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CHAPTER 210:  Heat Emergencies      1345 of improved outcomes with extracorporeal rewarming and the prolonged patient tolerance for CPR argue for the early identification of stage III and IV patients and priority transfer to an ECLS/ECMO center. Unfor tunately, many physicians are not aware of this benefit, and many healthcare systems are not prepared to transfer patients in cardiac arrest. The creation of critical care pathways that outline triage, initial management, transport destinations, and care goals within a given healthcare system has the potential to improve outcomes, in a similar manner to cardiovascular care pathways. 43 A New England Journal of Medicine current concepts article7 provides a preliminary framework, but considerable local and regional work is still required to create a functional system. The provincial health authority in British Columbia, Canada, has implemented a regional clinical practice guideline and care pathway, 44 and Poland has improved patient outcomes by creating the world’s first dedicated centralized severe hypothermia treatment center.45  DROWNING, AVALANCHE, AND TRAUMA Drowning, avalanche burial, and trauma are three situations that war rant special consideration in the context of hypothermia. Patients removed from cold water should be extracted in a horizontal position in an effort to decrease the risk of orthostatic and hydrostatic changes triggering rescue collapse. The majority of drowning is submersion, where the patient immediately goes under the water, suffers a hypoxic cardiac arrest, and then develops hypothermia. With the exception of children, who may undergo simultaneous hypoxic cardiac arrest and rapid cooling, most submersion patients are unlikely to benefit from prolonged resuscitation (normothermic hypoxic cardiac arrest with brain death prior to cooling). The less common immersion patient may benefit from prolonged resuscitation; this patient is initially immersed in cold water but able to breathe air, cooling ensues, and the patient eventually suffers a presumed hypothermic cardiac arrest and may or may not become secondarily submerged. A case series of survival in adolescents with prolonged CPR after cold water immersion has been reported. 40 See Chapter 215, “Drowning, ” for detailed discussion of drowning. With avalanche burial, most episodes of cardiac arrest are caused by asphyxia or trauma. 46 Avalanche burial results in much slower cooling than cold water exposure, and it will take from 35 minutes to several hours for the patient’s core temperature to drop below 32°C (assuming initial normothermia). Therefore, if the patient is recovered in cardiac arrest after less than 35 minutes of burial, hypothermia is not the cause of cardiac arrest. For patients recovered after 35 minutes of burial, in the absence of obvious traumatic death, an airway packed with snow, or an accurate core temperature >32°C, accidental hypothermia may be the cause of cardiac arrest and prolonged resuscitation may be indicated. Cardiac arrest secondary to blunt trauma has a dismal prognosis (<1% survival), 47 and a core temperature <35°C further increases the odds of death by at least 2.4.18 Therefore, it is reasonable to apply normothermic termination of resuscitation guidelines to patients suspected of blunt traumatic arrest, even in the presence of hypothermia.

ry to blunt trauma has a dismal prognosis (<1% survival), 47 and a core temperature <35°C further increases the odds of death by at least 2.4.18 Therefore, it is reasonable to apply normothermic termination of resuscitation guidelines to patients suspected of blunt traumatic arrest, even in the presence of hypothermia.  AUSTERE ENVIRONMENTS In the rare circumstances of stage IV hypothermia in an austere environment, when ongoing CPR during transport is not possible, it may be reasonable to transport without CPR (particularly if the patient has pulseless electrical activity) until such a time as CPR can be maintained or a definitive care center is reached. The decision to not perform CPR in an austere environment may be risky given that prehospital CPR is performed in the vast majority of stage IV hypothermia literature; however, there are two published cases that have shown good outcomes despite CPR interruptions 41,48 and one case where CPR was not performed at all during transport.49 There is considerable controversy about whether or not to perform CPR for stage IV patients with pulseless electrical activity.50,51 It is this author’s opinion that the benefits of CPR far outweigh the risks for the patient with absent vital signs, regardless of the ECG findings. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Heat Emergencies Frank LoVecchio INTRODUCTION AND EPIDEMIOLOGY Heat emergencies represent a continuum of disorders from heat cramps to heat stress that, when severe, culminate in heat stroke. The incidence of heat-related emergencies varies with the weather, although other factors may have a greater impact. 1 During heat waves and severe droughts, fatality rates spike.1 Physiologic acclimatization and cultural adaptation provide protection from heat stroke for people who live in warmer cli mates. From 1999 to 2010, there were 8081 heat-related deaths in the United States. 1 The heat wave during the summer of 2003 is estimated to have caused 14,800 deaths in France. 