- Email: [email protected]
Heat-Associated Illness
24
24
Heat-Associated Illness Michael V. Callahan
KEY FEATURES • Heat-associated illnesses are a spectrum of clinical syndromes ranging from minor heat exhaustion to life-threatening conditions characterized by rhabdomyolysis, renal failure, and encephalopathy. • In the tropics, loss of shade trees, crowding, urban heat islands, droughts, high solar exposure, and high humidity all increase the incidence and severity of heat illness. • Hydration status, extremes of age, co-morbidities, and the use of certain traditional remedies, pharmaceuticals, methamphetamines, and other recreational drugs and alcohol all increase heat illness. • Mass gatherings such as festivals, refugee camps, and pilgrimages can result in large numbers of heat casualties, which can overwhelm local medical resources and personnel. • Treatment of heat illness requires an understanding of the physiology of heat load and heat loss; heightened clinical vigilance; and prompt, effective use of cooling therapies and, in rare cases, adjunct drug therapy.
DEFINITION Heat illnesses result from an imbalance of metabolic heat production or environmental heat loading and inadequate heat dissipation.1 In healthy adults, thermoregulation dissipates metabolic and exogenous heat to maintain body temperatures between 36°C and 37.8°C. Extreme heat loads can overwhelm thermoregulatory responses, resulting in heat illness. Heat illness syndromes should not be confused with fever, which is a physiologic increase in the temperature set point of the body, or with malignant hyperthermia, a hereditary metabolic hyperthermic response to certain pharmaceuticals or anesthetic gases. If overheating continues and the patient is left untreated, milder forms of heat illness, such as heat edema, may progress to more severe manifestations of heat illness, such as heat stroke, which, if untreated, can have a case fatality rate of 63%. The key syndromes associated with different heat illnesses are listed in Table 24.1.
EPIDEMIOLOGY Heat illness is common among athletes, soldiers, foundry workers, and during mass gatherings in hot conditions such as the annual Hajj pilgrimage2,3 and summertime music festivals in both Northern and Southern Hemispheres. Among young athletes, the most severe form of heat illness—heat stroke—is the second leading cause of death.4 In tropical regions, heat casualties are common and may be increasing in developing economies as more workers are required to work under sweltering conditions. In many settings, inadequate access to cool havens or to cold, potable water increases the risk of heat illness. Epidemiologic studies on heat illness conducted in the United States and Europe5,6 indicate the groups at highest risk of heat illness are children under 4 years of age, the elderly, those with renal and endocrine disorders, and institutionalized
and hospitalized patients.7,8 In particular, the importance of sweatbased evaporative cooling is demonstrated by the higher incidence of heat illness in the elderly and in patients being treated with anti-cholinergic medication.9,10 At this time, there are no convincing studies demonstrating differences in risk of heat illness between genders. Acclimatization to heat can reduce the risk of heat illness. Acclimatization involves near- and long-term physiologic adaptation; key findings include rapid correction of water loss and improved sodium preservation and gradual normalization of plasma electrolytes, altered blood perfusion to the skin, and reduced sodium concentrations in sweat and urine. New arrivals to tropical climes undergo limited acclimatization over a 2- to 4-week period; subsequent advances in acclimatization are both limited and not conclusively established by current studies.
PATHOPHYSIOLOGY Heat illnesses are the result of excessive heat loads from the environment, the body’s inability to dissipate heat, or a combination of the two. In healthy individuals, the body compensates for heat stress by thermoregulatory processes and, less effectively, through adaptive processes. As total body heat load rises, the thermoregulatory system responds by stimulating the pre-optic nucleus of the anterior hypothalamus, which causes the dilation of cutaneous blood vessels and an increase in sweat production.11 There are four primary mechanisms with which the human body dissipates heat to the environment: evaporation, radiation, convection, and conduction. Care providers who understand these mechanisms of heat loss may exploit these mechanisms either separately or synergistically to maximize the effect of cooling therapy. The major form of heat loss in hot, dry climates is evaporation of sweat or surface water from the skin or pulmonary system. Each of the four methods of heat loss is enhanced by compensatory physiologic processes, notably increases in sweat production, respiration and cardiac output, alterations in cutaneous and splanchnic blood flow, and reduction in physical activity. The physical mechanisms of heat loss are summarized in Table 24.2. Physiologic thermoregulation expands upon physical mechanisms of heat loss through a combination of cutaneous vasodilation, increased cutaneous and respiratory evaporative cooling, and increased cardiac output. Environmental conditions greatly influence the efficiency of thermoregulation. For example, large temperature gradients between the body and surrounding air, convective loss from high air flow, and low humidity all favor efficient cooling. Evaporative heat loss is limited by humidity greater than 75% and by impaired physiologic responses such as anhidrosis, perfusion abnormalities, low cardiac output, and the effect of certain medications or toxins, pesticides, and chemical weapons. Other major methods of heat loss, such as radiation of infrared energy from the skin, conduction of heat through contact with surrounding materials, and convective heat loss, are less efficient when environmental temperatures are higher than skin temperatures. The body also has a limited ability to acclimatize to heat stress through increased shunting of blood to the skin, improved water preservation, and increased aldosterone production to retain sodium. Unacclimatized individuals exposed to heat stress initially have high urine and sweat sodium content, which reduces circulating plasma volume. Reduced renal blood flow from sodium and water loss stimulates aldosterone secretion, which increases plasma sodium levels, which, in turn, increases intravascular fluid
189
190
PART 1 Clinical Practice in the Tropics
TABLE 24.1 Clinical Spectrum of Heat Illness
TABLE 24.2 Physical Heat Loss
Syndromes
Clinical Features
Evaporation
Heat edema
Self-limiting swelling of hands and feet resulting from cutaneous vasodilation and dependent pooling of interstitial fluid; resolves with early acclimatization.
Heat rash (miliaria)
Pruritic, red vesicles found on skin covered by non-breathable clothing or sleeping pads. Occlusion of eccrine sweat ducts by keratinocytes leads to dilation and rupture. Secondary infection with bacteria including (in recent years) methicillinresistant Staphylococcus aureus is common. Repeated occlusion of sweat ducts results in progression of inflammation and, if untreated, chronic dermatitis.
Evaporative cooling aids the efficiency of cutaneous heat transfer to the environment and is the primary mechanism of heat loss in healthy individuals. Evaporative cooling through respiration is critical for dogs, upon which many classic heat stroke studies are based, but appear to be much less significant in humans compared with evaporation from the skin.
Conduction
Conduction is heat transfer through contact with a cooler material; the efficiency of conductive heat transfer varies with the properties of the conductive material, the temperature differential between surfaces, and surface area. Conductive heat loss is improved when contact surfaces are of dense composition, contiguous, or wet.
Radiation
Radiation is the loss of heat energy as electromagnetic waves and accounts for up to 65% of total heat loss for temperatures <37°C. When environmental temperatures are higher than body temperatures, the direction of heat exchange is reversed, resulting in a net heat gain.
Convection
Convection is the loss of heat to surrounding air; as with radiation, the direction of heat transfer reverses when the air temperature is higher than the skin temperature.
Heat cramps
Cramping of large muscle groups after exercise; common in unacclimatized individuals and those unaccustomed to physical exercise in hot conditions. The syndrome is attributed to inefficient sodium recovery and hypernatremic sweat; resolves with acclimatization.
