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Heat stroke

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2], Usama Talib, BSc, MD [3]
Synonyms and keywords:Heat apoplexy, Heat exhaustion, Heat hyperpyrexia, Overheating, Thermoplegia, Heat stress, Heat illness, Siriasis

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

Heat stroke is defined as severe illness characterized by a core temperature >40°C and central nervous system abnormalities such as delirium, convulsions, or coma resulting from exposure to environmental heat (classic heat stroke) or strenuous physical exercise (exertional heat stroke). It must be differentiated from other causes of altered mental status and fever, such as Neuroleptic malignant syndrome, Malignant hyperthermia, Serotonin syndrome, and sepsis based on patient’s background, history, symptoms and laboratory findings. Treatment is cooling by using standard protocols.

Historical perspective

Heat stroke was first described by Hippocrates in 400 BC. The prevention and treatment of heat stroke were then described by Avicenna in 1020. Recent treatment advances are because of military experiences with heat exposure.

Classification

Heat stroke is classified to 2 types: Exertional heat stroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period in a hot environment and classic nonexertional heat stroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young individuals.[1]

Pathophysiology

Heat stress means perceived discomfort and physiologic strains during heat exposure. A series of physiologic events occur to adapt heat. These events include thermoregulation (with acclimatization), an acute-phase response, and production of heat shock proteins. If these sequence of actions fails to prevents body from high temperature, heat stress progresses to heat stroke. Thermoregulation, acclimatization, acute phase responses, and heat shock proteins are the important factors in response to heat stroke. Hypothalamus is the center of thermoregulation.[1][2][3][4] Increase in the peripheral body temperature will activate sympathetic response through thermoregulatory action of hypothalamus to deliver more blood flow by vasodilation of surface cutaneous veins. This increase in blood flow will cause sweating. The elevated blood temperature will cause tachycardia, increase in cardiac output, and increase in minute ventilation. [5][6][7] Blood shift from internal organs to the skin may cause decreased visceral perfusion and predispose them to ischemia. Increased sweating will cause loss of salt and water up to 2 liters per hour. Therefore, dehydration may worsen thermoregulation.[7][8]

Causes

Excessive exercise in warm weather is the most common cause heat stroke.[9]

Differentiating Heat stroke from other Diseases

Heat stroke must be differentiated from other disease that may cause alteration in mental status and hyperthermia including: Neuroleptic malignant syndrome, Malignant hyperthermia, Serotonin syndrome, and sepsis.[10][11][12][13][14][15]

Epidemiology and demographics

The United States Centers for Disease Control (CDC) reports an average of 9000 cases per year among high school athletes. The highest incidence of heat stroke in the United States has been reported among football players. Young athletes are more prone to exertional heat stroke while, classic heat stroke is more common among elderly. Men are more affected by heat stroke than women.

Risk factors

Common risk factors for heat stroke include: excessive exercise in hot weather, lack of air movement, lack of water access, high humidity, obesity, acute illness, and certain drugs.[16][17][18][19][20]

Screening

There is insufficient evidence to recommend routine screening for heat stroke.

Natural history, complications, and prognosis

If heat stroke left untreated it may result in severe complications and even death. The complications of heat stroke include: multiple organ failure, acute renal failure, myocardial injury and  DIC. Timely resuscitation and fluid replacement decreases the mortality and can prevent sustained brain injury, which is the most important prognostic factor.

History and Symptoms

High body temperature (hyperthermia) and dysfunction of the CNS must coexist for the confirmation of the diagnosis of heat stroke. A history of an existing disease, outdoor activity, exposure to heat, extensive exertion and improper hydration may be observed.[21][22][23]

Physical Examination

A detailed physical examination should be performed in case of a suspicion of heat stroke. The physical examination of a patient with heat stroke may yield a disoriented, comatosed individual with fever, hypotension, skin redness, skin burn, tachycardia, muscle spasms or pain and hyperventilation.[24]

