Table of Contents
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Abstract
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Case Presentations
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Introduction
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Critical Appraisal Of The Literature
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Epidemiology
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Physiology
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Mechanisms Of Heat Transfer
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Thermoregulation
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Prevention And Acclimatization
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Mass Gatherings, Field Care, And Prehospital Care
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Measurement Of Patient Core Temperature In The Field
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Field And Prehospital Treatment
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Emergency Department Evaluation Of Heat Illness
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History
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Physical Examination
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Central Nervous System
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Cardiovascular System
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Lungs
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Abdomen
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Skin
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Diagnostic Studies For Heat Illness
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Treatment For Heat Illness In The ED
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Exertional Heat Stroke Treatment
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Rehydration
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Preventing End-Organ Damage
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Active Cooling Techniques
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Water Immersion Therapy
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Mist-And-Fan Technique
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Ice Packs And Internal Cooling
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Classic Heat Stroke Treatment
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Rehydration
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Classic Heat Stroke–Associated Sodium Abnormalities
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Preventing End-Organ Damage
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Cooling Techniques
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Other Cooling Modalities
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Risks Of Cooling
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Putting It All Together
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Treatment Of Other Heat-Related Conditions
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Prickly Heat (Miliaria)
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Heat Edema
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Heat Tetany And Cramps
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Special Populations
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The Very Young
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The Very Old
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The Agitated Patient
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Patients With Drug-Induced Hyperthermia
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Controversies And Cutting Edge In The Management Of Heat Illness
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Disposition Of Patients With Heat Illness
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Risk Management Pitfalls For Heat Illness
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Time- And Cost-Effective Strategies For Managing Heat Illness In The ED
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Case Conclusions
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Clinical Pathway For Differential Diagnosis Of Heat Illness
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Clinical Pathway For Treatment Of Noninfectious Heat Illness
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Tables And Figures For Heat Illness
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References
Abstract
Heat illness spans a broad spectrum of disease, with outcomes ranging from benign rash to fatal heat stroke. Heat illness is broadly divided into 2 types: classic and exertional. Both types occur as a result of exposure to elevated temperature with inadequate thermoregulation; however, classic illness occurs without preceding physical activity. Treatment consists of rapid cooling, fluid replacement, and physiologic support. Other milder forms of heat illness include heat fatigue, heat syncope, heat edema, and heat rash. Drugs, drug combinations, drug side effects, and infections can also cause or complicate heat illness and these manifestations may not respond to standard cooling maneuvers and treatments alone; each requires specific additional therapy or antidotes to reverse the cycle of heat and organ damage. This review examines the physiology, diagnosis, and treatment of exertional, classic, and drug-induced hyperthermia. Field and prehospital diagnosis and treatment are also reviewed, with recommendations for rehydration and monitoring in rhabdomyolysis.
Case Presentations
On a late summer afternoon shift, a 16-year-old adolescent boy presents to the ED via EMS after collapsing during football practice. The medics state that he complained of dizziness and staggered to the edge of the field before he fell to the ground. The medics call out vital signs: blood pressure, 102/60 mm Hg; heart rate, 120 beats/min; and respiratory rate, 16 breaths/min. They did not measure a temperature, but state that he feels hot to the touch. The patient is brought to the resuscitation room where you begin your evaluation. The patient is awake, but very lethargic and unresponsive to verbal commands. You notice he is flushed, his skin is hot to the touch, and he is sweating. The rectal temperature is 40.3°C. You begin volume resuscitation with normal saline, remove his athletic equipment and clothing, and order laboratory studies. As the nurse tells you that the patient is no longer responding to verbal or noxious stimuli, you wonder if you should intubate him. You consider the quickest and most effective way to cool the patient with the resources available in your department. As you assess what other treatments the patient may need during his resuscitation, the nurse tells you there is a new patient in the next room.