Heat tetany
Hyperthermia-associated hyperventilation causes a primary respiratory alkalosis, which in turn can cause perioral paresthesia, carpopedal or laryngeal spasm, and Chvostek’s sign.
Heat exhaustion
Danger: symptoms include nausea, vomiting, fatigue, weakness, and occasionally, diarrhea; clinical findings include orthostatic hypotension, tachycardia, syncope, hyperthermia (core temperature <40°C; 104°F) and minor mental status changes such as poor attention span. Caution: Heat exhaustion and heat stroke have overlapping symptoms; the primary differentiating criterion is that heat stroke is associated with more severe CNS disturbances and core body temperatures above 40°C.
Heat stroke
Life threatening: heat stroke is a medical emergency characterized by core temperature >40°C (105°F) and CNS disturbances in patients with a history of heat exposure. Anhidrosis (absence of sweating) is often present but is no longer a criteria for diagnosis. Age, chronic disease, and medications increase probability of heat stroke, which if untreated, leads to organ dysfunction and death. Caution: Heat stroke is often missed in patients who may not have been physically active.
Adapted from Bouchama, A, Knochel, JP. Heat stroke. N Engl J Med 2002;346:1978 and Tek D, Olshaker JS. Heat illness. Emerg Med Clin of North Amer 1992;10;299.
volume.9 Under extreme physiologic conditions and high heat stress, vasodilation can be significant, leading to peripheral venous pooling, extravasation of fluids, and reduced cardiac output. At temperatures above 42°C (≈108°F), mitochondrial enzymes are inhibited, oxidative phosphorylation becomes uncoupled, and ischemia of hepatocytes and renal parenchymal cells occurs. Heat damage to hepatorenal vascular beds results in microthrombi formation and prolonged prothrombin time (PT) and partial thromboplastin time (PTT); if cooling is not instituted, disseminated intravascular coagulation (DIC) can occur, leading to multi-organ system failure and death.12
ASSESSMENT AND INVESTIGATIONS The first priority in patient assessment is to confirm airway, breathing, and circulation. Attempts should be made to remove or protect the patient from continued heat exposure. While assessment is underway, equipment and personnel should be recruited to assist with cooling. If multiple cases are involved, a referral center should be notified
to increase capability for multiple casualty cooling. Initial treatment includes removal of clothing and preparation of cold water baths, water mist-convection systems, and focal cooling of superficial venous vessels such as the antecubital fossa, axilla, popliteal fossa, and inguinal region. Critically overheated patients require more aggressive interventions such a cool water immersion, cold intravenous fluids, and if expertise permits, peritoneal lavage. If initial assessment suggests severe heat injury, peripheral intravenous access should be established and normal saline or lactated Ringer’s solution should be initiated at 200 mL/hr. If available, unhumidified oxygen should be delivered by nasal cannula. Initial workup starts with a detailed history and thorough physical examination. The history should prioritize past medical conditions, careful documentation of therapeutic and recreational medication, and diet and hydration history. Hyperthermic patients should have baseline vital signs assessed every 15 minutes, and sphygmomanometer sites should be marked with indelible ink to ensure accurate measurements are obtained between serial readings and among different care providers. Baseline body temperature needs to be established using a quality non-glass medical thermometer. Rectal temperatures are preferred, as oral, axillary, and inguinal thermometry is unreliable in patients with perfusion shunt abnormalities; however, these locations can be used to monitor trends in body temperature if rectal measurements are unsafe. If prolonged resuscitation is anticipated, a thermometry probe should be placed in the rectum or esophagus. If none is available and the situation is dire, an invasive monitor can be improvised using an outdoor thermometer, where the probe is covered with a prophylactic condom or rubber glove and inserted into the rectum immediately past the anal verge. Modern low-cost wireless thermometers have been adapted for rectal patient monitoring by mountain rescue teams with even more success. Trends in body temperature monitoring during transport are helpful in triage and the selection of hospital-based cooling therapies (e.g., cutaneous, intravenous, peritoneal, extracorporeal). Mental status and the presence of focal neurologic problems should be assessed during transport and the early phases of cooling therapy. Within the central nervous system (CNS), the cerebellum is particularly sensitive to heat stroke, and therefore cerebellar examination such as finger–nose–finger, heel-to-shin rub, and dysdiadochokinesia studies should be performed. The oral cavity should be examined
CHAPTER 24 Heat-Associated Illness
for evidence of gingival bleeding or evidence of chronic methamphetamine use, and the rectal examination performed to assess for tone, and stool in the vault tested for hemoglobin, which each may warn of cryptic coagulopathy. Pulmonary examination should assess for rales. Skin examination will help determine the patient’s hydration status, and the presence of miliaria and the presence of needle tracks or skin-popping sites should be assessed. Muscle examinations should include active and passive flexion of shoulders, thighs, and calves; the presence of localized pain may indicate muscle breakdown. Urine should be collected by a Foley if necessary and inspected for evidence of myoglobin, hemoglobin, and sediment. Disposable urine analysis “dipsticks” are useful in guiding initial therapy and need to protect the kidneys from hemoglobinuria or myoglobinuria. In recent years, the proliferation of point-of-care handheld blood chemistry units in field clinics increases the probability that basic blood chemistry may be obtained. The current-generation cartridges for these handheld units require refrigeration; if test results are inconsistent with the clinical picture, the provider should suspect that the cartridges were unrefrigerated or are outdated. If quantitative coagulation studies are not available, a whole-blood clotting assay can be used to assess for coagulopathy, and a Weintraub sedimentation tube can be used to assess for hemoconcentration. The improvised coagulopathy and hemoconcentration tests discussed are most accurate when conducted with “controls” provided by a healthy bystander. Table 24.3 summarizes laboratory tests that are helpful in assessing heat illness casualties.
DIAGNOSIS The differential diagnosis of heat illness requires a history of heat exposure, a careful medical history and list of medications, a detailed physical examination, serum chemistries, and urine analysis. Infectious etiologies and rare causes of hyperthermia need to be ruled out. The differential diagnosis should include environmental heat stroke, exertional heat stroke, drug-induced hyperthermia, malignant hyperthermia, neuroleptic malignant syndrome, endocrine and hypothalamic disorders, and fictitious hyperthermia. The less severe heat illnesses such as heat edema and heat syncope are suggested by advanced age, deconditioning, low cardiac reserve, anti-cholinergic medication, pesticide exposure, and recent arrival to the tropics from cooler regions. Miliaria, a distinct heat dermatosis, is differentiated from other tropical skin maladies by the timing, distribution, and physical appearance of skin vesicles. Miliaria responds promptly to antihistamines or dilute topical chlorhexidine. Heat cramps are the second most common malady among unacclimatized individuals; diagnosis is suggested by resolution of cramps with rest and cool treatment, stretching, hydration, and electrolyte repletion. The two most dangerous heat illnesses— heat exhaustion and heat stroke—have overlapping clinical features and are discussed next.