Laboratory Findings

The laboratory finding scene in patients with a heat stroke include hypophosphatemia, hypokalemia, hypoglycemia, tension of arterial carbon dioxide is usually less than 20 mm Hg. Respiratory alkalosis is seen in non-exertional heat stroke where as lactic acidosis and respiratory alkalosis in exertional heat stroke.[25]

CT scan

A CT scan may be required in heat stroke patient with central nervous system(CNS) findings. CT scan can show the loss of gray white matter discrimination (GWMD) which can be associated with the CNS findings associated with heat stroke.[26][27]

MRI

An MRI can show variable findings depending on the degree of damage from heat stroke. Findings may include cerebellar and cerebral atrophy. Parietooccipital, and hippocampal lesions may also be noticed in an MRI scan.[28][29]

Medical Therapy

The heat stroke is primarily managed by removing the patient from the environment to minimize heat exposure and to ionitiate rapid cooling protocols.[30]

Primary Prevention

The primary prevention strategies for both classic and exertional heat stroke include acclimatization to the heat, appropriate scheduling of outdoor activities, staying well hydrated, minimizing physical activity, spending more time indoors and increasing consumption of salty foods.[31]

Secondary Prevention

The secondary prevention strategies for heat stroke are similar to the primary prevention.[32]

References

  1. ↑ Yang YL, Lin MT (1999). “Heat shock protein expression protects against cerebral ischemia and monoamine overload in rat heatstroke”. Am. J. Physiol. 276 (6 Pt 2): H1961–7. PMID 10362676.
  2. ↑ Li PL, Chao YM, Chan SH, Chan JY (2001). “Potentiation of baroreceptor reflex response by heat shock protein 70 in nucleus tractus solitarii confers cardiovascular protection during heatstroke”. Circulation. 103 (16): 2114–9. PMID 11319204.
  3. ↑ Welch WJ (1992). “Mammalian stress response: cell physiology, structure/function of stress proteins, and implications for medicine and disease”. Physiol. Rev. 72 (4): 1063–81. PMID 1438579.
  4. ↑ Grossman, Moses (1997). “Fever: Basic Mechanisms and Management”. JAMA: The Journal of the American Medical Association. 278 (5): 441. doi:10.1001/jama.1997.03550050105047. ISSN 0098-7484.
  5. ↑ Buono MJ, Sjoholm NT (1988). “Effect of physical training on peripheral sweat production”. J. Appl. Physiol. 65 (2): 811–4. PMID 3170430.
  6. ↑ NELSON N, EICHNA LW (1947). “Thermal exchanges of man at high temperatures”. Am. J. Physiol. 151 (2): 626–52. PMID 18901907.
  7. ↑ 7.0 7.1 Adams WC, Fox RH, Fry AJ, MacDonald IC (1975). “Thermoregulation during marathon running in cool, moderate, and hot environments”. J Appl Physiol. 38 (6): 1030–7. PMID 1141115.
  8. ↑ Deschamps A, Levy RD, Cosio MG, Marliss EB, Magder S (1989). “Effect of saline infusion on body temperature and endurance during heavy exercise”. J. Appl. Physiol. 66 (6): 2799–804. PMID 2745343.
  9. ↑ Bouchama A, Knochel JP (2002). “Heat stroke”. N. Engl. J. Med. 346 (25): 1978–88. doi:10.1056/NEJMra011089. PMID 12075060.
  10. ↑ Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC (2016). “The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)”. JAMA. 315 (8): 801–10. doi:10.1001/jama.2016.0287. PMC 4968574. PMID 26903338.
  11. ↑ Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, Rubenfeld G, Kahn JM, Shankar-Hari M, Singer M, Deutschman CS, Escobar GJ, Angus DC (2016). “Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)”. JAMA. 315 (8): 762–74. doi:10.1001/jama.2016.0288. PMC 5433435. PMID 26903335.