2 In the Russian heat wave in July/ August 2010, there were an estimated 15,000 deaths, with additional morbidity from associated forest fires and smoke injury. PATHOPHYSIOLOGY  MECHANISMS OF HEAT TRANSFER Controlled by the hypothalamus, body temperature is regulated through the delicate balance of heat production, accumulation, and dissipation. Heat is generated by cellular metabolism and the mechanical work of skeletal muscle. Heat accumulates from radiation from the sun and contact with hot objects. Heat is absorbed when the ambient tempera ture rises above body temperature. As core temperature rises, the auto nomic nervous system is stimulated to promote sweating and cutaneous vasodilatation. The body has several mechanisms for dissipating heat to the environment, including radiation (the transfer of heat by electromagnetic waves from a warmer object to a colder object), conduction (heat exchange between two surfaces in direct contact), convection (heat transfer by air or liquid moving across the surface of an object), and evaporation (heat loss by vaporization of water, or sweat). Evaporation is the principal mechanism of heat loss in a hot environment, but this becomes ineffec tive above a relative humidity of 75%. Radiation and evaporation dis sipate most body heat at lower ambient temperatures (<35°C [<95°F]). The effect of wind on heat loss depends on wind velocity. Wind moves heat away from the skin by convection, but above 32.2°C (90°F) and 35% humidity, convection does not remove heat well. 4 This is why the use of fans alone is not effective in preventing heat stroke during periods of high environmental temperature and humidity.

t of wind on heat loss depends on wind velocity. Wind moves heat away from the skin by convection, but above 32.2°C (90°F) and 35% humidity, convection does not remove heat well. 4 This is why the use of fans alone is not effective in preventing heat stroke during periods of high environmental temperature and humidity. When the ambient temperature rises to >35°C (>95°F), the body can no longer radiate heat to the environment and becomes dependent on evaporation for heat transfer. As humidity increases, the potential for evaporative heat loss decreases. The combination of high temperature and high humidity essentially blocks the two main physiologic mecha nisms that the body uses to dissipate heat. Elevations of temperature are accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia.  RESPONSE TO HEAT STRESS Controlled by the hypothalamus, the body maintains a core temperature between 36°C and 38°C (96.8°F and 100.4°F). Native thermal regulation mechanisms begin to fail at core temperatures of <35°C (<95°F) and >40°C (>104°F). 5 It is possible to maintain core temperatures of 40°C to 42°C (104.0°F to 107.6°F) for short periods without adverse effect. 5 The physiologic response to heat stress consists of four primary mechanisms: dilatation of blood vessels, particularly in the skin; increased sweat production; decreased heat production; and behavioral heat control. During exercise in hot environments, the heart rate increases to compensate for the decrease in stroke volume from the cutaneous vas cular dilation and to maintain cardiac output. 6 Patients with underlying cardiovascular disease or pharmacologic or physiologic impairment of CHAPTER Tintinalli_Sec16_p1333-1418.indd 1345 8/2/19 8:22 PM

in hot environments, the heart rate increases to compensate for the decrease in stroke volume from the cutaneous vas cular dilation and to maintain cardiac output. 6 Patients with underlying cardiovascular disease or pharmacologic or physiologic impairment of CHAPTER Tintinalli_Sec16_p1333-1418.indd 1345 8/2/19 8:22 PM 1346 SECTION 16: Environmental Injuries these mechanisms may not be able to elevate cardiac output. Heat stress may also result in arrhythmias, myocardial ischemia, and exacerbation of congestive heart failure. Elevated cholinergic stimulation to the skin results in increased sweat production. Sharp increases in the rate of sweat production normally occur with core temperature elevations above 37°C (98.6°F). 7 Cutaneous vascular dilation and sweating increase as the body temperature rises until a homeostatic stall of heat production is reached when the rate of heat production in response to exercise equals heat loss. 8 Interestingly, sweating activation in older adults requires a greater rise in skin tem perature (1.5°C, or 2.7°F) compared to younger adults.9  EFFECT OF MEDICATIONS Medications often interfere with heat-removal mechanisms. Notable drugs are anticholinergic agents, diuretics, phenothiazine, β-blockers, calcium channel blockers, and sympathomimetic agents. 10 Anticholinergic agents impair sweating and the cardiovascular response to heat. Diuretics lead to volume depletion and decreased cardiac output. Phenothiazines have anticholinergic properties and deplete central stores of dopamine, which interfere with the hypothalamic thermoregulatory center. Medications such as β-blockers and calcium channel blockers decrease the cardiovascular response to heat and reduce peripheral blood flow and the ability to sweat. Sympathomimetics cause cutaneous vasoconstriction and inhibit sweating. Alcohol inhibits secretion of antidiuretic hormone, which leads to dehydration, and blunts the psychological heat-avoidance response. Heroin, cocaine, and amphetamines disrupt the function of endogenous endorphins and adrenocorticotropic hormones that are involved in heat adaptation mechanisms. Amphetamines and cocaine increase muscle activity and lead to heat production. Lysergic acid diethylamide and phencyclidine act on the CNS to induce a hypermetabolic state.  