191
Heat exhaustion is a broadly defined clinical syndrome characterized by history of heat exposure, fatigue, and other protean clinical findings and the absence of an alternative diagnosis. Core body temperature in heat exhaustion is <40°C. The most common symptoms seen among hundreds of over-heated casualties attending outdoor music festivals and the Hajj are nausea and vomiting, headache, and weakness. Respiratory rate may be elevated. The cardiac and pulmonary examination may be normal; however, tachycardia may be present from concomitant dehydration. The presence of sweating in heat exhaustion patients is an important finding, as it is frequently decreased or absent in heat stroke patients. The patient’s mental status may suggest mild confusion, and complaints may include dizziness. Symptoms of heat exhaustion tend to resolve within several hours after oral hydrations, rest, and basic interventions that lower skin temperature. Several cases of rebound hyperthermia observed at the Hajj suggest that elderly patients and the very young (age <4 years) should be more closely monitored until euthermia is stable for over 3 hours. Heat stroke is a life-threatening condition defined by a core body temperature >40°C and mental status or neurologic symptoms that do not respond to initial cooling therapy (rest, cold treatment, and hydration).12 Patients may be combative, with delirium, seizure, obtundation, or coma. Clues to differentiate heat stroke from heat exhaustion include significant mental status changes, diarrhea, and dry skin in heat stroke. A minority of heat stroke casualties may present with sweating; however, this usually stops as thermoregulation continues to fail. Complications of heat stroke include acute renal failure from rhabdomyolysis, liver failure, DIC, acute respiratory distress syndrome, seizure, coma, and death.1 Select diagnostic features for differentiating heat stroke and heat exhaustion are listed in Table 24.4. The differential diagnosis of hyperthermia is listed in Table 24.5.
MANAGEMENT AND OUTCOMES Treatment of heat illness is provided in Table 24.6. Management strategies exploit all four principal mechanisms of heat loss and cold therapy targeted to specific body locations (Fig. 24.1). Minor heat illnesses are self-limiting if the patient is provided with fluids, rest, and access to a cool environment. The majority of cases require only fluids and electrolytes for resolution of symptoms. Heat edema is prevented by exercise at high temperatures before travel to the tropics, optimization of diuretics and beta-blockers, and use of supportive compressive stockings. Heat exhaustion is a more serious form of hyperthermia that requires close evaluation to ensure further deterioration is inhibited. TABLE 24.4 Differential Diagnosis of Heat Exhaustion and Heat Stroke Factor
Heat Exhaustion
Heat Stroke
Patient age
All ages
Often young/healthy
Symptoms
Nausea ± vomiting
Nausea ± diarrhea
TABLE 24.3 Laboratory Assessment of Heat Illness
Body temperature
<40°C
>40°C
MILD CASES: Obtain urine analysis; test for pH, specific gravity, urine sediment, and hemoglobinuria and myoglobinuria.
CNS status
Normal: mild confusion
Delirium, ataxia, dysarthria, seizures, coma
MODERATE CASES: Add basic blood chemistries; test for sodium, potassium, chloride, bicarbonate, blood urea nitrogen, and creatinine.
Vital signs
± Tachypneic
Tachypneic, tachycardia, hypotensive
SEVERE CASES (E.G., CNS DISTURBANCES): Add aspartate transaminase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), uric acid, calcium, phosphate, coagulation studies (PT and PTT, fibrinogen); consider arterial blood gas for accurate determination of physiologic pH.
Dermatologic findings
Sweating; ± miliaria
Little or no sweat
Laboratory results
Normal
Elevated transaminases (AST > ALT); DIC, urine: muddy brown casts; Cr elevated; CBC: WBC elevated
Note: In ongoing clinical trials assessing performance of endurance athletes, point-of-care assessment of elevated creatine kinase, MM form (CPK MM) has been highly predictive of heat stroke.
Cr, Creatinine; CBC, complete blood count; WBC, white blood count.
24
192
PART 1 Clinical Practice in the Tropics
TABLE 24.5 Differential Diagnosis of Hyperthermia Environmental exposure Sepsis Encephalitis Brain abscess Meningitis Tetanus Typhoid fever Thyroid storm Pheochromocytoma Catatonia Malignant hyperthermia
Hypothalamic stroke Status epilepticus Cerebral hemorrhage Neuroleptic malignant syndrome Alcohol, sedative-hypnotic withdrawal Salicylate, lithium toxicity Sympathomimetic toxicity Anticholinergic toxicity Dystonic reactions Serotonin syndrome
Radiation
Evaporation
External core cooling sites: large surface veins
TABLE 24.6 Treatment of Heat Illness Heat Illness
Treatment Strategies
All
Rest, hydration, electrolytes, access to cool haven: initiate rapid cooling for temperatures >40°C and any patient with mental status changes.
Heat edema
Elevation of legs, cold compresses on arms and legs or cold baths.
Heat syncope
Move to cool location, rest, fluids.
Heat syncope and dehydration
Electrolyte replacement, consider discontinuing anti-hypertensive and anti-cholinergic medications.
Heat cramps
Rest, hydration, electrolytes.
Heat tetany with hyperventilation
Move to cool environment, restore normal respiration rates; in severe cases, rebreathing carbon monoxide or use of benzodiazepines.
Heat exhaustion
As above. Provide oral or intravenous hydration, mist water convective cooling, and focal use of ice packs on large superficial veins, axilla, and inguinal regions (see Fig. 24.1).
Heat stroke
Rapid cooling is the priority; use cold water immersion with rectal temperature monitoring; patient should be removed when rectal temperature reaches 39°C. Patients with coronary artery disease may develop coronary spasm with ice water immersion; patients with coronary risk factors should be treated less aggressively with mist water and convective cooling.
Initial treatment includes accurate determination of core temperature; blood chemistry monitoring; and initial treatment using radiant, evaporative, and convective cooling of exposed skin and oral electrolyte solutions. In recent years, treatment-resistant heat exhaustion has been associated with use of methamphetamines, emphasizing the need for a thorough history and use of urine and serum toxicology testing. If symptoms progress, or mental status changes fail to improve, the patient should be treated with intravenous normal saline. Both normal and abnormal serum chemistries should be rechecked after hydration and urine output are restored. Patients should be monitored until core body temperature has normalized. Heat exhaustion patients who have deteriorating mental status should have core temperature rechecked to confirm the diagnosis and should resume more aggressive cold therapy. Heat stroke is a medical emergency that is associated with high mortality. Treatment for heat stroke requires prompt, aggressive physical cooling. All measures for dissipating heat should be maximized: evaporation, radiation, convection, and conductive cooling. Treatment of heat stroke in the tropics may be limited by inadequate water for cooling baths, unavailability of air conditioning, and unreliable electricity to power fans. Patient
Convection
Conduction Fig. 24.1 Thermoregulation and therapeutic cooling.
monitoring during treatment may be complicated by lack of quality thermometers or supportive laboratory tests. Initial presenting heat stroke casualties may warn of a surge of patients requiring cooling therapy. A solitary heat illness casualty referred from a mass gathering such as a soccer match, outdoor music festival, or refugee camp should prompt medical control to evaluate the possibility of large numbers of heat casualties and the resource list to effectively care for them. For mass casualty heat illness, evaporative and convective cooling are the most field-viable and scalable treatment options. Unlike water immersion and invasive techniques such as peritoneal lavage, evaporative cooling allows for constant patient monitoring, the use of additional “layered” cooling strategies, and the ability to treat multiple patients at one station. Evaporative cooling requires water to apply to the skin and an air movement source, such as an electric fan. The patient is undressed and placed supine close to the fan. The skin is moistened with water using a sponge or mist bottle. If patient preference, local cultures, or religious beliefs prevent disrobing, the patient may be covered with a thin sheet that is kept wet; however, this dramatically reduces evaporative heat loss. Effective treatment of heat patients with devout religious beliefs, such as female pilgrims to the Hajj, is more effective when performed by female health care workers of the same religious and cultural background. Patients cooled with convective mist water systems need to be re-assessed regularly to ensure stable correction of body temperatures. Alcohol and other low-vaporpressure fluids should not be applied to the skin, as dilated cutaneous blood vessels may increase absorption, leading to intoxication. In many tropical clinics the only resources available for cooling the patient are ice packs: if supplies are limited, cold packs should be applied directly to large superficial veins on flexor surfaces such as the antecubital and popliteal fossa, axilla, and inguinal region.