As you walk into the next room, you see a 35-year-old woman with her husband at her bedside. He says his wife was treated for nausea and vomiting at an urgent care center the previous day. When she woke up today, she was confused, sweating, and her arms and legs seemed "stiff.” As you begin your evaluation, you ask the ED clerk to obtain the records from the outside facility. On examination, the patient is febrile at 39.4°C, diaphoretic, and disoriented. Her heart rate is 133 beats/min and her blood pressure is 170/110 mm Hg. On motor examination, she exhibits cogwheel rigidity. You place an IV and administer a benzodiazepine, which does little to alleviate her symptoms. You ask yourself: What next?
Introduction
Heat-related illnesses exist along a continuum from the less severe symptoms of heat edema to the potentially fatal syndrome of heat stroke. (See Table 1.) Heat-related illnesses are classically defined in review literature by exposure without alteration of hypothalamic thermoregulation.1,2 In contrast, fever is defined by changes to the hypothalamic set point by pyrogenic cytokines.1 Heat stroke is a life-threatening condition and requires the highest level of clinical attention. The cardinal sign of heat stroke is a change in mental status and it is associated with a significant mortality. Delirium, convulsions (particularly during cooling), multisystem organ failure, coma, and death can occur. Any substance or situation that alters thermoregulatory function can precipitate severe, life-threatening disease. As there are no tests to confirm the diagnosis of heat stroke, other conditions presenting in a similar way should be considered and investigated. A list of differential diagnoses is provided in Table 2. Heat-related illnesses occur when the body’s cooling mechanisms are unable to control the natural rise in body temperature caused by metabolism, physical activity, or exposure to warm temperature. The true prevalence is difficult to estimate, as many cases go unreported. Heat-related illnesses can be multifactorial, but are most commonly seen in improperly conditioned patients participating in physical activities in environments with hot, humid weather (exertional), and in patients unable to escape a heated environment (classic). The challenge for the emergency clinician is twofold: first, the severity of heat illness must be established and prompt cooling therapy must be started. Second, the emergency clinician must be aware of toxicological substances, infectious processes, and other medical conditions that can cause symptoms that mimic heat illness.
The majority of heat illness cases are benign and easily reversed. After evaluation, diagnosis, and cooling treatment, the vast majority of patients presenting with mild to moderate disease can be discharged from the emergency department (ED). Important exceptions include heat stroke and lesser forms of heat illness occurring in patients who are elderly or debilitated or who have multiple comorbidities. Such conditions may result in major physiologic stress in situations of passive ambient heat exposure. This issue of Emergency Medicine Practice reviews the types of heat illness, their diagnosis, and their management. Knowing how to rapidly cool the patient, what sequelae to anticipate, and which processes mimic heat stroke can prevent mortality.
Critical Appraisal Of The Literature
A systematic search of the literature through May 2014 was undertaken using PubMed and the Cochrane Database of Systematic Reviews. The search was performed using the terms heat illness, heat stroke, neuroleptic malignant syndrome, serotonin syndrome, aspirin overdose, sympathomimetic overdose, rhabdomyolysis, and lithium toxicity. Limitations of the studies included poor study design, small sample sizes, and lack of appropriate controls in those studies examining treatment.
Risk Management Pitfalls For Heat Illness
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“The patient did not respond to multiple doses of diazepam and he required general anesthesia and intubation.” Persistent agitation after control of temperature or inability to control temperature should prompt consideration of other causes and contributors to heat illness. Sympathomimetic intoxication associated with heat illness will respond well to benzodiazepines, but anticholinergic syndrome and neuroleptic malignant syndrome will not. Before moving to general anesthesia, emergency clinicians should consider specific antidotes and treatments for unusual causes of hyperthermia.