RISK FACTORS In addition to patients on the medications discussed in the previous section, populations at higher risk of developing heat emergencies include the elderly, young children, athletes, persons with limited mobility, and alcoholics. 7,8 Other risk factors for exertional heat emergencies include obesity, dehydration, and vigorous exertion in the heat without proper training and acclimatization. Lack of air-conditioning and social isola tion are also risk factors for nonexertional heat emergencies. 7,8 Individuals with a history of heat stroke are at greater risk for another episode. Patients with congenital absence of sweat glands, progressive systemic scleroderma, hyperthyroidism, and pheochromocytoma are also at increased risk for heat stroke.  ACCLIMATION Acclimation is the adaptation of the body to environmental changes. It involves a number of physiologic and biochemical adjustments that allow an individual to withstand heat stresses that would otherwise result in substantial morbidity and mortality. Acclimation lowers the thermal set point in the hypothalamus, which triggers the onset of sweating at lower core temperatures, and the rate of sweating may double in the acclimated human. Aldosterone secretion is boosted, and sodium conservation results from more efficient reabsorption from the sweat. Plasma volume expands, heart rate decreases for any given heat load, and exercise tolerance improves.

et of sweating at lower core temperatures, and the rate of sweating may double in the acclimated human. Aldosterone secretion is boosted, and sodium conservation results from more efficient reabsorption from the sweat. Plasma volume expands, heart rate decreases for any given heat load, and exercise tolerance improves. Dilation of cutaneous blood vessels occurs at a lower core temperature to promote earlier cooling. In most individuals, acclimation can be achieved over 7 days to several weeks. 11 Once removed from the hot environment, the body will de-acclimate to the original physiologic parameters within 1 to 2 weeks.12,13  MODELS OF HEAT INJURY The pathology of heat stroke is not completely understood, and although heat stroke is triggered by hyperthermia, there is evidence that second ary endotoxemia triggers a systemic inflammatory response, coagulopathy, and multiorgan failure. 14,15 Heat exhaustion and heat stroke occur when the body’s thermoregulatory responses are impaired or overwhelmed and are no longer capable of maintaining homeostasis. Excessive heat is directly toxic to cells, causes an acute-phase reaction with release of inflammatory cytokines, and damages vascular endothelium. Nearly all cells respond to sudden heating by producing heat stress proteins, whose mechanism of action is still not completely understood. 14,15 Escalating cellular temperature results in denaturation of proteins, interruption of cellular processes, and cell death. Temperatures of >41.6°C (>106.9°F) can produce cellular injury in hours. As tempera ture rises, cellular damage occurs more quickly and extensively. Tem peratures >49°C (>120.2°F) typically result in immediate cell death and tissue necrosis. 15 The enhanced vascular permeability due to damaged vascular endothelium results in activation of the coagulation cascade and disseminated intravascular coagulation. Classic Classic heat injury occurs during periods of high environmen tal heat stress. Physical exertion is not required if the heat gain occurs at environmental temperatures and humidity levels that overwhelm the native heat loss mechanisms. The increase in core temperature seen in this setting is often slow, occurring over a period of hours to days. Because of this slow rise in heat burden, volume and electrolyte abnor malities are common. High-risk populations include the elderly, the young, and those with psychological, physiologic, and pharmacologic impairments of heat loss mechanisms (e.g., diabetes; Raynaud’s disease; drugs such as anticholinergics, diuretics, antipsychotics, cocaine). Epi demiologic studies of classic heat injury typically identify the elderly, living alone or without social support and without air-conditioning. Exertional Exertional heat injury usually affects individuals who are participating in athletic events or performing jobs under conditions of high heat stress. Risk factors include dehydration, concurrent illness, obesity, wearing too much clothing, and poor cardiovascular fitness. In this setting, heat production and heat gain from the environment exceed the capacity of heat removal processes. Physical exercise is the most common single source of internal heat production. Without an efficient cooling mechanism, progressive dehydration and hyperpyrexia continue to the level of cardiovascular and metabolic failure. Confinement Hyperpyrexia Confinement hyperpyrexia is a special category of nonexertional hyperpyrexia and can occur in several cir cumstances, such as when children are left inside cars, when stowaways are abandoned inside closed vehicles or railroad cars, and when work ers are occupationally exposed to heat inside enclosed spaces.