CHAPTER 24 Heat-Associated Illness
If ice is used, it should be wrapped in a damp cloth and applied to superficial veins using non-compressive pressure (see Fig. 24.1). Chemical cold packs, such as those found in modern first aid kits, lack sufficient cold capacity to treat heat casualties; however, they should be used if nothing else is available. Cold (ice) water immersion is the most effective method for rapid cooling. Clinical experience indicates ice water immersion lowers body core temperature at twice the rate of convective mist-water cooling (mist water and electric fan). The advantage of cold water baths is that the rate of cooling can be controlled by either changing the water temperature or adjusting the depth of immersion. In immersion cooling, the patient is undressed and placed in a tub of suitable depth to allow water to cover the extremities; cold immersion should only be used on alert patients. Heat stroke patients with co-morbidities, such as underlying cardiac disease, should be monitored for arrhythmias or syncope and, if the situation is not critical, cooled using less aggressive methods. In developed regions, immersion cooling has fallen out of favor because of difficulties with patient telemetry. In refugee camps and mass gatherings, however, a water bath is often in constant use to treat heat illnesses. Invasive cooling techniques are only to be used when cold water misting, evaporative cooling, and cool water immersion are ineffective and the patient is critically overheated. Invasive cooling may correct temperature unevenly and result in unpredictable cooling rates, over-cooling, and possibly death. Current invasive cooling methods include gastric and peritoneal lavage with cold fluids, cooled intravenous fluids, and cooled inhalational gas. The use of ice water gastric lavage is contraindicated in patients who have altered mental status or who are unable to protect their airway. Severe heat illness casualties treated with gastric lavage should be intubated to protect the airway. Cold intravenous fluids require careful control, as proximal access and rapid infusion rates can induce cardiac arrhythmias. Cold peritoneal lavage is an invasive technique that requires sterile access and should not be used in patients suspected of having abdominal adhesions or who are pregnant. Cooled oxygen and oral hydration fluids lack sufficient cold capacity to treat all but the most trivial of heat illnesses, but are low-risk adjunct treatments when combined with other approaches. New technologies designed to cool soldiers and athletes in hot climates include small circulating water baths that encircle a single foot or hand. A commercial vacuum cooling glove that
Fig. 24.2 Commercial vacuum cooling glove.
193
makes use of recirculating water is illustrated in Fig. 24.2. Each of these technologies requires a power source or re-charge of a cold source such as ice. Real-world studies of all current-generation “wearable” cooling technologies have been mixed; the clinician is encouraged to not substitute a complex, costly, and unproven technology for the clinically proven technologies described earlier. Regardless of the cooling method used, care providers should continuously monitor core temperature to ensure cooling does not overshoot the desired temperature.13 In cases involving rapid cooling of the core, treatment should be interrupted when core temperature drops below 40°C. The objective is to drop core temperature into a range where normal thermoregulation can again take control. Under field conditions such as the Hajj or Sudanese refugee camps, oral, rectal, and axillary temperature monitoring has under-estimated elevated core temperature and over-estimated the effectiveness of non-invasive cooling. Scanning thermometry devices are quick, require little training, and are non-invasive but rely on powered devices that require recalibration and careful maintenance. Adjunct treatments that complement therapeutic cooling are limited. Dehydration is treated quickly with intravenous fluids or, in conscious patients, with water or sports drinks. Sports drinks should be diluted before use to prevent osmotic loading of the gastrointestinal (GI) tract, which, in turn, can cause GI distress. Antipyretic medications and drugs used to treat malignant hyperthermia have no value in the treatment of heat illnesses and should not be used.13 One common complication of effective cooling with ice packs or immersion is shivering, which generates more body heat. In these situations, the careful use of short-acting benzodiazepines is reasonable. Although chlorpromazine is also used to treat shivering, the secondary alpha-1 blocking activity may make hypotension worse and therefore should not be used. Successful management of heat illness requires prompt recognition, triage, identification of exacerbating factors such as drug or alcohol ingestion, and efficient use of limited therapeutic cooling resources. Heat illness casualties require repeat assessment to ensure the orderly return to normothermia and to ensure overheating and under-cooling are avoided. REFERENCES
1. Tek D, Olshaker JS. Heat illness. Emerg Med Clin North Am 1992;10:299–310. 2. Centers for Disease Control and Prevention (CDC). Heat-related deaths – four states, July–August 2001, and United States, 1979–1999. MMWR Morb Mortal Wkly Rep 2002;51:567–70. 3. Al-Harthi SS, Nouh MS, Al-Arfaj H, et al. Non-invasive evaluation of cardiac abnormalities in heat stroke pilgrims. Int J Cardiol 1992;37:151–4. 4. Rav-Acha M, Hadad E, Epstein Y, et al. Fatal exertional heat stroke: a case series. Am J Med Sci 2004;328:84–7. 5. Centers for Disease Control and Prevention (CDC). Heat-related deaths – Chicago, Illinois, 1996–2001, and United States, 1979–1999. MMWR Morb Mortal Wkly Rep 2003;52:610–13. 6. Misset B, De Jonghe B, Bastuji-Garin S, et al. Mortality of patients with heatstroke admitted to intensive care units during the 2003 heat wave in France: a national multiple-center risk-factor study. Crit Care Med 2006;34:1087. 7. Centers for Disease Control and Prevention (CDC). Heat-related deaths – four states, July–August 2001, and United States, 1979–1999. MMWR Morb Mortal Wkly Rep 2002;51:567–70. 8. Sierra Pajares Ortiz M, et al. Daily mortality in the Madrid community during 1986–1991 for the group between 45 and 64 years of age: its relationship to air temperature. Rev Esp Salud Publica 1997;71:149–60. 9. Simon HB. Hyperthermia. N Engl J Med 1993;329:483–7. 10. Dann EJ, Berkman N. Chronic idiopathic anhydrosis – a rare cause of heat stroke. Postgrad Med 1992;68:750–2. 11. Khosla R, Guntapalli KK. Heat-related illness. Crit Care Clin 1999;15:251–63. 12. Bouchama A, Knochel JP. Heat stroke. N Engl J Med 2002;346:1978–88. 13. Bouchama A, Cafege A, Devol EB, et al. Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Crit Care Med 1991;19:176–80.
