heat stroke

HS is categorized as either classic (CHS) or exertional (EHS) (see Table 2).

Classic heatstroke This form of HS typically occurs during periods of high ambient temperatures; epidemics in temperate climates correlate with spring or early summer heat waves. The number of HS cases escalates about 24 hours after very hot days; abnormally high night temperatures particularly increase the risk for CHS. Persons older than 75 years or those who have preexisting medical conditions, children younger than 5 years, and urban dwellers are most vulnerable.^7-9,12 Access to an air-conditioned environment is the most important factor for preventing CHS.^3,5-7

About half of heat-related deaths occur in adults older than 65 years, who are at increased risk for a number of reasons.⁹ When dehydrated, they tend to maintain blood volume via a compensatory loss of fluids from the intracellular compartment.¹³ They also have an altered response to heat stress, including reductions in sweat gland function, skin blood flow, and cardiac output.¹⁴

Young children produce more metabolic heat than do adults and have less efficient mechanisms for dissipating heat. Children are also less likely to reduce activity in extreme heat and can experience a faster rise in core temperature when dehydrated.⁹

Exertional heatstroke This form of HS occurs when the skin and lungs are unable to dissipate heat generated by working skeletal muscle.^12,15-17 With heavy exercise, net heat production can rapidly result in extreme hyperthermia. The greatest predisposing factor to EHS is prolonged physical activity in high ambient temperature.^15,16,18 Dehydration, insufficient caloric intake, and electrolyte imbalances can all exacerbate EHS.¹⁶ Normally, compensatory mechanisms such as sweating, increased respiration, changes in circulatory distribution, and renal function can moderate this heat gain.¹⁰ EHS occurs when these mechanisms fail.⁸

Those who are young and in apparent good health are the most common victims of EHS, most likely because this age-group often participates in strenuous activity in high temperatures.^{8,10,12,15-17} HS is the third leading cause of death among athletes in the United States.^19,20 People can suffer EHS while participating in organized sports. Occupation may also increase risk: For example, foundry workers, firefighters, and military personnel may experience EHS.⁹ In 1995 alone, 700 deaths reportedly resulted from EHS.¹² Among survivors, evidence of brain damage is reported to be as high as 14% to 20%.^6,21,22 

Physiology

The hypothalamus is the central integrator for maintaining temperature in a homeothermic range.^7,9 It receives afferent signals from thermoreceptors in the skin and CNS and responds by activating elements of both the sympathetic and parasympathetic pathways.⁷ The body’s initial reactions to heat stress include peripheral vasodilation, activation of sweat glands, and tachycardia. These mechanisms combine to transfer internal heat to the body surface, where it can dissipate under most conditions.^7,9,14 Adaptation, which generally takes several days in a hot climate, includes increases in plasma volume, sweating capacity, and cardiovascular performance.⁷

Whether CHS or EHS is the cause, the underlying pathophysiology of HS is the same. It occurs when the body’s thermoregulatory system fails in the face of heat stress, which develops from a combination of metabolic production plus environmental heat.⁹ Homeostatic mechanisms favor thermogenesis and heat retention. Humans have a limited capacity to dissipate excess body heat effectively, and the two primary mechanisms for heat dissipation—peripheral vasodilation and perspiration—are inefficient in excessive heat or humidity.

Heat transfer The rate of heat exchange increases when the temperature difference between substances increases and when the surface area available for heat exchange is augmented. Insulation of any kind interferes with heat transfer, so it is important to uncover a patient with HS as much as possible.

The four methods of heat transfer are radiation, evaporation, conduction, and convection.

Radiation involves the transfer of heat via electromagnetic waves. The quantity of heat transferred via radiation is directly related to the mass and proximity of the objects. The effects of radiation are felt in direct sunlight or when standing near a fire. While radiation can add to heat stress, it does not play a role in treating HS. In urban areas, buildings and asphalt create a “heat island effect” by absorbing heat during the day and radiating it throughout the night, contributing to increased HS risk in urban areas during heat waves.

Conduction involves the direct transfer of heat from one substance to another. There is minimal conductive heat transfer in warm, still air, although water is approximately 30 times more effective than air for conducting heat. As such, immersing a patient in cool water can be an extremely efficient method for treating HS in some settings, although monitoring and rapid access to the patient are limited. Immersion has been used effectively for treating athletes and soldiers.^8,15,23

Convection, as wind or water current, greatly magnifies conductive heat transfer by continually restoring the thermal gradient at the boundary layer between two substances. Fanning a patient augments cooling because it continually replaces the air in contact with the skin.