  12. ↑ Carbone JR (2000). “The neuroleptic malignant and serotonin syndromes”. Emerg. Med. Clin. North Am. 18 (2): 317–25, x. PMID 10767887.
  13. ↑ Bodner RA, Lynch T, Lewis L, Kahn D (1995). “Serotonin syndrome”. Neurology. 45 (2): 219–23. PMID 7854515.
  14. ↑ Ener RA, Meglathery SB, Van Decker WA, Gallagher RM (2003). “Serotonin syndrome and other serotonergic disorders”. Pain Med. 4 (1): 63–74. PMID 12873279.
  15. ↑ Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB (2010). “Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006”. Anesth. Analg. 110 (2): 498–507. doi:10.1213/ANE.0b013e3181c6b9b2. PMID 20081135.
  16. ↑ Bricknell MC (1994). “Heat illness in Cyprus”. J R Army Med Corps. 140 (2): 67–9. PMID 8907832.
  17. ↑ Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO (2009). “Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980-2006”. Circulation. 119 (8): 1085–92. doi:10.1161/CIRCULATIONAHA.108.804617. PMID 19221222.
  18. ↑ “Heat illness among high school athletes — United States, 2005-2009”. MMWR Morb. Mortal. Wkly. Rep. 59 (32): 1009–13. 2010. PMID 20724966.
  19. ↑ Capacchione JF, Muldoon SM (2009). “The relationship between exertional heat illness, exertional rhabdomyolysis, and malignant hyperthermia”. Anesth. Analg. 109 (4): 1065–9. doi:10.1213/ane.0b013e3181a9d8d9. PMID 19617585.
  20. ↑ Armstrong LE, Casa DJ, Watson G (2006). “Exertional hyponatremia”. Curr Sports Med Rep. 5 (5): 221–2. PMID 16934202.
  21. ↑ Simon HB (1994). “Hyperthermia and heatstroke”. Hosp Pract (Off Ed). 29 (8): 65–8, 73, 78–80. PMID 7914522.
  22. ↑ Bricknell MC (1994). “Heat illness in Cyprus”. J R Army Med Corps. 140 (2): 67–9. PMID 8907832.
  23. ↑ Leon LR, Bouchama A (2015). “Heat stroke”. Compr Physiol. 5 (2): 611–47. doi:10.1002/cphy.c140017. PMID 25880507.
  24. ↑ Tek D, Olshaker JS (1992). “Heat illness”. Emerg Med Clin North Am. 10 (2): 299–310. PMID 1559470.
  25. ↑ Kim RC, Collins GH, Cho C, Ichikawa K, Givelber H (1980). “Heat stroke. Report of three fatal cases with emphasis on findings in skeletal muscle”. Arch Pathol Lab Med. 104 (7): 345–9. PMID 6893120.
  26. ↑ Cha SY, Kang TH, Kim SJ, Lee HY, Kim HJ, Jung DS; et al. (2013). “Selective anterograde amnesia associated with hippocampal and splenial damage after heat stroke”. Clin Neurol Neurosurg. 115 (9): 1867–70. doi:10.1016/j.clineuro.2013.03.003. PMID 23602221.
  27. ↑ Tek D, Olshaker JS (1992). “Heat illness”. Emerg Med Clin North Am. 10 (2): 299–310. PMID 1559470.
  28. ↑ Kuzume D, Inoue S, Takamatsu M, Sajima K, Kon-No Y, Yamasaki M (2015). “[A case of heat stroke showing abnormal diffuse high intensity of the cerebral and cerebellar cortices in diffusion weighted image]”. Rinsho Shinkeigaku. 55 (11): 833–9. doi:10.5692/clinicalneurol.cn-000755. PMID 26399667.
  29. ↑ Li J, Zhang XY, Zou ZM, Wang B, Xia JK (2015). “Heat stroke: typical MRI and (1)H-MRS features”. Clin Imaging. 39 (3): 504–5. doi:10.1016/j.clinimag.2014.12.011. PMID 25586637.
  30. ↑ Leon LR, Bouchama A (2015). “Heat stroke”. Compr Physiol. 5 (2): 611–47. doi:10.1002/cphy.c140017. PMID 25880507.
  31. ↑ Leon LR, Bouchama A (2015). “Heat stroke”. Compr Physiol. 5 (2): 611–47. doi:10.1002/cphy.c140017. PMID 25880507.
  32. ↑ Bouchama A, Knochel JP (2002). “Heat stroke”. N Engl J Med. 346 (25): 1978–88. doi:10.1056/NEJMra011089. PMID 12075060.
Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

Heat stroke was first described by Hippocrates in 400 BC. Its prevention and treatment then described by Avicenna in 1020. Recent treatment advances is because of military experiences with heat exposure.

