AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Heat illness is a major cause of preventable morbidity worldwide, especially in regions characterized by high ambient temperatures. The major heat-related illnesses, heat exhaustion and heatstroke, involve varying degrees of thermoregulatory failure that occur when individuals are exposed to elevated temperatures.

Heat exhaustion, the most common heat-related illness, involves mild-to-moderate dysfunction of temperature control associated with elevated ambient temperatures and/or strenuous exercise resulting in dehydration and salt depletion. It may rapidly progress to heatstroke when the body's thermoregulatory mechanisms become overwhelmed and fail. Heatstroke is extreme hyperthermia, typically above 104ºF (40ºC), associated with a systemic inflammatory response, which leads to end-organ damage with universal involvement of the CNS.

Heatstroke traditionally is divided into exertional and classic varieties, which are defined by the underlying etiology but are clinically indistinguishable. Exertional heatstroke typically occurs over hours in younger athletic patients who exercise at elevated temperatures for a sufficient period of time to cause the rate of heat production to exceed the capacity of the body to dissipate heat. Classic heatstroke more commonly develops during heat waves when air temperatures exceed 102.5ºF (39.2ºC) for 3 or more consecutive days in older or debilitated patients who are unable to avoid extreme environmental conditions. In both cases, thermoregulatory mechanisms fail if the stress becomes too great, which results in accelerated hyperthermia with an increased expression of heat shock proteins, an exaggerated acute-phase response, and end-organ dysfunction.

Pathophysiology

All heat illnesses exist along a continuum and share similar elements. In all cases, the root cause is rate of heat gain exceeding the ability of the body to dissipate the thermal load. If the responsible factors are not corrected, the individual will invariably develop heatstroke. Progression to heatstroke and end-organ dysfunction is related to the physiologic responses to hyperthermia, the direct toxicity of the heat, and subsequent inflammatory response.

Thermoregulation

Core temperature is determined by heat gained from the environment and heat produced by the body itself. This heat gain must be carefully regulated to maintain a core temperature of approximately 98.6°F (37°C). In the absence of adequate thermoregulatory mechanisms, the basal metabolic rate at rest may lead to an increase in body temperature of approximately 1.1°C/h. Heat production from muscles during heavy exercise can be 15 times the resting rate. Core temperatures measured after long distance races have been found to be as high as 105.8°F (40.6°C) in conscious athletes and 109.4°F (43°C) in those who have collapsed. The rate of heat rise may be further escalated in the setting of high environmental temperatures and humidity.

Heat transfer from the body occurs via the following 4 mechanisms:

• Conduction is the transfer of heat via direct physical contact with a cooler object; it accounts for 2% of the body's heat loss.
• Convection is the dissipation of heat from the body to the air and water vapor surrounding the body; it accounts for 10% of the body's heat loss. When air temperature exceeds body temperature, the body gains heat energy.
• Radiation is the transfer of heat to the environment via electromagnetic waves; it accounts for most heat dissipation. As long as there is a temperature gradient between the body and the air, 65% of the body's heat is lost by radiation.
• Evaporation is the transfer of heat by transformation of perspiration and saliva into a vapor; it accounts for 30% of the body's heat loss.

The body's dominant forms of heat loss in a hot environment are radiation and evaporation. However, when air temperature exceeds 95°F (35°C), radiation of heat from the body ceases and evaporation becomes the only means of heat loss. Evaporation is maximally efficient in a dry environment. If humidity reaches 100%, evaporation of sweat is no longer possible and the body loses its ability to dissipate heat.

Acclimatization to heat takes days to weeks and allows a person to safely be active at temperatures that would have previously been dangerous. This adaptive mechanism includes earlier onset of sweating, increased sweat volume, more dilute sweat, enhanced cardiovascular performance, activation of the renin-angiotensin-aldosterone axis, salt conservation with expansion of plasma volume, increased glomerular filtration rate, and the ability to resist rhabdomyolysis.