24
24
Heat-Associated Illness Michael V. Callahan
KEY FEATURES • Heat-associated illnesses are a spectrum of clinical syndromes ranging from minor heat exhaustion to life-threatening conditions characterized by rhabdomyolysis, renal failure, and encephalopathy. • In the tropics, loss of shade trees, crowding, urban heat islands, droughts, high solar exposure, and high humidity all increase the incidence and severity of heat illness. • Hydration status, extremes of age, co-morbidities, and the use of certain traditional remedies, pharmaceuticals, methamphetamines, and other recreational drugs and alcohol all increase heat illness. • Mass gatherings such as festivals, refugee camps, and pilgrimages can result in large numbers of heat casualties, which can overwhelm local medical resources and personnel. • Treatment of heat illness requires an understanding of the physiology of heat load and heat loss; heightened clinical vigilance; and prompt, effective use of cooling therapies and, in rare cases, adjunct drug therapy.
DEFINITION Heat illnesses result from an imbalance of metabolic heat production or environmental heat loading and inadequate heat dissipation.1 In healthy adults, thermoregulation dissipates metabolic and exogenous heat to maintain body temperatures between 36°C and 37.8°C. Extreme heat loads can overwhelm thermoregulatory responses, resulting in heat illness. Heat illness syndromes should not be confused with fever, which is a physiologic increase in the temperature set point of the body, or with malignant hyperthermia, a hereditary metabolic hyperthermic response to certain pharmaceuticals or anesthetic gases. If overheating continues and the patient is left untreated, milder forms of heat illness, such as heat edema, may progress to more severe manifestations of heat illness, such as heat stroke, which, if untreated, can have a case fatality rate of 63%. The key syndromes associated with different heat illnesses are listed in Table 24.1.
EPIDEMIOLOGY Heat illness is common among athletes, soldiers, foundry workers, and during mass gatherings in hot conditions such as the annual Hajj pilgrimage2,3 and summertime music festivals in both Northern and Southern Hemispheres. Among young athletes, the most severe form of heat illness—heat stroke—is the second leading cause of death.4 In tropical regions, heat casualties are common and may be increasing in developing economies as more workers are required to work under sweltering conditions. In many settings, inadequate access to cool havens or to cold, potable water increases the risk of heat illness. Epidemiologic studies on heat illness conducted in the United States and Europe5,6 indicate the groups at highest risk of heat illness are children under 4 years of age, the elderly, those with renal and endocrine disorders, and institutionalized
and hospitalized patients.7,8 In particular, the importance of sweatbased evaporative cooling is demonstrated by the higher incidence of heat illness in the elderly and in patients being treated with anti-cholinergic medication.9,10 At this time, there are no convincing studies demonstrating differences in risk of heat illness between genders. Acclimatization to heat can reduce the risk of heat illness. Acclimatization involves near- and long-term physiologic adaptation; key findings include rapid correction of water loss and improved sodium preservation and gradual normalization of plasma electrolytes, altered blood perfusion to the skin, and reduced sodium concentrations in sweat and urine. New arrivals to tropical climes undergo limited acclimatization over a 2- to 4-week period; subsequent advances in acclimatization are both limited and not conclusively established by current studies.
PATHOPHYSIOLOGY Heat illnesses are the result of excessive heat loads from the environment, the body’s inability to dissipate heat, or a combination of the two. In healthy individuals, the body compensates for heat stress by thermoregulatory processes and, less effectively, through adaptive processes. As total body heat load rises, the thermoregulatory system responds by stimulating the pre-optic nucleus of the anterior hypothalamus, which causes the dilation of cutaneous blood vessels and an increase in sweat production.11 There are four primary mechanisms with which the human body dissipates heat to the environment: evaporation, radiation, convection, and conduction. Care providers who understand these mechanisms of heat loss may exploit these mechanisms either separately or synergistically to maximize the effect of cooling therapy. The major form of heat loss in hot, dry climates is evaporation of sweat or surface water from the skin or pulmonary system. Each of the four methods of heat loss is enhanced by compensatory physiologic processes, notably increases in sweat production, respiration and cardiac output, alterations in cutaneous and splanchnic blood flow, and reduction in physical activity. The physical mechanisms of heat loss are summarized in Table 24.2. Physiologic thermoregulation expands upon physical mechanisms of heat loss through a combination of cutaneous vasodilation, increased cutaneous and respiratory evaporative cooling, and increased cardiac output. Environmental conditions greatly influence the efficiency of thermoregulation. For example, large temperature gradients between the body and surrounding air, convective loss from high air flow, and low humidity all favor efficient cooling. Evaporative heat loss is limited by humidity greater than 75% and by impaired physiologic responses such as anhidrosis, perfusion abnormalities, low cardiac output, and the effect of certain medications or toxins, pesticides, and chemical weapons. Other major methods of heat loss, such as radiation of infrared energy from the skin, conduction of heat through contact with surrounding materials, and convective heat loss, are less efficient when environmental temperatures are higher than skin temperatures. The body also has a limited ability to acclimatize to heat stress through increased shunting of blood to the skin, improved water preservation, and increased aldosterone production to retain sodium. Unacclimatized individuals exposed to heat stress initially have high urine and sweat sodium content, which reduces circulating plasma volume. Reduced renal blood flow from sodium and water loss stimulates aldosterone secretion, which increases plasma sodium levels, which, in turn, increases intravascular fluid
189
190
PART 1 Clinical Practice in the Tropics
TABLE 24.1 Clinical Spectrum of Heat Illness
TABLE 24.2 Physical Heat Loss
Syndromes
Clinical Features
Evaporation
Heat edema
Self-limiting swelling of hands and feet resulting from cutaneous vasodilation and dependent pooling of interstitial fluid; resolves with early acclimatization.
Heat rash (miliaria)
Pruritic, red vesicles found on skin covered by non-breathable clothing or sleeping pads. Occlusion of eccrine sweat ducts by keratinocytes leads to dilation and rupture. Secondary infection with bacteria including (in recent years) methicillinresistant Staphylococcus aureus is common. Repeated occlusion of sweat ducts results in progression of inflammation and, if untreated, chronic dermatitis.
Evaporative cooling aids the efficiency of cutaneous heat transfer to the environment and is the primary mechanism of heat loss in healthy individuals. Evaporative cooling through respiration is critical for dogs, upon which many classic heat stroke studies are based, but appear to be much less significant in humans compared with evaporation from the skin.
Conduction
Conduction is heat transfer through contact with a cooler material; the efficiency of conductive heat transfer varies with the properties of the conductive material, the temperature differential between surfaces, and surface area. Conductive heat loss is improved when contact surfaces are of dense composition, contiguous, or wet.
Radiation
Radiation is the loss of heat energy as electromagnetic waves and accounts for up to 65% of total heat loss for temperatures <37°C. When environmental temperatures are higher than body temperatures, the direction of heat exchange is reversed, resulting in a net heat gain.
Convection
Convection is the loss of heat to surrounding air; as with radiation, the direction of heat transfer reverses when the air temperature is higher than the skin temperature.
Heat cramps
Cramping of large muscle groups after exercise; common in unacclimatized individuals and those unaccustomed to physical exercise in hot conditions. The syndrome is attributed to inefficient sodium recovery and hypernatremic sweat; resolves with acclimatization.