Historical perspective

The bible acknowledged several sunstroke death in farmers and workers. Juddith’s husband died because of sunstroke. Ancient Greek and Romans described how Sirius brought fever to men, describing the occasional use of term Siriasis as heat stroke.

  • Hippocrates, in 400 BC, first described how the violent heat from the sun may cause convulsion and fever.
  • Approximately in 400 BC, Herodotus, described how the Spartans were affected by thirst because of heat.
  • Heat stroke prevention, first described in 332 BC, when Alexander the great advised his army to do not march in sunny days without enough water supplies.
  • Avicenna, in 1020 described preventive measures and precaution for travelling in sunny days to avoid heat stroke in his book, The Canon of Medicine.
  • Edwin Babbit, is an American physician who described the impractical treatment for heat stroke in 1800.
  • In 1865, the first recorded death of a U.S. Navy sailor occurred due to heat stroke.
  • IN 1927, Wakefield and Hall, described the presenting features of heat stroke and its treatment.
  • During Civil Wars in 1885, 313 people died because of heat stroke.
  • Significant advances in understanding heat stroke developed during the Spanish-American War of 1898 by the U.S. Navy.
  • In a 1935 lecture presented to the Royal Society of Medicine in London, D.H.K. Lee differentiated heat stroke, heat exhaustion, and heat cramps as distinct illnesses with distinct etiologies.
  • During World War II, approximately 250 fatal cases of heat stroke occurred in the U.S. military, mostly in military basic training camps in the southern United States.
  • Army in 1943, stated, the most effective means of reducing pyrexia is by securing evaporation of water from the skin.

References

Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

On the basis of temperature, heat stroke must be differentiated from heat wave, heat stress, heat exhaustion, hyperthermia and multi-organ dysfunction syndrome. Heat stroke is classified to 2 types: Exertional heat stroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period in a hot environment and classic nonexertional heat stroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons.[1]

Classification

Heat related problems may be classified based on the temperature and the clinical presentation. The following table summarizes the related terms.[1][2]

Condition Definition
Heat wave Three or more consecutive days during which the air temperature is >32.2°C.
Heat stress Perceived discomfort and physiological strain associated with exposure to a hot environment, especially during physical work.
Heat stroke Severe illness characterized by a core temperature >40°C and central nervous system abnormalities such as delirium, convulsions,

or coma resulting from exposure to environmental heat (classic heat stroke) or strenuous physical exercise (exertional heat stroke).

Heat exhaustion Mild-to-moderate illness due to water or salt depletion that results from exposure to high environmental heat or strenuous physical

exercise; signs and symptoms include intense thirst, weakness, discomfort, anxiety, dizziness, fainting, and headache; core temperature

may be normal, below normal, or slightly elevated (>37°C but <40°C).

Hyperthermia A rise in body temperature above the hypothalamic set point when heat-dissipating mechanisms are impaired (by drugs or disease) or

overwhelmed by external (environmental or induced) or internal (metabolic) heat.

Multiorgan-dysfunction

syndrome

Continuum of changes that occur in more than one organ system after an insult such as trauma, sepsis, or heat stroke.

Heat stroke is classified to 2 types.