Initially, the body attempts to control the core temperature. A rise in body temperature activates heat receptors in both the hypothalamus and the periphery, which results in increased shunting of blood to the periphery. Increased minute ventilation and sweating maximize evaporative heat loss. These responses may be blunted in chronically ill patients or patients with cardiovascular disease. Patients on medications that cause salt and water depletion or impair physiologic cardiovascular responses are at an increased susceptibility to heat injury. Loss of the ability to excrete sweat is thought to be a result of rising venous pressure or direct thermal damage and may play a role in the inability to dissipate heat. If these compensatory mechanisms fail, central vasoconstriction and peripheral vasodilatation decrease resulting in less heat carried away from the core, and hyperthermia develops.

Heat damage

Thermal maximum is a measure of the magnitude and duration of heat that cells can encounter before they begin to denature proteins. Individuals may begin to sustain cellular damage anywhere from 45 minutes to 8 hours after exposure to core temperatures of 107.6°F (42°C). Nearly all cells respond to heat stressors by producing heat-shock proteins to prolong cell survival at otherwise lethal temperatures. They are believed to act as molecular chaperones to prevent denaturation. The increased quantity of heat-shock proteins is protective against not only heat but ischemia, hypoxia, endotoxin, and inflammatory cytoxins as well. Conditions associated with low levels of these protective proteins such as advanced age, lack of acclimatization, and genetic polymorphisms may place these patients at increased risk for thermal injury.

Inflammatory response

An acute-phase response occurs to heat stress, which produces various mediators of the inflammatory response to protect against injury and promote repair. These cytokines and interleukins mediate fever, hypothalamic-pituitary-adrenal axis, and activate other elements of the stress response. It is thought that heat injury causes an exaggerated response similar to sepsis. Splanchnic hypoperfusion, from shunting of blood volume to the periphery, may increase production of reactive oxygen and nitrogen species. These byproducts with inflammatory mediators may act to increase intestinal permeability resulting in endotoxemia. These factors combine to further impair thermoregulation and the body's ability to prevent damage culminating in hypotension, hyperthermia, and heatstroke.

Frequency

United States

According to the Centers for Disease Control and Prevention (CDC) from 1979-2002, a total of 4,780 heat-related deaths in the United States were attributable to weather conditions and that, during 1993-2002, the incidence of such deaths was 3-7 times greater in Arizona than in the United States overall. The exact number of persons seeking treatment for heat-related disorders is not recorded but reaches the thousands.

International

Incidence of heat-related disorders is increased in areas with higher ambient temperatures. The incidence further rises when customs or beliefs cause large groups of people to be exposed to the elements for extended periods of time such as Hajj, the annual Muslim pilgrimage to the Sacred Mosque in Mecca, Saudi Arabia.

Mortality/Morbidity

• Risk of death is related directly to peak temperature, duration of exposure, and acclimatization period.
• Estimates of fatalities caused by heat-related illness in the United States range from hundreds to several thousand per year. The mortality rate in patients with heatstroke has been reported to be 10-70%, with the highest number of deaths occurring when treatment is delayed for more than 2 hours.
• Heat waves increase the mortality rate. The European summer heat wave of 2003 was exceptionally harsh in both duration and intensity. In France alone, the number of heat-related deaths reached 14,800 by August 20.

Sex

The male-to-female ratio is 1:1.

Age

• Elderly persons are at increased risk for heat-related illness because of underlying illness, medication use, declining adaptive thermoregulatory mechanisms, poor access to air-conditioning, cognitive obstacles to self-care, and limited social support networks.
• Neonates have an increased risk of heat-related illness because of poorly developed thermoregulatory mechanisms and inability to make behavioral adjustments.
• In the review of Naughton et al, of the 80 heat-related deaths during the Chicago 1999 heat wave, 47% of deaths occurred among those older than 65 years.¹

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Hyperthermia, and resulting heat illness, occurs following exposure to heat stress when thermoregulatory mechanisms are overwhelmed by excessive environmental heat or impaired heat dissipation.