yperpyrexia Confinement hyperpyrexia is a special category of nonexertional hyperpyrexia and can occur in several cir cumstances, such as when children are left inside cars, when stowaways are abandoned inside closed vehicles or railroad cars, and when work ers are occupationally exposed to heat inside enclosed spaces. Between January 1990 and December 2014 in the United States, 3115 nonfatal heat injuries and 729 fatalities were reported in children who were left intentionally in motor vehicles during hot days. 17 Nonventilated vehicle compartments in a hot environment may reach temperatures of 54°C to 60°C (129.2°F to 140.0°F) in <10 minutes. 17 In the August 2003 heat wave in France, a risk factor for heat stroke mortality was heat exposure at home or in a non–air-conditioned healthcare facility.  SPECIFIC TYPES OF HEAT ILLNESS Heat emergencies comprise a range of disorders from minor (heat edema, prickly heat, heat cramps, and heat exhaustion) to major (heat stroke). Minor heat emergencies are primarily diagnosed and differentiated from heat stroke on clinical grounds. HEAT EDEMA Heat edema is a self-limited process manifested by mild swelling of the feet, ankles, and hands that appears within the first few days of exposure to a hot environment. Heat edema is due to the cutaneous vasodilata tion and orthostatic pooling of interstitial fluid in gravity-dependent extremities. An increase in the secretion of aldosterone and antidiuretic hormone in response to the heat stress contributes to the mild edema. In general, heat edema is found in elderly nonacclimatized individuals who are physically active after a period of sitting while traveling in a vehicle or airplane. Occasionally, heat edema occurs after prolonged standing. The edema is mild and does not impair or interfere with normal activi ties. Very rarely, pitting edema of the ankles may develop but does not progress to the pretibial region. Tintinalli_Sec16_p1333-1418.indd 1346 8/2/19 8:22 PM

aveling in a vehicle or airplane. Occasionally, heat edema occurs after prolonged standing. The edema is mild and does not impair or interfere with normal activi ties. Very rarely, pitting edema of the ankles may develop but does not progress to the pretibial region. Tintinalli_Sec16_p1333-1418.indd 1346 8/2/19 8:22 PM CHAPTER 210:  Heat Emergencies      1347 History and physical examination are usually sufficient to exclude systemic causes of edema in healthy patients. In the elderly, new pedal edema from heat should be differentiated from early congestive heart failure or deep venous thrombosis. Heat edema usually resolves spontaneously in a few days. Elevation of the legs and the use of support hose facilitate removal of the interstitial fluid; diuretics have no role. PRICKLY HEAT Prickly heat is a pruritic, maculopapular, and erythematous rash over normally clothed areas of the body. Also known as lichen tropicus , miliaria rubra , or heat rash , it is an acute inflammation of the sweat ducts caused by blockage of the sweat pores by macerated stratum corneum (Figure 210-1). The sweat ducts become dilated under pressure and ultimately rupture, producing superficial vesicles in the malpighian layer of the skin on a red base. Itching is the predominant clinical feature during this phase and can be treated successfully with antihistamines. Wearing clean, light, and loose-fitting clothing and avoiding sweat-generating situations can prevent prickly heat. Cala mine lotion, topical steroids, and oral vitamin C can be of benefit. Chlorhexidine in a light cream or salicylic acid cleaning solution may provide some relief. With prolonged or repeated heat exposure, a keratin plug fills the sweat duct, causing obstruction in the stratum malpighian layer. When the duct ruptures a second time, the resultant vesicle will be driven deeper into the dermis. This vesicle simulates the white papules of piloerection and is not pruritic. This is known as the profunda stage of prickly heat (miliaria profunda) and can readily advance into a chronic dermatitis. Infection with Staphylococcus aureus or methicillin-resistant S. aureus is a common complication. The skin can be desquamated by applying 1% salicylic acid to the affected area three times a day. HEAT CRAMPS Heat cramps are painful, involuntary, spasmodic contractions of skeletal muscles, usually those of the calves, although they may involve the thighs and shoulders. These cramps usually occur in individuals who are sweating profusely and replace fluid losses with water or other hypotonic solutions. Heat cramps may occasionally occur during exer cise or, more commonly, during a rest period following several hours of vigorous physical activity. Nonacclimated or unconditioned individuals who are just starting manual labor in a hot environment are at risk for heat cramps. Although heat cramps are self-limited and do not cause significant morbidity, the pain associated with them can precipitate an ED visit. In general, heat cramps are short in duration, are limited to a definitive group of muscles, and almost never involve enough muscle mass to cause rhabdomyolysis. The pathogenesis of heat cramps is believed to involve a relative deficiency of sodium, potassium, or magnesium and fluid at muscle level. Patients with severe heat cramps may have hyponatremia and hypochloremia. 20 Rhabdomyolysis is rare and occurs secondary to diffuse and protracted muscle spasm. 15 Treatment consists of fluid and salt replacement (PO or IV) and rest in a cool environment. For mild cases, or if an overwhelming number of patients require treatment, a 0.1% to 0.2% saline solution can be given PO. Two 650-milligram salt tablets dissolved in a quart of water provide a 0.1% saline solution.