Evaporation is the transformation of a liquid to a gas. When water evaporates from the body’s surface, it uses enormous quantities of heat energy. Evaporating perspiration is the primary mechanism for dissipating heat from the body in a hot environment. The drier the air is, the more effective the evaporation. In low humidity, this mechanism can often dissipate all of the heat produced by heavy exercise. When environmental humidity is high, sweat accumulates on skin and clothing, greatly reducing the efficiency of evaporative heat loss.  

Diagnosis and complications

The patient with HS generally presents with an elevated temperature, neurologic impairment, tachypnea, and tachycardia.^22,23 The hallmark of HS, neurologic dysfunction associated with an elevated core temperature, results from both increased intracranial pressure and decreased arterial BP leading to a marked reduction of cerebral perfusion pressure.^8,11,12,22 The patient may have decreased visual acuity, impaired recent and remote memory, ataxic gait, decreased coordination in a nonfocal pattern, lethargy, delirium, or coma.^8,11,12 Perspiration is often markedly decreased because of dehydration, and the skin is hot to the touch.^8,12 Anhidrosis is more likely in persons with CHS than with EHS.^9,20 A sublethal core temperature elevation can lead to cellular damage and rhabdomyolysis, heart failure, acute renal failure (ARF), and electrolyte abnormalities.^7,9,19 Delayed complications include disseminated intravascular coagulation (DIC), hepatic failure, and multiorgan-dysfunction syndrome.^7,8,23

Rhabdomyolysis may result from a combination of hyperthermia, dehydration, and excessive muscle activity, leading to the systemic release of toxic intracellular substances such as myoglobin. Myalgia with the presence or history of dark brown urine, along with transient elevations of creatine phosphokinase unrelated to cardiac or inflammatory conditions, are diagnostic evidence of rhabdomyolysis.^23,24 This syndrome can lead to metabolic acidosis, hyperkalemia, ARF, coagulopathies, respiratory and hepatic insufficiency, and hypocalcemia.^23,24 If there is no evidence of rhabdomyolysis, ARF is most likely due to heart failure, severe dehydration, or vasodilation. The mainstay of treatment for ARF is aggressive rehydration to facilitate diuresis and, in the case of rhabdomyolysis, dilution of the circulating toxins.

DIC, which is most evident 3 to 5 days after insult, results from concurrent activation of both the coagulation and fibrinolytic systems.⁷ If multiorgan failure can be averted, DIC may resolve over several days. When DIC does occur, replace coagulation factors by administering blood products.²⁴

Fulminant hepatic failure is a common late finding in patients suffering from HS. Hepatic cells appear to be particularly sensitive to thermal injury when the perfusion of the splanchnic organs is redistributed to cutaneous capillary beds in order to increase heat dissipation.¹² Historically, low-dose dopamine has been used in such situations, in the belief that it minimizes splanchnic vasoconstriction and prevents development of multiorgan dysfunction.^12,24

Finally, there are similarities between acute HS and septic shock. When circulation is shunted to the periphery, ischemia of the visceral organs can lead to absorption of bacterial endotoxins and the activation of inflammatory mediators.^7,17 This, coupled with decreased function of the immune response seen in HS patients, can be quite deleterious.⁷ Suppression of neutrophil phagocytosis during the acute phase of EHS has been correlated with the severity of physical exertion and body temperature and with an increased likelihood of infections in patients with HS.^7,17  

Evaluation and treatment

An organized approach to evaluation and treatment of HS is necessary to achieve an optimal outcome (see Table 3).^7,9,20 With effective primary treatment, mortality can be less than 10%.^9,20,25-27 The patient’s airway, cardiorespiratory status, and core temperature should be monitored continuously. IV access should be obtained and the patient rehydrated with normal saline or lactated Ringer’s solution, keeping cardiopulmonary status in mind.⁸ Diagnostic studies should include a CBC, rapid serum glucose level, coagulation studies, electrolyte panel, hepatic panel, creatine phosphokinase (CPK), serum alcohol level, toxicology screen, arterial blood gases, chest radiograph, ECG, and urinalysis, including urine pH, myoglobin, and HCG. Neuroimaging studies such as CT may be needed.¹⁹ Because of the potential for serious late sequelae, it may be necessary to observe the patient beyond the acute recovery phase and to obtain serial measurements of liver function, electrolytes (including calcium, phosphorus, and magnesium), CPK, serum urea nitrogen and creatinine, as well as urinary pH and myoglobin, CBC, platelets, prothrombin time, and partial thromboplastin time.