• Heat exhaustion
• • Symptoms often are nonspecific and may be insidious in onset; these symptoms often resemble a viral illness.
  • Fatigue, weakness, and fainting
  • Nausea and vomiting
  • Headache and myalgias
  • Dizziness
  • Muscle cramps and myalgias
  • Irritability
• Heatstroke
• • The progression to this condition may include any or all of the symptoms of heat exhaustion.
  • The critical features of heatstroke are hyperthermia above 40°C and CNS dysfunction, which has a sudden onset in 80% of cases.
  • Symptoms may be subtle and include impaired judgment, bizarre behavior, hallucinations, altered mental status, confusion, disorientation, and coma.
  • Patients may be sweating. Although anhydrosis is considered a classic feature of heatstroke, more than half of presenting patients are sweating, especially in cases of exertional heatstroke. Anhydrosis usually is a late finding.

Physical

• Heat exhaustion
• • Weakness
  • Vomiting
  • Orthostatic pulse and blood pressure changes
  • Sweating (absent or present)
  • Piloerection
  • Tachycardia
  • Temperature usually is less than 106°F (41°C) and may be normal.
• Heatstroke
• • Assume that any patient presenting with an elevated temperature, signs of CNS dysfunction, and a history of heat exposure has heatstroke and treat immediately.
  • All or some of the findings of heat exhaustion may be present in heatstroke.
  • The patient's temperature is usually higher than 106°F (41°C). Initial temperature readings may be normal or only marginally elevated if prehospital cooling measures were used.
  • The patient may exhibit signs of a hyperdynamic cardiovascular system, including tachycardia, hyperventilation, increased pulse pressure, decreased cardiac output, decreased diastolic blood pressure, decreased systemic vascular resistance, increased cardiac index, and increased central venous pressure. Tachyarrhythmias may not be amenable to cardioversion.
  • CNS dysfunction includes seizure, coma, delirium, bizarre behavior, opisthotonus, hallucinations, decerebrate rigidity, cerebellar dysfunction, oculogyric crisis, and fixed and dilated pupils.
  • Coagulation disorders include disseminated intravascular coagulation (DIC) and result in signs such as purpura, conjunctival hemorrhage, melena, bloody diarrhea, hemoptysis, hematuria, myocardial bleeding, and CNS hemorrhage.
  • Skin findings may range from warm and dry to diaphoretic. Many individuals with temperatures higher than 41°C are sweating diffusely. Anhydrosis typically is a late finding in heatstroke and is more common in classic than in exertional heatstroke.
  • Respiratory symptoms include tachypnea, alkalosis, and respiratory decompensation secondary to acute respiratory distress syndrome (ARDS).
  • Genitourinary symptoms include hematuria, oliguria, or anuria that may occur as signs of acute renal failure.
  • Unlike malignant hyperthermia and neuroleptic malignant syndrome, heatstroke is not characterized by muscular rigidity. Muscle cramps or flaccidity may be noted.

Causes

As stated above, the primary cause is failure of thermoregulation due to heat stress. Several agents express toxicity via unregulated heat production (eg, malignant hyperthermia); endocrinopathy (eg, thyroid storm) and presence of comorbid disease can also contribute.

• Illnesses
• • Heart disease
  • Skin diseases (eg, scleroderma, ectodermal hyperplasia)
  • Extensive burns
  • Dehydration (eg, vomiting, diarrhea)
  • Endocrine disorders (eg, hyperthyroidism, diabetes, pheochromocytoma)
  • Neurologic diseases (eg, autonomic neuropathies, parkinsonism, dystonias)
  • Delirium tremens
  • Fever
• Behavior
• • Exercise or labor in a hot environment
  • Lack of air conditioning or proper ventilation
  • Inappropriate clothing (eg, occlusive, heavy, vapor-impermeable)
  • Lack of acclimatization
  • Decreased fluid intake
  • Hot environments (eg, inside of tent or automobile in the sun, hot tub, sauna)
• Drugs/toxins
• • Beta-blockers
  • Anticholinergics
  • Diuretics
  • Ethanol
  • Antihistamines
  • Cyclic antidepressants
  • Sympathomimetics (eg, cocaine, amphetamines)
  • Phenothiazines
  • Lithium
  • Salicylates
• Other risk factors
• • Salt or water depletion
  • Obesity
  • Living alone
  • Confined to bed
  • Extremities of age