e spasm. 15 Treatment consists of fluid and salt replacement (PO or IV) and rest in a cool environment. For mild cases, or if an overwhelming number of patients require treatment, a 0.1% to 0.2% saline solution can be given PO. Two 650-milligram salt tablets dissolved in a quart of water provide a 0.1% saline solution. 13,20 Many electrolyte solution drinks (sports drinks) are commercially available and are much more palat able. Patients with more severe symptoms require IV rehydration with normal saline. Heat cramps can be prevented by maintaining adequate dietary salt intake or by drinking commercial electrolyte beverages. Salt tablets by themselves should not be used, because the tablets are a gastric irritant and cause nausea and vomiting. HEAT STRESS  CLINICAL FEATURES AND DIAGNOSIS Heat stress is part of the continuum of heat illness but does not meet criteria for heat stroke. Heat stress can result from either water or sodium depletion, but is typically a combination of both. Water depletion tends to occur in the elderly and in persons working in hot environments with inadequate water replacement. Salt depletion tends to occur in nonac climatized individuals who replace fluid losses with large amounts of hypotonic solutions. Heat stress presents with symptoms that include headache, nausea, vomiting, malaise, dizziness, and muscle cramps as well as signs of dehydration, such as tachycardia and orthostatic hypotension or near-syncope. Rhabdomyolysis may be present on rare occasions (see Chapter 89, “Rhabdomyolysis”). Because of the ill-defined and non specific symptoms, heat exhaustion is often a diagnosis of exclusion. On physical examination, the temperature may be normal or elevated, usually not above 40°C (104°F). Patients with heat exhaustion (stress) do not manifest signs of CNS impairment (Table 210-1). Laboratory studies almost universally demonstrate hemoconcentration, although the specific electrolyte abnormalities seen depend on the ratio of fluid and electrolyte losses to intake. Patients who have had no fluid intake of any kind exhibit hypernatremia, whereas those who partly rehydrate with salt-containing fluids develop isotonic hypovo lemia with normal sodium and chloride levels. Serum potassium and magnesium levels are variable.  TREATMENT Heat stress is treated with volume and electrolyte replacement and rest. Removal from the heat-stressed environment is essential. Patients with mild heat stress may be treated with oral electrolyte solutions. Rapid infusion of moderate amounts of IV fluids (1 to 2 L of normal saline) may be necessary in patients who demonstrate significant tissue hypoperfusion. Ideally, the choice of IV solution should be guided by FIGURE 210-1. Miliaria   rubra   (prickly   heat). [Image   used  with  permission   of Peter  Lio, MD.] TABLE 210-1 Signs and Symptoms of Heat Emergencies Heat Cramps Heat Stress (Exhaustion) Heat Stroke Muscle cramps Symptoms seen in heat cramps plus: Symptoms seen in heat stress (exhaustion) plus: Normal to mildly elevated temperature Normal to elevated temperature (<40°C [<104°F]) Elevated temperature (>40°C [>104°F]) Sweating Nausea, vomiting, headache, malaise, dizziness Neurologic abnormalities: inappropriate behavior, confusion, delirium, ataxia, coma, seizures Orthostatic hypotension Anhidrosis or sweating Tintinalli_Sec16_p1333-1418.indd 1347 8/2/19 8:23 PM