  • Exertional heat stroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period in a hot environment.
  • Classic nonexertional heat stroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons.[1]

References

  1. ↑ 1.0 1.1 Leon LR, Bouchama A (2015). “Heat stroke”. Compr Physiol. 5 (2): 611–47. doi:10.1002/cphy.c140017. PMID 25880507.
  2. ↑ Bouchama A, Knochel JP (2002). “Heat stroke”. N. Engl. J. Med. 346 (25): 1978–88. doi:10.1056/NEJMra011089. PMID 12075060.
|}
Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

Heat stress means perceived discomfort and physiologic strains during heat exposure. A series of physiologic events occur to adapt heat. These events include thermoregulation (with acclimatization), an acute-phase response, and production of heat shock proteins. If these sequence of actions fails to prevents body from high temperature, heat stress progresses to heat stroke. Thermoregulation, acclimatization, acute phase responses, and heat shock proteins are the important factors in response to heat stroke. Hypothalamus is the center of thermoregulation.[1][2][3][4] Increase in the peripheral body temperature will activate sympathetic response through thermoregulatory action of hypothalamus to deliver more blood flow by vasodilation of surface cutaneous veins. This increase in blood flow will cause sweating. The elevated blood temperature will cause tachycardia, increase in cardiac output, and increase in minute ventilation. [5][6][7] Blood shift from internal organs to the skin may cause decreased visceral perfusion and predispose them to ischemia. Increased sweating will cause loss of salt and water up to 2 liters per hour. Therefore, dehydration may worsen thermoregulation. [7][8]

Pathophysiology

Heat stress means perceived discomfort and physiologic strains during heat exposure. A series of physiologic events occur to adapt heat. These events include thermoregulation (with acclimatization), an acute-phase response, and production of heat shock proteins. If these sequence of actions fails to prevents body from high temperature, heat stress progresses to heat stroke.

 
 
 
 
 
 
 
 
Heat stroke
High body temperature with CNS dysfunction
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Tissue thermal injury
Necrotic/apoptotic cell death
 
 
 
 
Coagulopathies
Fibrin deposition Excessive bleeding
 
 
 
 
Immune modulators
Endotoxin, cytokines
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Systemic inflammatory response syndrome
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Multi-organ failure and death
 
 
 
 
 
 

Pathogenesis

Thermoregulation

The core body temperature is set to 37 °C. Thermoregulatory center is located in hypothalamus, every 1 °C in body temperature activates the peripheral and central receptors to maintain core body temperature at 37 °C.[4] Increase in the peripheral body temperature will activate sympathetic response through thermoregulatory action of hypothalamus to deliver more blood flow by vasodilation of surface cutaneous veins. This increase in blood flow will cause sweating. The elevated blood temperature will cause tachycardia, increase in cardiac output, and increase in minute ventilation. [5][6][7] Blood shift from internal organs to the skin may cause decreased visceral perfusion and predispose them to ischemia. Increased sweating will cause loss of salt and water up to 2 liters per hour. Therefore, dehydration may worsen thermoregulation. [7][8]

Acclimatization

The process of body adaptation to heat which, might take up to 3 weeks is called acclimatization. Acclimatization, involves enhancement of cardiovascular performance, activation of the renin–angiotensin–aldosterone axis, salt conservation by the sweat glands and kidneys, an increase in the capacity to secrete sweat, expansion of plasma volume, an increase in the glomerular filtration rate, and an increase in the ability to resist exertional rhabdomyolysis.[9]

Acute-Phase Response

Endothelial cells, leukocytes, and epithelial cells incorporate a variety of cytokines (mainly interleukin-1 and interleukin-6) to protect against tissue injury and promote repair. A similar event occur in sepsis.[10]

Heat-Shock Response

Heat-shock proteins are secreted in response to heat to protect cells from injury. Heat-shock proteins bind to proteins and act as chaperons to prevent them from denaturation. [1][2][3]

Microscopic findings

Severe heat stroke causes vascular congestion and/or hemorrhage, thrombi, increased inflammatory cells, and disruption of architecture in many internal organs including: liver, jejunum, spleen, lungs, and kidneys. Angiotelectasis, congestion, and thickening of the lung matrix are another pathological findings.[11]

Gross pathological findings

Hyperemia and edema associated with microhemorrhages are common pathological findings in post mortem surveys.