Heat tetany
Hyperthermia-associated hyperventilation causes a primary respiratory alkalosis, which in turn can cause perioral paresthesia, carpopedal or laryngeal spasm, and Chvostek’s sign.
Heat exhaustion
Danger: symptoms include nausea, vomiting, fatigue, weakness, and occasionally, diarrhea; clinical findings include orthostatic hypotension, tachycardia, syncope, hyperthermia (core temperature <40°C; 104°F) and minor mental status changes such as poor attention span. Caution: Heat exhaustion and heat stroke have overlapping symptoms; the primary differentiating criterion is that heat stroke is associated with more severe CNS disturbances and core body temperatures above 40°C.
Heat stroke
Life threatening: heat stroke is a medical emergency characterized by core temperature >40°C (105°F) and CNS disturbances in patients with a history of heat exposure. Anhidrosis (absence of sweating) is often present but is no longer a criteria for diagnosis. Age, chronic disease, and medications increase probability of heat stroke, which if untreated, leads to organ dysfunction and death. Caution: Heat stroke is often missed in patients who may not have been physically active.
Adapted from Bouchama, A, Knochel, JP. Heat stroke. N Engl J Med 2002;346:1978 and Tek D, Olshaker JS. Heat illness. Emerg Med Clin of North Amer 1992;10;299.
volume.9 Under extreme physiologic conditions and high heat stress, vasodilation can be significant, leading to peripheral venous pooling, extravasation of fluids, and reduced cardiac output. At temperatures above 42°C (≈108°F), mitochondrial enzymes are inhibited, oxidative phosphorylation becomes uncoupled, and ischemia of hepatocytes and renal parenchymal cells occurs. Heat damage to hepatorenal vascular beds results in microthrombi formation and prolonged prothrombin time (PT) and partial thromboplastin time (PTT); if cooling is not instituted, disseminated intravascular coagulation (DIC) can occur, leading to multi-organ system failure and death.12
ASSESSMENT AND INVESTIGATIONS The first priority in patient assessment is to confirm airway, breathing, and circulation. Attempts should be made to remove or protect the patient from continued heat exposure. While assessment is underway, equipment and personnel should be recruited to assist with cooling. If multiple cases are involved, a referral center should be notified
to increase capability for multiple casualty cooling. Initial treatment includes removal of clothing and preparation of cold water baths, water mist-convection systems, and focal cooling of superficial venous vessels such as the antecubital fossa, axilla, popliteal fossa, and inguinal region. Critically overheated patients require more aggressive interventions such a cool water immersion, cold intravenous fluids, and if expertise permits, peritoneal lavage. If initial assessment suggests severe heat injury, peripheral intravenous access should be established and normal saline or lactated Ringer’s solution should be initiated at 200 mL/hr. If available, unhumidified oxygen should be delivered by nasal cannula. Initial workup starts with a detailed history and thorough physical examination. The history should prioritize past medical conditions, careful documentation of therapeutic and recreational medication, and diet and hydration history. Hyperthermic patients should have baseline vital signs assessed every 15 minutes, and sphygmomanometer sites should be marked with indelible ink to ensure accurate measurements are obtained between serial readings and among different care providers. Baseline body temperature needs to be established using a quality non-glass medical thermometer. Rectal temperatures are preferred, as oral, axillary, and inguinal thermometry is unreliable in patients with perfusion shunt abnormalities; however, these locations can be used to monitor trends in body temperature if rectal measurements are unsafe. If prolonged resuscitation is anticipated, a thermometry probe should be placed in the rectum or esophagus. If none is available and the situation is dire, an invasive monitor can be improvised using an outdoor thermometer, where the probe is covered with a prophylactic condom or rubber glove and inserted into the rectum immediately past the anal verge. Modern low-cost wireless thermometers have been adapted for rectal patient monitoring by mountain rescue teams with even more success. Trends in body temperature monitoring during transport are helpful in triage and the selection of hospital-based cooling therapies (e.g., cutaneous, intravenous, peritoneal, extracorporeal). Mental status and the presence of focal neurologic problems should be assessed during transport and the early phases of cooling therapy. Within the central nervous system (CNS), the cerebellum is particularly sensitive to heat stroke, and therefore cerebellar examination such as finger–nose–finger, heel-to-shin rub, and dysdiadochokinesia studies should be performed. The oral cavity should be examined
CHAPTER 24 Heat-Associated Illness
for evidence of gingival bleeding or evidence of chronic methamphetamine use, and the rectal examination performed to assess for tone, and stool in the vault tested for hemoglobin, which each may warn of cryptic coagulopathy. Pulmonary examination should assess for rales. Skin examination will help determine the patient’s hydration status, and the presence of miliaria and the presence of needle tracks or skin-popping sites should be assessed. Muscle examinations should include active and passive flexion of shoulders, thighs, and calves; the presence of localized pain may indicate muscle breakdown. Urine should be collected by a Foley if necessary and inspected for evidence of myoglobin, hemoglobin, and sediment. Disposable urine analysis “dipsticks” are useful in guiding initial therapy and need to protect the kidneys from hemoglobinuria or myoglobinuria. In recent years, the proliferation of point-of-care handheld blood chemistry units in field clinics increases the probability that basic blood chemistry may be obtained. The current-generation cartridges for these handheld units require refrigeration; if test results are inconsistent with the clinical picture, the provider should suspect that the cartridges were unrefrigerated or are outdated. If quantitative coagulation studies are not available, a whole-blood clotting assay can be used to assess for coagulopathy, and a Weintraub sedimentation tube can be used to assess for hemoconcentration. The improvised coagulopathy and hemoconcentration tests discussed are most accurate when conducted with “controls” provided by a healthy bystander. Table 24.3 summarizes laboratory tests that are helpful in assessing heat illness casualties.
DIAGNOSIS The differential diagnosis of heat illness requires a history of heat exposure, a careful medical history and list of medications, a detailed physical examination, serum chemistries, and urine analysis. Infectious etiologies and rare causes of hyperthermia need to be ruled out. The differential diagnosis should include environmental heat stroke, exertional heat stroke, drug-induced hyperthermia, malignant hyperthermia, neuroleptic malignant syndrome, endocrine and hypothalamic disorders, and fictitious hyperthermia. The less severe heat illnesses such as heat edema and heat syncope are suggested by advanced age, deconditioning, low cardiac reserve, anti-cholinergic medication, pesticide exposure, and recent arrival to the tropics from cooler regions. Miliaria, a distinct heat dermatosis, is differentiated from other tropical skin maladies by the timing, distribution, and physical appearance of skin vesicles. Miliaria responds promptly to antihistamines or dilute topical chlorhexidine. Heat cramps are the second most common malady among unacclimatized individuals; diagnosis is suggested by resolution of cramps with rest and cool treatment, stretching, hydration, and electrolyte repletion. The two most dangerous heat illnesses— heat exhaustion and heat stroke—have overlapping clinical features and are discussed next.