ted temperature (<40°C [<104°F]) Elevated temperature (>40°C [>104°F]) Sweating Nausea, vomiting, headache, malaise, dizziness Neurologic abnormalities: inappropriate behavior, confusion, delirium, ataxia, coma, seizures Orthostatic hypotension Anhidrosis or sweating Tintinalli_Sec16_p1333-1418.indd 1347 8/2/19 8:23 PM 1348 SECTION 16: Environmental Injuries laboratory determinations, but isotonic salt solutions may be used until specific electrolyte abnormalities are identified. In general, hospitaliza tion is not required. Patients with congestive heart failure or severe electrolyte disturbances may require admission, because of the time needed to correct fluid and/or electrolyte deficits. Heat stress with an elevated temperature can progress to heat stroke even after the patient is removed from the hot environment. Therefore, patients with heat stress who do not respond to approximately 30 minutes of fluid replacement and removal from the hot environment should be cooled until the core temperature drops to ≤39°C (102°F). Patients should not be prematurely labeled as having heat stress without observation and reassessment. HEAT STROKE Heat stroke is an acute life-threatening emergency with high mortality and is fatal if left untreated.  CLINICAL FEATURES The cardinal features of heat stroke are hyperthermia (>40 °C [>104° F]) and altered mental status. See also symptoms listed in Table 210-1. Although patients presenting with classic (nonexer tional) heat stroke may exhibit anhidrosis, the absence of sweat is not considered a diagnostic criterion because sweat is present in over half of patients with heat stroke. The CNS is particularly vulnerable in heat stroke. The cerebellum is highly sensitive to heat, and ataxia can be an early neurologic finding. Virtually any neurologic abnormality may be present in heat stroke, including irritability, confusion, bizarre behavior, combativeness, hal lucinations, plantar responses, decorticate and decerebrate posturing, hemiplegia, status epilepticus, and coma. Seizures are quite common, especially during cooling. Neurologic injury is a function of the maxi mum temperature reached and the duration of exposure. The distinction between exertional and classic (nonexertional) heat stroke is not clinically important, because immediate cooling and sup port of organ system function are the therapeutic goals for both. A delay in cooling increases the mortality rate.  DIAGNOSIS There are no diagnostic tests for heat stroke, and the differential diag nosis is extensive. Therefore, the diagnosis of heat stroke is determined by history and clinical presentation, and exclusion of other processes (Table 210-2). Laboratory Evaluation Diagnostic studies are directed toward detecting end-organ damage and excluding other diseases. Helpful studies include a CBC, comprehensive metabolic panel with arterial blood gas analysis, coagulation profile, creatine phosphokinase level, myoglobin level, urinalysis, ECG, and chest radiograph. CT of the head and lumbar puncture may be indicated to rule out other causes of altered mental status. The partial pressure of arterial carbon dioxide is often <20 mm Hg due to hyperventilation. Patients with exertional heat stroke often have lactic acidosis, and hypoglycemia may occur.  PREHOSPITAL CARE Remove the patient from the hot environment immediately, and per form standard resuscitation measures. Check point-of-care glucose if there is altered mental status. Start cooling by removing clothing and implementing one of the following methods: spray the patient with water and provide airflow over the patient (ideal method but not always practical during transportation); place wet towels or sheets over the patient’s body; or place ice on the patient.