References

  1. ↑ 1.0 1.1 Yang YL, Lin MT (1999). “Heat shock protein expression protects against cerebral ischemia and monoamine overload in rat heatstroke”. Am. J. Physiol. 276 (6 Pt 2): H1961–7. PMID 10362676.
  2. ↑ 2.0 2.1 Li PL, Chao YM, Chan SH, Chan JY (2001). “Potentiation of baroreceptor reflex response by heat shock protein 70 in nucleus tractus solitarii confers cardiovascular protection during heatstroke”. Circulation. 103 (16): 2114–9. PMID 11319204.
  3. ↑ 3.0 3.1 Welch WJ (1992). “Mammalian stress response: cell physiology, structure/function of stress proteins, and implications for medicine and disease”. Physiol. Rev. 72 (4): 1063–81. PMID 1438579.
  4. ↑ 4.0 4.1 Grossman, Moses (1997). “Fever: Basic Mechanisms and Management”. JAMA: The Journal of the American Medical Association. 278 (5): 441. doi:10.1001/jama.1997.03550050105047. ISSN 0098-7484.
  5. ↑ 5.0 5.1 Buono MJ, Sjoholm NT (1988). “Effect of physical training on peripheral sweat production”. J. Appl. Physiol. 65 (2): 811–4. PMID 3170430.
  6. ↑ 6.0 6.1 NELSON N, EICHNA LW (1947). “Thermal exchanges of man at high temperatures”. Am. J. Physiol. 151 (2): 626–52. PMID 18901907.
  7. ↑ 7.0 7.1 7.2 7.3 Adams WC, Fox RH, Fry AJ, MacDonald IC (1975). “Thermoregulation during marathon running in cool, moderate, and hot environments”. J Appl Physiol. 38 (6): 1030–7. PMID 1141115.
  8. ↑ 8.0 8.1 Deschamps A, Levy RD, Cosio MG, Marliss EB, Magder S (1989). “Effect of saline infusion on body temperature and endurance during heavy exercise”. J. Appl. Physiol. 66 (6): 2799–804. PMID 2745343.
  9. ↑ Knochel JP (1990). “Catastrophic medical events with exhaustive exercise: “white collar rhabdomyolysis““. Kidney Int. 38 (4): 709–19. PMID 2232508.
  10. ↑ Kurahashi K, Kajikawa O, Sawa T, Ohara M, Gropper MA, Frank DW, Martin TR, Wiener-Kronish JP (1999). “Pathogenesis of septic shock in Pseudomonas aeruginosa pneumonia”. J. Clin. Invest. 104 (6): 743–50. doi:10.1172/JCI7124. PMC 408437. PMID 10491409.
  11. ↑ Liu ZF, Li BL, Tong HS, Tang YQ, Xu QL, Guo JQ, Su L (2011). “Pathological changes in the lung and brain of mice during heat stress and cooling treatment”. World J Emerg Med. 2 (1): 50–3. PMC 4129731. PMID 25214983.
Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

Excessive exercise in warm weather is the most common cause heat stroke.[1]

Causes

Excessive exercise in warm weather is the most common cause heat stroke.[1]

References

  1. ↑ 1.0 1.1 Bouchama A, Knochel JP (2002). “Heat stroke”. N. Engl. J. Med. 346 (25): 1978–88. doi:10.1056/NEJMra011089. PMID 12075060.
Differentiating Any Disease from other Diseases

Differentiating Any Disease from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

Heat stroke must be differentiated from other disease that may cause alteration in mental status and hyperthermia including: Neuroleptic malignant syndrome, Malignant hyperthermia, Serotonin syndrome, cocaine use and sepsis.[1][2][3][4][5][6]

Differentiating Heat stroke from other Diseases

Differentiation between 2 types of heat stroke (Classic vs Exertional) is based on history, clinical findings, and laboratory findings.[7][8] The following table summarizes their differentiating feature.