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“The patient came in febrile and altered, but now he is better. He can definitely go home.” Before discharging anyone with heat illness or heat stroke, consider the factors that are associated with mortality (such as advanced age, comorbidities, immobility, social isolation, cardiovascular disease, and male sex). Also remember that rhabdomyolysis is a frequent complication of heat illness and that factors such as CPK > 10000 IU/L, hyperkalemia, and metabolic acidosis are associated with a higher likelihood of acute kidney injury. Assess a checklist of criteria that are associated with safe discharge, including working air conditioning and social support. Be sure that symptoms are resolved and that any marked vital sign or laboratory abnormality has normalized before discharge.
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“Haloperidol, lorazepam, and cooling maneuvers could not reverse the heat stroke and heat-induced psychosis; I have no idea why the patient died.” Benzodiazepines are a good starting choice when sedation is necessary. Phenothiazines, because of their potential extrapyramidal side effects and their anticholinergic effects, are not a good choice in hyperthermia and agitation. The anticholinergic effects can markedly decrease the ability of the body to sweat and the extrapyramidal effects can worsen hyperthermia. They can also cause neuroleptic malignant syndrome.
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“The patient was given naloxone, and thereafter developed severe agitation. He must have been doing a speedball. Just keep giving him diazepam.” A speedball is a mixture of heroin and cocaine. When the heroin is reversed with naloxone, the sympathomimetic effects are unmasked and the patient may become agitated. Occasionally, heroin is mixed with an anticholinergic such as scopolamine. In this case, when the heroin is reversed, a full-blown anticholinergic syndrome may result. You can distinguish between sympathomimetic and anticholinergic toxidromes by remembering how they differ. The anticholinergic patient will tend be more profoundly delirious, and will have dry, flushed skin, urinary retention, and a quiet abdomen, whereas the patient abusing sympathomimetic drugs will tend to be manic, will tend to sweat profusely, and will respond better to benzodiazepines.
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“Please give the febrile marathoner with heat exhaustion 3 L of normal saline and then recheck his vital signs.” Healthy patients who participate in marathons or other high-endurance events or scenarios can develop hyponatremia. In the exertional heat illness group, it is important to check serum sodium level before administering a large amount of saline.
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“But I treat all my agitated patients with haloperidol.” Sedation of the patient with heat illness merits careful consideration. Benzodiazepines are safe, but they may obscure the real cause of hyperthermia. It is important to try to establish the likely cause of hyperthermia before sedating the patient. If you do judge that a sedative is necessary, benzodiazepines are the safest and most generally useful class.
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“The patient is altered because he is old, febrile, and demented.” It may be the case that a fever can, by itself, cause alteration of mental status in an elderly patient, but bear in mind that elderly patients with immobility and dementia are at increased risk for heat stroke. Additionally, the elderly are more likely to be on complex combinations of medications, which may predispose them to heat-related illness.
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“Please give that 98-year-old a quick 3 L of normal saline and when you are done, let me know.” The elderly, in general and especially with heat illness, can become hyponatremic. If the sodium level is very low and it is corrected too quickly, central pontine myelinolysis can occur. To avoid complications of hyponatremia and hypernatremia reversal, a sodium level should be obtained as quickly as possible so that sodium derangement may be corrected appropriately. Additionally, conditions such as congestive heart failure or renal disease can thwart the ability of the elderly patient to tolerate rapid resuscitation even if the fluid deficit is fairly large. Careful but continuous fluid administration with frequent rechecking is prudent.
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“Her legs were swollen so I prescribed furosemide. I had no idea she would get dehydrated after discharge, fall, and break her hip.” Heat edema occurs frequently, especially early in the heat season and it often resolves with acclimatization. Treatment emphasizes support stockings and elevating the extremities, not on diuretics.
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“He looked great at discharge. I couldn't believe he died the next day at football practice.” Young patients with exertional heat exhaustion or heat stroke can quickly recover and appear well. However, their ability to regulate temperature may be impaired, and they should be returned to play slowly over time, with close monitoring.
Tables And Figures For Heat Illness
References
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study will be included in bold type following the reference, where available. In addition, the most informative references cited in this paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference.
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