EM@3AM: Heat Stroke

Author: Sofia Rodriguez, DO (EM Resident Physician, UTSW, Dallas, TX) // Edited by: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 72-year-old female is brought into your ED in Texas during a heat wave. Her daughter found her confused in her home. She believes the power has been out for several days. The patient has no complaints but appears lethargic and is intermittently confused. Her granddaughter mentions she usually has no memory issues and takes no medications.

Triage vital signs (VS): BP 100/82, HR 112, T 102F oral, RR 22, SpO2 98% on RA.

You ask the nurse to get a rectal temperature, which reads 105.1F. The patient’s skin is warm and dry. She is confused, but the rest of her exam is unremarkable.

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?

Diagnosis: Heat Stroke


  • Heat-related illness is a set of preventable conditions ranging from mild forms (e.g., heat exhaustion, heat cramps) to potentially fatal heat stroke.
  • Hyperthermia is not synonymous with fever, which is induced by cytokine activation and regulated at the level of the hypothalamus. A temperature above 40ºC (or 104ºF) is generally considered to be consistent with severe hyperthermia. [1]
  • Heat stroke is differentiated from heat exhaustion by the presence of neurological changes.
  • Several characteristics define heat stroke: a core body temperature greater than 104°F (40°C), neurological signs such as confusion, seizures, or loss of consciousness, exposure to high environmental heat, and absence of other causes of hyperthermia. [1]
  • Nonexertional (or “classic”) heat stroke occurs in those who are exposed to a hot environment, especially in young and elderly persons (mostly > 70) with underlying chronic medical conditions that impair thermoregulation, prevent removal from a hot environment, or interfere with access to hydration or attempts at cooling. [1]
  • Exertional heat stroke occurs in otherwise healthy individuals who undergo strenuous activity in hot weather with high humidity, such as athletes and military trainees. [1]
  • Nonexertional (classic) heat stroke has a higher mortality than exertional heat stroke. The death rate from exertional heat stroke is relatively low (3 to 5%) compared to classic heat stroke (10 to 65%). [2,3]
  • The increased mortality rate is likely due to the higher prevalence of comorbidities and older age in the classic population. If immediate rapid cooling is successful, there has been a zero-fatality rate for young exertional heat-stroke patients. [3]
  • Patients who present to the emergency department with a core body temperature of 105.8°F (41°C) or greater and prolonged hyperthermia have mortality rates as high as 80%, although this number includes patients with non-exertional heat stroke, which has a higher mortality rate. [4]



  • The pathophysiology of heat stroke is complex and includes protein denaturation, endotoxin release, and thermoregulatory failure, which contribute to systemic inflammatory response syndrome (similar to septic shock) leading to multi-organ failure and death. [5]
  • The organs most affected by elevated core temperatures are the brain and liver, but all organ systems can be affected. [6]
  • Prognosis is related to the time spent in hyperthermia. [6]
  • As temperature increases there is an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. [7]
  • Above 42ºC (108ºF), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function. A cytokine-mediated systemic inflammatory response develops, and production of heat-shock proteins is increased. [7]


History and Exam:

  • History: Patients may complain of weakness, lethargy, nausea, or dizziness. The presentation of elderly patients with heat stroke may be subtle and nonspecific early in the course of the disease.
  • Exam: In addition to an elevated core body temperature, common vital sign abnormalities include sinus tachycardia, tachypnea, a widened pulse pressure, and hypotension. [8]
    • Physical exam findings may include flushing due to cutaneous vasodilation, crackles due to noncardiogenic pulmonary edema, GI bleeding due to shunting of blood from the splanchnic circulation to the skin and muscles, and evidence of neurologic dysfunction, such as altered mentation, slurred speech, agitation, ataxia, delirium, seizures, and coma. [7]
    • Dehydration is common.
    • Anhidrosis is common, but its absence does not rule out heat stroke.
    • Hematochezia may be present due to intestinal ischemia.



  • Sepsis, encephalitis, meningitis, malaria, thyroid storm, DKA, CVA, anticholinergic toxicity, salicylate toxicity, serotonin syndrome, stimulant toxicity, neuroleptic malignant syndrome, malignant hyperthermia, baclofen withdrawal, EtOH or benzodiazepine withdrawal