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Fever, sepsis
Typhoid fever
Malignant hyperthermia
Hypothalamic infarct
Serotonin syndrome
Drug-induced fluid loss
Cardiac arrhythmias
Drug withdrawal (hypersympathetic states)
CNS trauma
Pheochromocytoma

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Laboratory evaluation for heat exhaustion and heatstroke is used primarily to detect end-organ damage.
• Hepatic transaminases: These are elevated almost universally in heatstroke. Reconsider the diagnosis of heatstroke if aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels are within the reference ranges.
• CBC, prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, and platelets: These tests may provide evidence of coagulation disorders and hemoconcentration.
• Electrolytes, BUN, and creatinine: Evaluate for acute renal failure, acid-base disorders, uremia, and hyperkalemia.
• Blood glucose: Hypoglycemia may occur because of increased use of glucose or hepatic damage leading to impaired gluconeogenesis.
• Creatine kinase (CK): The CK level is elevated in rhabdomyolysis, especially in exertional heatstroke.
• Arterial blood gases (ABGs): These measurements are useful to evaluate acid-base status, pulmonary function, and tissue oxygenation. Nonexertional cases typically have respiratory alkalosis, while exertional cases may have both respiratory alkalosis and lactic acidosis.
• Urinalysis
• • Proteinuria, hematuria, myoglobinuria, or granular casts provide evidence of acute renal failure or rhabdomyolysis.
  • Urine specific gravity typically is increased.

Imaging Studies

• Chest radiography
• • Perform chest radiography (CXR) to evaluate for ARDS, aspiration, and pneumonia.
  • CXR may be useful in excluding differential diagnoses (eg, thermal myocardial dysfunction, which may result in a pulmonary edema pattern on CXR film despite dehydration).
• CT scan of the head
• • Evaluate for CNS edema and hemorrhage.
  • This test is important to exclude differential diagnoses in patients with altered level of consciousness.

Procedures

• Rectal thermometer probe for constant core temperature monitoring.
• Foley catheter: Monitor urine output during rehydration or in the presence of renal failure.
• Swan-Ganz catheter: This is useful to guide fluid management in patients with hemodynamic instability, especially if renal or cardiac function is compromised.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Prehospital Care

Immediate cooling and support of organ-system dysfunction is essential for those with heat exhaustion or heatstroke.

• Remove the patient from the hot environment, remove excess clothing, and transfer to a shady place, a cool vehicle, or a cool building.
• Support airway, breathing, and circulation with intravenous (IV) fluids, supplemental oxygen, and assisted ventilation, as indicated.
• Initiate cooling measures with any resources available but do not impede transfer to hospital if heatstroke is suspected.
• • Apply tepid water to the patient and fan the patient to increase water vapor pressure gradient and promote evaporative cooling.
  • Apply ice packs to the patient's neck, axillae, and groin. Alternatively, cover, do not tightly wrap, the patient with a wet sheet.
  • Transport the patient with air conditioning turned on or with windows open.