191
Heat exhaustion is a broadly defined clinical syndrome characterized by history of heat exposure, fatigue, and other protean clinical findings and the absence of an alternative diagnosis. Core body temperature in heat exhaustion is <40°C. The most common symptoms seen among hundreds of over-heated casualties attending outdoor music festivals and the Hajj are nausea and vomiting, headache, and weakness. Respiratory rate may be elevated. The cardiac and pulmonary examination may be normal; however, tachycardia may be present from concomitant dehydration. The presence of sweating in heat exhaustion patients is an important finding, as it is frequently decreased or absent in heat stroke patients. The patient’s mental status may suggest mild confusion, and complaints may include dizziness. Symptoms of heat exhaustion tend to resolve within several hours after oral hydrations, rest, and basic interventions that lower skin temperature. Several cases of rebound hyperthermia observed at the Hajj suggest that elderly patients and the very young (age <4 years) should be more closely monitored until euthermia is stable for over 3 hours. Heat stroke is a life-threatening condition defined by a core body temperature >40°C and mental status or neurologic symptoms that do not respond to initial cooling therapy (rest, cold treatment, and hydration).12 Patients may be combative, with delirium, seizure, obtundation, or coma. Clues to differentiate heat stroke from heat exhaustion include significant mental status changes, diarrhea, and dry skin in heat stroke. A minority of heat stroke casualties may present with sweating; however, this usually stops as thermoregulation continues to fail. Complications of heat stroke include acute renal failure from rhabdomyolysis, liver failure, DIC, acute respiratory distress syndrome, seizure, coma, and death.1 Select diagnostic features for differentiating heat stroke and heat exhaustion are listed in Table 24.4. The differential diagnosis of hyperthermia is listed in Table 24.5.
MANAGEMENT AND OUTCOMES Treatment of heat illness is provided in Table 24.6. Management strategies exploit all four principal mechanisms of heat loss and cold therapy targeted to specific body locations (Fig. 24.1). Minor heat illnesses are self-limiting if the patient is provided with fluids, rest, and access to a cool environment. The majority of cases require only fluids and electrolytes for resolution of symptoms. Heat edema is prevented by exercise at high temperatures before travel to the tropics, optimization of diuretics and beta-blockers, and use of supportive compressive stockings. Heat exhaustion is a more serious form of hyperthermia that requires close evaluation to ensure further deterioration is inhibited. TABLE 24.4 Differential Diagnosis of Heat Exhaustion and Heat Stroke Factor
Heat Exhaustion
Heat Stroke
Patient age
All ages
Often young/healthy
Symptoms
Nausea ± vomiting
Nausea ± diarrhea
TABLE 24.3 Laboratory Assessment of Heat Illness
Body temperature
<40°C
>40°C
MILD CASES: Obtain urine analysis; test for pH, specific gravity, urine sediment, and hemoglobinuria and myoglobinuria.
CNS status
Normal: mild confusion
Delirium, ataxia, dysarthria, seizures, coma
MODERATE CASES: Add basic blood chemistries; test for sodium, potassium, chloride, bicarbonate, blood urea nitrogen, and creatinine.
Vital signs
± Tachypneic
Tachypneic, tachycardia, hypotensive
SEVERE CASES (E.G., CNS DISTURBANCES): Add aspartate transaminase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), uric acid, calcium, phosphate, coagulation studies (PT and PTT, fibrinogen); consider arterial blood gas for accurate determination of physiologic pH.
Dermatologic findings
Sweating; ± miliaria
Little or no sweat
Laboratory results
Normal
Elevated transaminases (AST > ALT); DIC, urine: muddy brown casts; Cr elevated; CBC: WBC elevated
Note: In ongoing clinical trials assessing performance of endurance athletes, point-of-care assessment of elevated creatine kinase, MM form (CPK MM) has been highly predictive of heat stroke.
Cr, Creatinine; CBC, complete blood count; WBC, white blood count.
24
192
PART 1 Clinical Practice in the Tropics
TABLE 24.5 Differential Diagnosis of Hyperthermia Environmental exposure Sepsis Encephalitis Brain abscess Meningitis Tetanus Typhoid fever Thyroid storm Pheochromocytoma Catatonia Malignant hyperthermia
Hypothalamic stroke Status epilepticus Cerebral hemorrhage Neuroleptic malignant syndrome Alcohol, sedative-hypnotic withdrawal Salicylate, lithium toxicity Sympathomimetic toxicity Anticholinergic toxicity Dystonic reactions Serotonin syndrome
Radiation
Evaporation
External core cooling sites: large surface veins
TABLE 24.6 Treatment of Heat Illness Heat Illness
Treatment Strategies
All
Rest, hydration, electrolytes, access to cool haven: initiate rapid cooling for temperatures >40°C and any patient with mental status changes.
Heat edema
Elevation of legs, cold compresses on arms and legs or cold baths.
Heat syncope
Move to cool location, rest, fluids.
Heat syncope and dehydration
Electrolyte replacement, consider discontinuing anti-hypertensive and anti-cholinergic medications.
Heat cramps
Rest, hydration, electrolytes.
Heat tetany with hyperventilation
Move to cool environment, restore normal respiration rates; in severe cases, rebreathing carbon monoxide or use of benzodiazepines.
Heat exhaustion
As above. Provide oral or intravenous hydration, mist water convective cooling, and focal use of ice packs on large superficial veins, axilla, and inguinal regions (see Fig. 24.1).
Heat stroke
Rapid cooling is the priority; use cold water immersion with rectal temperature monitoring; patient should be removed when rectal temperature reaches 39°C. Patients with coronary artery disease may develop coronary spasm with ice water immersion; patients with coronary risk factors should be treated less aggressively with mist water and convective cooling.
Initial treatment includes accurate determination of core temperature; blood chemistry monitoring; and initial treatment using radiant, evaporative, and convective cooling of exposed skin and oral electrolyte solutions. In recent years, treatment-resistant heat exhaustion has been associated with use of methamphetamines, emphasizing the need for a thorough history and use of urine and serum toxicology testing. If symptoms progress, or mental status changes fail to improve, the patient should be treated with intravenous normal saline. Both normal and abnormal serum chemistries should be rechecked after hydration and urine output are restored. Patients should be monitored until core body temperature has normalized. Heat exhaustion patients who have deteriorating mental status should have core temperature rechecked to confirm the diagnosis and should resume more aggressive cold therapy. Heat stroke is a medical emergency that is associated with high mortality. Treatment for heat stroke requires prompt, aggressive physical cooling. All measures for dissipating heat should be maximized: evaporation, radiation, convection, and conductive cooling. Treatment of heat stroke in the tropics may be limited by inadequate water for cooling baths, unavailability of air conditioning, and unreliable electricity to power fans. Patient
Convection
Conduction Fig. 24.1 Thermoregulation and therapeutic cooling.
monitoring during treatment may be complicated by lack of quality thermometers or supportive laboratory tests. Initial presenting heat stroke casualties may warn of a surge of patients requiring cooling therapy. A solitary heat illness casualty referred from a mass gathering such as a soccer match, outdoor music festival, or refugee camp should prompt medical control to evaluate the possibility of large numbers of heat casualties and the resource list to effectively care for them. For mass casualty heat illness, evaporative and convective cooling are the most field-viable and scalable treatment options. Unlike water immersion and invasive techniques such as peritoneal lavage, evaporative cooling allows for constant patient monitoring, the use of additional “layered” cooling strategies, and the ability to treat multiple patients at one station. Evaporative cooling requires water to apply to the skin and an air movement source, such as an electric fan. The patient is undressed and placed supine close to the fan. The skin is moistened with water using a sponge or mist bottle. If patient preference, local cultures, or religious beliefs prevent disrobing, the patient may be covered with a thin sheet that is kept wet; however, this dramatically reduces evaporative heat loss. Effective treatment of heat patients with devout religious beliefs, such as female pilgrims to the Hajj, is more effective when performed by female health care workers of the same religious and cultural background. Patients cooled with convective mist water systems need to be re-assessed regularly to ensure stable correction of body temperatures. Alcohol and other low-vaporpressure fluids should not be applied to the skin, as dilated cutaneous blood vessels may increase absorption, leading to intoxication. In many tropical clinics the only resources available for cooling the patient are ice packs: if supplies are limited, cold packs should be applied directly to large superficial veins on flexor surfaces such as the antecubital and popliteal fossa, axilla, and inguinal region.