  • No single diagnostic test definitively confirms or excludes heat stroke; it is a clinical diagnosis that requires a high index of suspicion.
  • It is important to note that some thermometers have a maximum reading below the temperatures sometimes reached by patients suffering from heat stroke, thus a thermometer (rectal or esophageal) that is accurate at high temperatures must be used when assessing heat stroke patients.
  • Core temperature continuous monitoring is ideal (e.g. with bladder temperature monitor).
  • While heat stroke is a clinical diagnosis, laboratory testing should be performed to assess for end-organ damage and should include lactate, CBC, creatine kinase (to evaluate for rhabdomyolysis), glucose, BUN, creatinine, liver function tests, prothrombin time (PT), and partial thromboplastin time (PTT) because of the risk of heat-induced liver damage and disseminated intravascular coagulation. [9]
  • Hepatocellular injury is a well-documented complication of heat stroke [10]. In the United States, nearly 1000 annual cases of heat stroke are reported, but the frequency of severe liver injury in such patients is not well described. [11]
  • Mild to moderate hepatic injury in most cases of heat stroke is usually asymptomatic and can be reversed, with a subset of patients presenting with acute liver failure, requiring liver transplantation. [12, 13]
  • Laboratory study abnormalities may overlap in patients with heat stroke and with hyperthermia due to other conditions (i.e., can meet SIRS criteria).
  • ECG findings: patients with heat stroke may have sinus tachycardia, prolonged Q-T interval, diffuse nonspecific ST-T changes, and ST-T changes localized to the territory of a coronary artery. [14]
  • A head CT and analysis of the cerebrospinal fluid should be performed if central nervous system causes of altered mental status are suspected and/or the patient does not improve with cooling. [8]



  1. Address the ABCs.
  2. Rapid cooling
  • Patients may require definitive airway. Use rocuronium, and fluid replete prior to intubation if possible.
  • Patients are dehydrated. Resuscitate with cool IV fluids. Treat hypotension with fluids before vasopressors. Most patients improve with cooling and fluids.
  • When the etiology of hyperthermia is unclear but heat stroke remains a possibility, it is important to initiate cooling measures while diagnoses other than heat stroke are pursued. Improvement with cooling suggests that heat stroke is the diagnosis.
  • Rapid cooling: the way the patient is cooled matters.
  • Noninvasive methods are applied to the surface of the skin (ie. Ice-water immersion, evaporative plus convective cooling) while invasive methods are aimed at cooling the core of the body (bladder, thoracic, and gastric lavage with cooled fluids and cardiopulmonary bypass/ECMO). Ultimately, noninvasive techniques are effective first-line modalities for cooling.
  • Exertional heat stroke: Ice-water immersion has been shown to be rapid and highly effective, with a zero fatality rate in large case series of younger, fit patients. [3]
  • Nonexertional (classic) heat stroke: Evaporative and convective cooling is the method most often recommended because it is effective, noninvasive, easily performed, and does not interfere with other aspects of patient care. It is also associated with decreased morbidity and mortality. [3,15,16,17] With evaporative and convective cooling, the naked patient is sprayed with a mist of lukewarm water while fans are used to blow air over the moist skin. In elderly patients with classic heat stroke, immersion therapy is associated with increased mortality. [15]
  • Invasive cooling: There is little evidence to guide the use of chilled intravenous fluids or gastric, peritoneal, thoracic, or bladder cooling with cold lavage fluids [18, 19, 20].
    • The only available controlled studies regarding invasive cooling techniques were tested on animals. In these studies, peritoneal lavage and gastric lavage were less effective than evaporative methods. [21, 22]
    • Cold thoracic (using bilateral chest tubes) and peritoneal lavage results in rapid cooling. Peritoneal lavage is contraindicated in pregnant patients and those with previous abdominal surgery and gastric lavage may cause water intoxication. [23]
    • Cooled oxygen, cooling blankets, and cold (ie, room temperature, or approximately 22°C [71.6°F]) intravenous fluids may be helpful adjuncts but should not be used as a primary method of cooling. [23] Intravenous cooling may be useful as an adjunct in scenarios such as ambulance transport. [24]
    • There are limited data for use of cardiopulmonary bypass/ECMO. [3]
  • Based on current evidence, ice packs applied strategically to the neck, axilla, and groin; cooling blankets; and intravascular or external cooling devices are notrecommended as primary cooling methods but can be used to supplement primary cooling methods. [3]
  • Agitation from altered mental status or shivering induced by evaporative and convective cooling or other treatments may generate heat and can be suppressed with short-acting IV benzodiazepines, such as lorazepam (1-2 mg IV). Benzodiazepines may also improve core body cooling. [25]
  • Cooling measures should be stopped once a temperature of 38 to 39ºC (100.4 to 102.2ºF) has been achieved in order to reduce the risk of iatrogenic hypothermia. [8]
  • When cooling is completed within 30 minutes from collapse, the mortality rate approaches zero. [26]
  • Pharmacologic agents such as antipyretics or dantrolene have no role in the treatment of heat stroke. [15]
  1. Treatment of complications: Acute Respiratory Distress Syndrome (ARDS), disseminated intravascular coagulation (DIC), acute kidney injury, hepatic injury, hypoglycemia, rhabdomyolysis, and seizures [27]



  • Hospital admission is recommended for ongoing treatment of complications and observation even after cooling has been done and mental status has returned to baseline. [28]


Take Home Points:

  • Temperature > 104F should point you toward heat stroke, neuroleptic malignant syndrome, or malignant hyperthermia.
  • Cooling should be started immediately, even if diagnosis is unclear.
  • Nonexertional (classic) heat stroke = evaporative and convective cooling
  • Exertional heat stroke = cold water immersion
  • Stop cooling once a temperature of 38 to 39ºC (100.4 to 102.2ºF) is reached
  • No place for antipyretics