Emergency Department Care

• Heat exhaustion
• • Treat heat exhaustion with rest, removal from hot environment, and correction of dehydration and electrolyte abnormalities.
  • Patients may be cooled gently with ice packs applied to the neck, groin, and axillae.
  • For mild cases, oral rehydration with 0.1% isotonic sodium chloride solution usually is adequate.
  • For more severe cases, characterized by orthostasis or more severe symptomatology, IV fluids may be required.
  • The water deficit is best corrected slowly (one half of the total water depletion replaced in the first 3-6 h, with the remainder replaced over the next 6-9 h).
  • Monitor vital signs, including orthostatics and urine output, to guide fluid replacement.
  • Heat exhaustion should correct in 2-3 hours, slower resolution or failure to resolve should initiate consideration of other causes of elevated temperature or transfer to a higher level of care.
• Heatstroke
• • Rapidly conduct initial stabilization of airway, breathing, and circulation. Administer supplemental oxygen and IV crystalloid while core temperature is determined and clothing is removed.
  • Institute aggressive cooling measures as rapidly as possible to minimize end-organ damage. An ideal goal is to drop the patient's core temperature by 0.2°C/min. The endpoint core temperature is around 38°C to avoid overshoot.
  • Controversy remains over which method is faster, and no controlled head-to-head studies comparing times or outcomes between the various techniques are available.
  • Evaporative cooling is safe, effective, easily accomplished, and well tolerated. Undress the patient, spray with tepid (not cold) water, and cool by large fans to maximize evaporative heat loss. Proponents estimate that evaporating 1 g of water dissipates 7 times as much heat as melting the same quantity of ice.
  • Ice water or slush immersion is an alternative cooling method. Although ice water or slush immersion is effective at rapidly lowering body temperature, it is associated with more complications than evaporative cooling. Immersion in ice water causes peripheral vasoconstriction, shunts blood away from the periphery, and may lead to shivering and less heat dissipation. It is also uncomfortable for the patient, limits access for cardiac and vital sign monitoring, may prove difficult to get in and out of tub, and may result in hypothermic overshoot.
  • Adjunctive measures include ice packs applied to the patient's neck, axillae, and groin as well as cooling blankets.
  • Other modalities with anecdotal success include internal cooling methods, such as ice water gastric lavage and ice water rectal lavage, as well as invasive techniques such as ice water peritoneal and thoracic lavage, and cardiopulmonary bypass. Gastric or bladder lavage likely adds very little to the effect of evaporative cooling when performed properly and the former additionally carries the risk of aspiration.
  • Alcohol sponge baths are outdated and dangerous and should never be used in children or adults.

Consultations

Consultation with a pediatrician, internist, or intensivist may be required to arrange admission for a patient with heatstroke or severe heat exhaustion.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

No drugs significantly reduce core temperature in patients with heat illness. In contrast to patients with fever who develop elevated temperatures because of an elevated hypothalamic set point, hyperthermic patients do not benefit from antipyretic therapy. Salicylates can worsen coagulopathies, and acetaminophen in large doses can worsen hepatic damage.

The mainstay of therapy involves rapid cooling. Muscle relaxants and neuroleptics have been used in the past to treat complications of heat illness, shivering, and seizure prophylaxis, but clinical trials are lacking.

Avoid several drugs, including anticholinergics (decrease sweating), alpha-adrenergic agonists (increase peripheral resistance without increasing cardiac output), and antipyretics.

Drug Category: Neuroleptics

These agents have been used to suppress shivering during rapid cooling.

Drug Category: Benzodiazepines

These agents are used to treat seizures. By binding to specific receptor sites, these agents appear to potentiate the effects of gamma-aminobutyric acid (GABA) and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters.

Drug Category: Diuretics, osmotic

These agents are used to promote diuresis and prevent or treat acute renal failure.

Drug Category: Alkalinizing agents

Sodium bicarbonate is administered IV to alkalinize urine in patients with rhabdomyolysis. This may prevent toxicity caused by presence of myoglobin in acidic urine and crystallization of uric acid.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Patients requiring admission
• • All patients diagnosed with heatstroke should be admitted to a monitored bed.
  • Elderly patients who have decreased heat tolerance and underlying medical conditions require cardiac monitoring, frequent reassessment, and cautious fluid and electrolyte replacement.
  • Patients with significant electrolyte abnormalities should be admitted and treated until the alterations are corrected.
• Monitor rectal temperature.
• Consider central venous pressure monitoring.

Further Outpatient Care

• Refer elderly, bedridden, or socially isolated patients to social and community services. These patients may benefit from home health assistance.
• Upon discharge from the ED, instruct patients recovering from heat exhaustion to avoid heat for 24-48 hours and to drink increased amounts of fluid.

Transfer

• Patients with heatstroke may require transfer to a higher level of care if the hospital to which they present cannot provide intensive monitoring and treatment.
• Patients with severe complications of heatstroke also may require transfer.