re is altered mental status. Start cooling by removing clothing and implementing one of the following methods: spray the patient with water and provide airflow over the patient (ideal method but not always practical during transportation); place wet towels or sheets over the patient’s body; or place ice on the patient. Administer a bolus of normal saline (1 to 2 L) if hypotension is present. 15 Online medical direction is helpful when transport times are long and when EMS personnel in the given region rarely encounter heat stroke.  ED RESUSCITATION The goals of therapy are immediate cooling and aggressive support of organ system function. Continue standard resuscitation measures. Administer IV fluids at a rate that ensures adequate urine output. In elderly patients or patients with cardiovascular disease, consider invasive monitoring. Check glu cose levels. Monitor core temperature with an electronic rectal ther mometer, temperature probe–equipped urinary drainage catheter, or esophageal thermometer.  COOLING TECHNIQUES Currently, only physical methods of cooling are recommended, and there is no evidence to support one particular approach over another. In clinical practice, the primary physical cooling procedure is one that allows easy patient access, is readily available, is tolerated well by the patient, and is effective ( Table 210-3). With all cooling methods, the goal is to reduce the core temperature to approximately 39°C (102.2°F) and to avoid overshoot hypothermia. 7 No method has been proven superior.7 If the initial cooling method used does not lower temperature quickly, try another method.15,21 Evaporative Cooling Cooling by evaporation is practical and comfortable for the patient compared with other methods. Remove patient clothing and spray cool water ( ∼15°C [59°F]) on most of the patient’s body surface. Directing a fan over the patient facilitates evaporation. If the skin temperature is reduced <30°C (86°F), shivering will result in more heat production, and peripheral vasoconstriction will impair evaporation. To prevent hypothermic overshoot, some recommend using either tepid water warmed to 40°C (104°F) or exposing the patient to hot air (45°C [113°F]) with the fan. 21 This method is the foundation of several cooling units such as the Makkah cooling unit, which is widely used in the Middle East to treat pilgrims traveling to Mecca who succumb to heat stroke. The Makkah cooling unit is composed of a large hammock with built-in sprinklers that spray cool water (15°C [59°F]) over the patient’s body and powerful fans that blow warm air (45°C [113°F]) over the patient. The main problems with the Makkah cooling method are cost, portability, and the fact that evaporation rates are reduced in very humid environments. The two main difficulties associated with evaporative cooling are shivering and the inability of cardiac electrodes to adhere to the skin. Shivering is treated primarily with short-acting benzodiazepines and secondarily with phenothiazines. Phenothiazines may lower the seizure threshold and cause hypotension, and their anticholinergic properties impair sweating. Immersion Cooling Immersion cooling is performed by placing the undressed patient into a tub of ice water deep enough to cover the trunk and extremities, while keeping the patient’s head out of the water. Problems associated with immersion cooling include shivering, dis placement of monitoring leads, and inability to perform defibrillation or resuscitative procedures. Also, a tub or receptacle large enough to accommodate the patient may not be readily available.

mities, while keeping the patient’s head out of the water. Problems associated with immersion cooling include shivering, dis placement of monitoring leads, and inability to perform defibrillation or resuscitative procedures. Also, a tub or receptacle large enough to accommodate the patient may not be readily available. The efficiency of immersion cooling has been documented primarily in young, healthy TABLE 210-2 Differential Diagnosis of Heat Stroke Infection •  Sepsis  syndrome •  Meningitis •  Encephalitis •  Malaria •  Typhoid •  Tetanus Endocrine •  Thyroid  storm •  Pheochromocytoma •  Diabetic  ketoacidosis Neurologic •  Hypothalamic  bleeding or infarct •  Cerebrovascular  accident •  Status  epilepticus Toxicologic •  Anticholinergic  toxidrome •  Sympathomimetic  overdose •  Salicylate  overdose •  Serotonin  syndrome •  Malignant  hyperthermia •  Neuroleptic  malignant syndrome •   Withdrawal syndromes—alcohol and benzodiazepine withdrawal Tintinalli_Sec16_p1333-1418.indd 1348 8/2/19 8:23 PM

t •  Status  epilepticus Toxicologic •  Anticholinergic  toxidrome •  Sympathomimetic  overdose •  Salicylate  overdose •  Serotonin  syndrome •  Malignant  hyperthermia •  Neuroleptic  malignant syndrome •   Withdrawal syndromes—alcohol and benzodiazepine withdrawal Tintinalli_Sec16_p1333-1418.indd 1348 8/2/19 8:23 PM CHAPTER 210:  Heat Emergencies      1349 patients without comorbid diseases. The efficacy and safety of immer sion in patients with classic (nonexertional) heat stroke and patients with significant comorbid diseases (e.g., coronary artery disease) have not been established. Massage with ice water is an alternative for patients who cannot tolerate immersion, although its effectiveness as a single modality for cooling remains unclear. Invasive Cooling Measures When evaporation or immersion meth ods are not sufficient, invasive cooling may be considered. The most rapid method of cooling a heat stroke victim is cardiopulmonary bypass, although