Further Reading:


WikEM – Heat Stroke

IBCC Hyperthermia and Heat Stroke

EMRAP June 2019



  1. Peiris AN, Jaroudi S, Noor R. Heat Stroke. JAMA.2017;318(24):2503. doi:10.1001/jama.2017.18780
  2. Pease S, Bouadma L, Kermarrec N, Schortgen F, Régnier B, Wolff M. Early organ dysfunction course, cooling time and outcome in classic heatstroke. Intensive Care Med. 2009 Aug;35(8):1454-8.
  3. Gaudio FG, Grissom CK. Cooling Methods in Heat Stroke. J Emerg Med. 2016;50(4):607‐616.
  4. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heat-stroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177–2183.
  5. Pryor RR, Bennett BL, O’Connor FG, Young JM, Asplund CA. Medical evaluation for exposure extremes: heat. Wilderness Environ Med. 2015;26(4 suppl):S69–S75.
  6. Atha WF. Heat-related illness. Emerg Med Clin North Am. 2013;31(4):1097–1108.
  7. Ye N, Yu T, Guo H, Li J. Intestinal Injury in Heat Stroke. J Emerg Med 2019; 57:791.
  8. Tek D, Olshaker JS. Heat illness. Emerg Med Clin North Am 1992; 10:299.
  9. al-Mashhadani SA, Gader AG, al Harthi SS, et al. The coagulopathy of heat stroke: alterations in coagulation and fibrinolysis in heat stroke patients during the pilgrimage (Haj) to Makkah. Blood Coagul Fibrinolysis 1994; 5:731.
  10. Bianchi L, Ohnacker H, Beck K, Zimmerli-Ning M. Liver damage in heatstroke and its regression. A biopsy study. Hum Pathol. 1972;3:237–248.]
  11. Davis, Brian C et al. Heat stroke leading to acute liver injury & failure: A case series from the Acute Liver Failure Study Group. Liver international: official journal of the International Association for the Study of the Liver 2017;37(4): 509-513
  12. T. Hassanein, A. Razack, J. S. Gavaler, and D. H. Van Thiel, “Heatstroke: its clinical and pathological presentation, with particular attention to the liver,” American Journal of Gastroenterology 1992:87(10):1382–1389, 1992.]
  13. Martínez-Insfran LA, Alconchel F, Ramírez P, et al. Liver Transplantation for Fulminant Hepatic Failure Due to Heat Stroke: A Case Report. Transplant Proc 2019; 51:87.
  14. Akhtar MJ, al-Nozha M, al-Harthi S, Nouh MS. Electrocardiographic abnormalities in patients with heat stroke. Chest. 1993;104(2):411-414. doi:10.1378/chest.104.2.411
  15. Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care 2007; 11:R54.
  16. Lipman GS, Eifling KP, Ellis MA, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of heat-related illness. Wilderness Environ Med 2013; 24:351.
  17. Alzeer AH, Wissler EH. Theoretical analysis of evaporative cooling of classic heat stroke patients. Int J Biometeorol 2018; 62:1567.
  18. Atha WF. Heat-related illness. Emerg Med Clin North Am 2013; 31:1097.
  19. J.E. Smith. Cooling methods used in the treatment of exertional heat illness. Br J Sports Med, 39 (2005), pp. 503-507
  20. B.Z. Horowitz. The golden hour in heat stroke: use of iced peritoneal lavage. Am J Emerg Med, 7 (1989), pp. 616-619
  21. White JD, Kamath R, Nucci R, et al. Evaporation versus iced peritoneal lavage treatment of heatstroke: comparative efficacy in a canine model. Am J Emerg Med 1993; 11(1): 1–3
  22. White JD, Riccobene E, Nucci R, et al. Evaporation versus iced gastric lavage treatment of heatstroke: comparative efficacy in a canine model. Crit Care Med 1987; 15(8): 748–50
  23. Bouchama A, Knochel JP. Heat stroke. N Engl J Med 2002; 346:1978.
  24. Morrison KE, Desai N, McGuigan C, et al. Effects of Intravenous Cold Saline on Hyperthermic Athletes Representative of Large Football Players and Small Endurance Runners. Clin J Sport Med 2018; 28:493.
  25. Hostler D, Northington WE, Callaway CW. High-dose diazepam facilitates core cooling during cold saline infusion in healthy volunteers. Appl Physiol Nutr Metab 2009; 34:582.
  26. Casa DJ, Armstrong LE, Kenny GP, O’Connor FG, Huggins RA. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep. 2012;11(3):115–123.
  27. Epstein Y, Yanovich R. Heatstroke. N Engl J Med 2019; 380:2449.
  28. Pryor RR, Casa DJ, Holschen JC, O’Connor FG, Vandermark LW. Exertional heat stroke: strategies for prevention and treatment from the sports field to the emergency department. Clin Pediatr Emerg Med. 2013;14(4):267–278.

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