Deterrence/Prevention

• All heat-related illnesses are preventable.
• Identify susceptible populations and at risk behaviors. Have heat response plans (HRP) in place that can be activated in the event of extremes of temperature.
• Encourage community outreach programs for the most vulnerable patients.
• Reschedule strenuous physical activities for cooler periods of the day.
• Use air conditioning, fans, and adequate ventilation. Parents should never lock children in cars, and all cars should be locked when not in use.
• Drink less than 200 mOsm/L (400-500 mL) of cool fluids before exercising and 200-300 mL at frequent intervals during exercise.
• Athletes should not exercise in temperature extremes with concurrent illness.
• Wear light, loose-fitting, and light-colored clothing.
• Bath or shower in tepid water.
• Acclimatization typically requires 90 minutes per day of exercise in hot conditions for at least 1 week. Gradually increase exercise intensity and duration, especially athletes.
• Monitor body weight before and after exercise.
• • Weight loss of more than 7% of body weight represents severe water depletion. Cease exercise and rehydrate to normal weight.
  • Weight loss of 5-6% of body weight represents moderate water depletion. Hydrate to normal weight and proceed with light workouts.
  • Weight loss of 2-3% body weight represents mild water depletion. Rehydrate to normal body weight before engaging in further exercise.

Complications

• Heatstroke has been reported to affect almost every organ in the body except for the pancreas.
• • Cardiac - Sinus tachycardia, hypotension, ST-T segment changes on ECG, elevated cardiac enzyme levels, subendocardial hemorrhage, and ruptured cardiac muscle
  • Pulmonary - Pulmonary edema, aspiration, respiratory alkalosis (and tetany), and ARDS
  • Renal - Rhabdomyolysis, acute oliguric renal failure, and acute tubular necrosis
  • Electrolyte - Hypokalemia, hyperkalemia, hypocalcemia, hypernatremia, hypoglycemia, hyperuricemia, and lactic acidosis
  • Hematologic - Coagulopathy, DIC
  • Neurologic - Cerebellar deficits, hemiplegia, coma, dementia, personality changes, hemiparesis, aphasia, ataxia, dysarthria, and seizures
  • Hepatic - Jaundice, hepatocellular necrosis, and liver failure

Prognosis

• Worse prognosis is proportional to the length of time between onset of elevated core temperatures and initiation of cooling measures.
• With rapid cooling, adequate rehydration, and aggressive treatment of complications, the survival rate approaches 90% for patients with heatstroke.
• Poor prognostic signs
• • Coagulopathy with liver hepatocyte damage
  • Lactic acidosis (in classic, not exertional heatstroke)
  • Rectal temperature more than 42.2°C
  • Prolonged coma of more than 4 hours
  • Residual brain damage (occurs in up to 20% of patients and is a poor prognostic sign)
  • Acute renal failure
  • Hyperkalemia
  • AST level greater than 1000 U/L
  • Prolonged hyperthermia

Patient Education

• Public education about the signs, symptoms, and risks of heatstroke may facilitate early diagnosis and treatment.
• • Patients who experience heat illness should be educated about the early signs and symptoms of heat illness, the importance of adequate hydration, and the methods of minimizing future risk.
  • Coaches should be taught not only to recognize heat illness but also to take preventive measures.
• For excellent patient education resources, visit eMedicine's Environmental Exposures and Injuries Center; Exercise, Nutrition, and Weight Management Center; and Children's Health Center. Also, see eMedicine's patient education articles Heat Exhaustion and Heat Stroke, Heat Cramps, Dehydration in Adults, and Dehydration in Children.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to diagnose (or delay in diagnosis), with consequent failure to treat
• • Reliance on classic heatstroke symptoms for diagnosis (eg, extreme hyperpyrexia, anhydrosis) may be misleading.
  • Sweating often is maintained in heatstroke; loss of sweating is typically a late sign.
  • Prehospital cooling can decrease a patient's temperature at presentation to the ED.
  • The mortality rate may reach 70% if treatment is delayed more than 2 hours.
  • Heat exhaustion and heatstroke occupy points along a continuum. Patients may progress from heat exhaustion to heatstroke rapidly, even in the ED.
  • Failure to consider alternative diagnosis or inciting factors if the patient fails to respond to treatment modalities.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Aug 20, 2008