Characteristic Exertional Heat Stroke Classic Heat Stroke
Age Adults Early childhood or elderly
Health status Healthy and athlete Ill and debilitate
Weather condition Temperate or hot Heat wave
Activity Sustained or heavy exertion Sedentary
Medications or drug use Ergogenic aids, ecstasy, cocaine Diuretics, β-blockers, antihistamines,

antidepressants

Sweating Present Abscent
Laboratory findings Acid-base disturbance Metabolic acidosis Mixed metabolic and respiratory acidosis
Calcium ↓ Nl
Potassium ↓ or ↑ Nl
Phosphate ↑ ↓
Blood glucose ↓ ↑
Creatine kinase (CK) ↑↑↑ ↑
AST, ALT ↑↑↑ ↑
Complications Rhabdomyolysis Severe Mild
Acute renal failure Common (∼25%) Uncommon (∼5%)

Differentiating Heat stroke from other Diseases that may cause hyperthermia and altered mental status

Heat stroke must be differentiated from other conditions that may cause hyperthermia and altered mental status.[1][2][3][4][5][6]

Disease Symptoms and signs Labs Other findings
Heat stroke Electrolyte disturbances, increased CK, AST, and ALT Relevant history of excessive exercise and lack of water access
Sepsis
  • Altered mental status (confusion, altered consciousness, coma, or seizure)
  • Respiratory rate ≥22/minute
  • Systolic blood pressure ≤100 mmHg
 Thrombocytopenia, leukocytosis, leukopenia, elevated Cr
Malignant hyperthermia Hypercarbia (PaCO2) >65 mmHg, hyperkalemia History of receiving anaesthetic agent
Neuroleptic malignant syndrome Electrolyte disturbances, increased CK, LDH, ALP, AST, and ALT, leukocytosis, myoglobinuria. Relevant history of recent use of anti-psychotics
Serotonin syndrome Elevated CK, LDH, ALP, AST, and ALT History of recent use of SSRIs, SNRIs , or MAOIs.

References

  1. ↑ 1.0 1.1 Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC (2016). “The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)”. JAMA. 315 (8): 801–10. doi:10.1001/jama.2016.0287. PMC 4968574. PMID 26903338.
  2. ↑ 2.0 2.1 Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, Rubenfeld G, Kahn JM, Shankar-Hari M, Singer M, Deutschman CS, Escobar GJ, Angus DC (2016). “Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)”. JAMA. 315 (8): 762–74. doi:10.1001/jama.2016.0288. PMC 5433435. PMID 26903335.
  3. ↑ 3.0 3.1 Carbone JR (2000). “The neuroleptic malignant and serotonin syndromes”. Emerg. Med. Clin. North Am. 18 (2): 317–25, x. PMID 10767887.
  4. ↑ 4.0 4.1 Bodner RA, Lynch T, Lewis L, Kahn D (1995). “Serotonin syndrome”. Neurology. 45 (2): 219–23. PMID 7854515.
  5. ↑ 5.0 5.1 Ener RA, Meglathery SB, Van Decker WA, Gallagher RM (2003). “Serotonin syndrome and other serotonergic disorders”. Pain Med. 4 (1): 63–74. PMID 12873279.
  6. ↑ 6.0 6.1 Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB (2010). “Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006”. Anesth. Analg. 110 (2): 498–507. doi:10.1213/ANE.0b013e3181c6b9b2. PMID 20081135.
  7. ↑ Bouchama A, Knochel JP (2002). “Heat stroke”. N. Engl. J. Med. 346 (25): 1978–88. doi:10.1056/NEJMra011089. PMID 12075060.
  8. ↑ O’Connor FG, Casa DJ, Bergeron MF, Carter R, Deuster P, Heled Y, Kark J, Leon L, McDermott B, O’Brien K, Roberts WO, Sawka M (2010). “American College of Sports Medicine Roundtable on exertional heat stroke–return to duty/return to play: conference proceedings”. Curr Sports Med Rep. 9 (5): 314–21. doi:10.1249/JSR.0b013e3181f1d183. PMID 20827100.
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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

The United States Centers for Disease Control (CDC) reports an average of 9000 cases per year among high school athletes. The highest incidence of heat stroke in athletes in the United States has been reported among football players. Young athletes are more prone to exertional heat stroke while, classic heat stroke is more common among elderly. Men are more affected by heat stroke than women.