lack of availability and logistical problems are major disadvantages. Cold water gastric lavage, cold water urinary bladder lavage, and cold water rectal lavage are other adjunctive measures that can be performed in the ED but require patient cooperation, are labor intensive, have the potential for inducing water intoxication, and are of question able efficacy. Cold water peritoneal lavage is yet another option, but its effectiveness has not been validated. Other Cooling Measures Cooling blankets work slowly and should not be a sole treatment for heat stroke. IV infusion of cold fluids alone is not considered effective treatment. Applying ice packs to the neck, axillae, and groin does not lower temperature quickly enough to be used alone. There are no studies on the effectiveness of antipyretics. Dan trolene is not indicated for treatment of heat stroke.  COMPLICATIONS OF HEAT STROKE Heat stroke causes both early and late complications ( Table 210-4).7,15 Hypotension is a common initial finding. Usually the blood pressure will rise in response to fluid bolus and body cooling. The combination of low cardiac output and elevated central venous pressure warrants the use of vasoactive catecholamines such as dopamine or dobutamine if a 20 mL/kg fluid bolus does not result in improvement. Once the central venous pressure reaches 12 to 14 mm Hg and cooling is initiated, dopamine or dobutamine may be used to maintain a normal blood pressure. Inotropes that cause severe vasoconstriction by α-adrenergic stimulation, such as norepinephrine, may impede cooling by redirecting blood flow away from the skin. Fluid and electrolyte abnormalities vary depending on the type of onset and duration of the disorder, any underlying disease (especially cardiovascular disease), and any prior use of medications, such as diuretics. Hypokalemia due to total-body depletion of potassium may be noted, and hyperkalemia may result from acute renal failure and rhabdomyolysis. Hypernatremia is seen in severely dehydrated patients, whereas hyponatremia occurs in patients who hydrate with oral hypotonic solutions. Hematologic disorders may be apparent clinically and on laboratory evaluation. Findings of abnormal hemostasis include purpura, petechiae, and conjunctival, GI, renal, or pulmonary hemorrhage. Coagulation studies may show thrombocytopenia, hypoprothrombinemia, and hypofibrinogenemia. Thermal injury to the vascular endothelium can cause increased platelet aggregation, changes in capillary permeability, thermal deactivation of plasma proteins resulting in a decreased level of clotting factors, disseminated intravascular coagulation, and fibrinolysis. 15,22 Thermal injury to the liver is a common finding in heat stroke, although jaundice does not always develop.

platelet aggregation, changes in capillary permeability, thermal deactivation of plasma proteins resulting in a decreased level of clotting factors, disseminated intravascular coagulation, and fibrinolysis. 15,22 Thermal injury to the liver is a common finding in heat stroke, although jaundice does not always develop. Delayed elevation of hepatic enzyme levels, peaking 24 to 72 hours after the thermal insult, is attributed to centrilobular necrosis. Glucose homeostasis is affected. Hepatic damage is almost always reversible, with a full recovery. TABLE 210-3 Summary of Cooling Techniques Cooling Method Advantages Disadvantages Recommendations Evaporative cooling Provides effective cooling Readily available Practical Well tolerated Can cause shivering Less effective in humid environments Makes it difficult to maintain electrode positions Strongly recommended Immersion cooling Provides effective cooling Can cause shivering Poorly tolerated Not compatible with resuscitation settings Recommended Ice packs on neck, axillae, and groin Practical Can be added to other cooling methods Cooling times longer than other modalities Poorly tolerated Can be used as adjunct cooling method Cardiopulmonary bypass Provides fast and effective cooling  Invasive Not readily available Setup is labor intensive Recommended in severe or resistant cases when available Cooling blankets  Easy to apply  Have limited cooling efficacy Impede use of other cooling methods Not recommended when other methods available Cold water gastric, urinary bladder, rectal, or peritoneal lavage Advocated to cool the core when cardiopulmonary bypass not desirable or possible, however, efficacy not validated Invasive Labor intensive May lead to water intoxication Human experience is limited Effectiveness and safety not established TABLE 210-4 Complications of Heat Stroke Early Late Vital signs Hypotension Hypothermic overshoot Hyperthermic rebound Muscular Rhabdomyolysis Neurologic Delirium/coma Cerebral edema Seizure Encephalopathy Persistent neurologic deficit Cardiac Heart failure Myocardial injury Pulmonary Pulmonary edema Acute respiratory distress syndrome Renal Oliguria Renal failure, rhabdomyolysis GI Intestinal ischemia or infarction Pancreatic injury Hepatic dysfunction Metabolic

ologic Delirium/coma Cerebral edema Seizure Encephalopathy Persistent neurologic deficit Cardiac Heart failure Myocardial injury Pulmonary Pulmonary edema Acute respiratory distress syndrome Renal Oliguria Renal failure, rhabdomyolysis GI Intestinal ischemia or infarction Pancreatic injury Hepatic dysfunction Metabolic Hypokalemia Hyperkalemia Hypernatremia Hypocalcemia Hyponatremia Hyperuricemia Hematologic Thrombocytopenia Disseminated intravascular coagulation Tintinalli_Sec16_p1333-1418.indd 1349 8/2/19 8:23 PM