CHAPTER 24 Heat-Associated Illness
If ice is used, it should be wrapped in a damp cloth and applied to superficial veins using non-compressive pressure (see Fig. 24.1). Chemical cold packs, such as those found in modern first aid kits, lack sufficient cold capacity to treat heat casualties; however, they should be used if nothing else is available. Cold (ice) water immersion is the most effective method for rapid cooling. Clinical experience indicates ice water immersion lowers body core temperature at twice the rate of convective mist-water cooling (mist water and electric fan). The advantage of cold water baths is that the rate of cooling can be controlled by either changing the water temperature or adjusting the depth of immersion. In immersion cooling, the patient is undressed and placed in a tub of suitable depth to allow water to cover the extremities; cold immersion should only be used on alert patients. Heat stroke patients with co-morbidities, such as underlying cardiac disease, should be monitored for arrhythmias or syncope and, if the situation is not critical, cooled using less aggressive methods. In developed regions, immersion cooling has fallen out of favor because of difficulties with patient telemetry. In refugee camps and mass gatherings, however, a water bath is often in constant use to treat heat illnesses. Invasive cooling techniques are only to be used when cold water misting, evaporative cooling, and cool water immersion are ineffective and the patient is critically overheated. Invasive cooling may correct temperature unevenly and result in unpredictable cooling rates, over-cooling, and possibly death. Current invasive cooling methods include gastric and peritoneal lavage with cold fluids, cooled intravenous fluids, and cooled inhalational gas. The use of ice water gastric lavage is contraindicated in patients who have altered mental status or who are unable to protect their airway. Severe heat illness casualties treated with gastric lavage should be intubated to protect the airway. Cold intravenous fluids require careful control, as proximal access and rapid infusion rates can induce cardiac arrhythmias. Cold peritoneal lavage is an invasive technique that requires sterile access and should not be used in patients suspected of having abdominal adhesions or who are pregnant. Cooled oxygen and oral hydration fluids lack sufficient cold capacity to treat all but the most trivial of heat illnesses, but are low-risk adjunct treatments when combined with other approaches. New technologies designed to cool soldiers and athletes in hot climates include small circulating water baths that encircle a single foot or hand. A commercial vacuum cooling glove that
Fig. 24.2 Commercial vacuum cooling glove.
193
makes use of recirculating water is illustrated in Fig. 24.2. Each of these technologies requires a power source or re-charge of a cold source such as ice. Real-world studies of all current-generation “wearable” cooling technologies have been mixed; the clinician is encouraged to not substitute a complex, costly, and unproven technology for the clinically proven technologies described earlier. Regardless of the cooling method used, care providers should continuously monitor core temperature to ensure cooling does not overshoot the desired temperature.13 In cases involving rapid cooling of the core, treatment should be interrupted when core temperature drops below 40°C. The objective is to drop core temperature into a range where normal thermoregulation can again take control. Under field conditions such as the Hajj or Sudanese refugee camps, oral, rectal, and axillary temperature monitoring has under-estimated elevated core temperature and over-estimated the effectiveness of non-invasive cooling. Scanning thermometry devices are quick, require little training, and are non-invasive but rely on powered devices that require recalibration and careful maintenance. Adjunct treatments that complement therapeutic cooling are limited. Dehydration is treated quickly with intravenous fluids or, in conscious patients, with water or sports drinks. Sports drinks should be diluted before use to prevent osmotic loading of the gastrointestinal (GI) tract, which, in turn, can cause GI distress. Antipyretic medications and drugs used to treat malignant hyperthermia have no value in the treatment of heat illnesses and should not be used.13 One common complication of effective cooling with ice packs or immersion is shivering, which generates more body heat. In these situations, the careful use of short-acting benzodiazepines is reasonable. Although chlorpromazine is also used to treat shivering, the secondary alpha-1 blocking activity may make hypotension worse and therefore should not be used. Successful management of heat illness requires prompt recognition, triage, identification of exacerbating factors such as drug or alcohol ingestion, and efficient use of limited therapeutic cooling resources. Heat illness casualties require repeat assessment to ensure the orderly return to normothermia and to ensure overheating and under-cooling are avoided. REFERENCES
1. Tek D, Olshaker JS. Heat illness. Emerg Med Clin North Am 1992;10:299–310. 2. Centers for Disease Control and Prevention (CDC). Heat-related deaths – four states, July–August 2001, and United States, 1979–1999. MMWR Morb Mortal Wkly Rep 2002;51:567–70. 3. Al-Harthi SS, Nouh MS, Al-Arfaj H, et al. Non-invasive evaluation of cardiac abnormalities in heat stroke pilgrims. Int J Cardiol 1992;37:151–4. 4. Rav-Acha M, Hadad E, Epstein Y, et al. Fatal exertional heat stroke: a case series. Am J Med Sci 2004;328:84–7. 5. Centers for Disease Control and Prevention (CDC). Heat-related deaths – Chicago, Illinois, 1996–2001, and United States, 1979–1999. MMWR Morb Mortal Wkly Rep 2003;52:610–13. 6. Misset B, De Jonghe B, Bastuji-Garin S, et al. Mortality of patients with heatstroke admitted to intensive care units during the 2003 heat wave in France: a national multiple-center risk-factor study. Crit Care Med 2006;34:1087. 7. Centers for Disease Control and Prevention (CDC). Heat-related deaths – four states, July–August 2001, and United States, 1979–1999. MMWR Morb Mortal Wkly Rep 2002;51:567–70. 8. Sierra Pajares Ortiz M, et al. Daily mortality in the Madrid community during 1986–1991 for the group between 45 and 64 years of age: its relationship to air temperature. Rev Esp Salud Publica 1997;71:149–60. 9. Simon HB. Hyperthermia. N Engl J Med 1993;329:483–7. 10. Dann EJ, Berkman N. Chronic idiopathic anhydrosis – a rare cause of heat stroke. Postgrad Med 1992;68:750–2. 11. Khosla R, Guntapalli KK. Heat-related illness. Crit Care Clin 1999;15:251–63. 12. Bouchama A, Knochel JP. Heat stroke. N Engl J Med 2002;346:1978–88. 13. Bouchama A, Cafege A, Devol EB, et al. Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Crit Care Med 1991;19:176–80.
24