Appropriate treatment strategies for HS involve immediate reduction of the core body temperature and restoration of homeostasis.^7,25-27 The major factor determining outcome is the length of time that the temperature remains hyperthermic, so immediate measures should be directed toward decreasing the core temperature to less than 38.9°C (102°F) as rapidly as possible.^8,23,25

Techniques for cooling Cooling methods for treating HS in conditions with limited resources include moving the patient to the shade, removing excess clothing, and initiating active cooling with either cold water immersion or ice water slurry packs to the groin and axillae.^9,25 Where adequate medical facilities exist, evaporative cooling or even surgical bypass with extracorporeal cooling has been successful.^21,23

Armstrong and colleagues found that ice water immersion cooled patients with HS in nearly half the time when compared to wrapping the patient in wet towels to cool by air exposure.¹⁵ Ice water immersion increases cardiac output in persons who can safely generate a cardiac response.¹⁵ While immersion reduces core temperature rapidly, it is generally not well tolerated. Monitor vital signs and mental status continuously, and monitor trunk and extremities to preserve cutaneous blood flow. When the core temperature reaches 38.9°C (102°F), discontinue cold water immersion to prevent cutaneous vasoconstriction and hypothermia.

If the medical facility is well equipped, utilize a combination of evaporative and convective cooling methods.^7,9 An effective intervention is an ordinary spray bottle to mist the patient’s exposed skin, followed by use of an electric fan to blow room air over the patient. These techniques allow for unhindered monitoring and access to the patient as needed.

Any neurologic impairment usually resolves promptly with effective treatment. Accordingly, failure to recover to baseline mental status once the core temperature has been lowered is a poor prognostic sign.⁷ It is important to quickly reevaluate other potential causes for neurologic compromise and correct electrolyte imbalances before irreversible damage occurs.²³ Continue to monitor the patient for refractory hypothermia as a result of the cooling methods.²³

Antipyretic warning Antipyretics are contraindicated in HS. No studies demonstrate their effectiveness, and they are likely to complicate patient management by either impairing platelet function, as can happen with aspirin and NSAIDs, or stressing the vulnerable liver with acetaminophen.²³ 

New or experimental treatments

Dantrolene This agent is a neuromuscular blocking drug that depolarizes postsynaptic nicotinic receptors. It lowers temperature in patients with malignant hyperthermia by reducing the gain in temperature produced by shivering.²⁰ Bouchama and Knochel cite a double-blind, randomized study undertaken in 1991, which found that dantrolene was not effective in HS.⁷ Hadad and colleagues reviewed several studies and reported variable results, with no clear trend. Routine administration of dantrolene for treatment of HS is not currently supported by the literature.²⁸

Hypothermic retrograde jugular vein flush (HRJVF) Wen and colleagues determined that retrograde injection of 5 mL of cold saline into the external jugular vein of rats with experimentally induced HS resulted in reduced brain temperature at 15 minutes, decreased brain injury, and prolonged survival time, when compared to rats that were treated with peripheral cold saline perfusion.^21,22 The researchers showed that HRJVF using cold saline had a more favorable outcome than intracarotid cold saline infusion and that it was not complicated by arterial thrombosis.²¹ The researchers concluded that HRJVF has the ability to cool the brain by up to 3°C (5.4°F), which serves to protect that organ from the deleterious effects of HS by increasing or maintaining cerebral blood flow in rat models. No follow-up research on this technique appears to have been published. 

Prevention

HS is a preventable illness, as are most illnesses associated with environmental exposure.^7,9,25 The first step is to limit exposure to conditions that are conducive to the disorder. Using a combination of heat and humidity, the National Weather Service has produced a Heat Index Chart that can help predict when heat illnesses are a danger (see Figure 1, page 31). The National Weather Service also issues regional warnings when dangerously hot conditions are anticipated. Patients can minimize their risk for developing HS by following some basic guidelines (see Table 4). Educating patients about how to prevent heat illness should be part of standard health maintenance.²⁵    

© 2007 Haymarket Media, Inc. and the American Academy of Physician Assistants. All rights reserved.
Use of jaapa.com subject to License agreement. Please read our Disclaimer and Privacy policy.