Epidemiology and demographics

  • The United States Centers for Disease Control report a weighted average of 9237 cases of exercise heat stroke among high school athletes per year for the period 2005 to 2009.[1]
  • Its incidence has been increased among the United States military personnel in 2014 compared to 2013 despite preventive measures.

Incidence

  • In Saudi Arabia, the incidence varies seasonally, from 22 to 250 cases per 100,000 population.[2]
  • Epidemiologic studies showed an incidence of 17.6 to 26.5 cases per 100,000 population in urban areas of the United States during heat waves.[3]
  • The highest incidence of exertional heat stroke in athletes in the United States is among football players and it’s approximately 4.5 cases per 100,000 athlete exposures.[1]
  • There are various reports of death among American football players ranged from 1 to 31 from 1995 till 2008.

Age

Exertional heat stroke

Exertional heat stroke is more common in age group 15-50 years.

Classic heat stroke

Classic heat stroke is more common in early childhood and elderly.

Sex

Exertional heat stroke is more common among men than in women.

Race

Heat stroke is more common among Asian/Pacific Islander than other ethnicities.

References

  1. ↑ 1.0 1.1 “Heat illness among high school athletes — United States, 2005-2009”. MMWR Morb. Mortal. Wkly. Rep. 59 (32): 1009–13. 2010. PMID 20724966.
  2. ↑ Gatrad AR, Sheikh A (2005). “Hajj: journey of a lifetime”. BMJ. 330 (7483): 133–7. doi:10.1136/bmj.330.7483.133. PMC 544433. PMID 15649928.
  3. ↑ Jones TS, Liang AP, Kilbourne EM, Griffin MR, Patriarca PA, Wassilak SG, Mullan RJ, Herrick RF, Donnell HD, Choi K, Thacker SB (1982). “Morbidity and mortality associated with the July 1980 heat wave in St Louis and Kansas City, Mo”. JAMA. 247 (24): 3327–31. PMID 7087075.
Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

Common risk factors for heat stroke include: excessive exercise in hot weather, lack of air movement, lack of water access, high humidity, obesity, acute illness, and certain drugs.

Risk Factors

Common risk factors to develop heat stroke could be divided in to 4 major groups:[1][2][3][4][5]

Environmental factors

  • Heat waves
  • High humidity
  • Lack of air movement
  • Urban heat islands
  • Lack of air conditioning

Compromised health condition

Genetic conditions

Medications

Classic heat stroke

Exertional heat stroke

References

  1. ↑ Bricknell MC (1994). “Heat illness in Cyprus”. J R Army Med Corps. 140 (2): 67–9. PMID 8907832.
  2. ↑ Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO (2009). “Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980-2006”. Circulation. 119 (8): 1085–92. doi:10.1161/CIRCULATIONAHA.108.804617. PMID 19221222.
  3. ↑ “Heat illness among high school athletes — United States, 2005-2009”. MMWR Morb. Mortal. Wkly. Rep. 59 (32): 1009–13. 2010. PMID 20724966.
  4. ↑ Capacchione JF, Muldoon SM (2009). “The relationship between exertional heat illness, exertional rhabdomyolysis, and malignant hyperthermia”. Anesth. Analg. 109 (4): 1065–9. doi:10.1213/ane.0b013e3181a9d8d9. PMID 19617585.
  5. ↑ Armstrong LE, Casa DJ, Watson G (2006). “Exertional hyponatremia”. Curr Sports Med Rep. 5 (5): 221–2. PMID 16934202.

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Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

There is insufficient evidence to recommend routine screening for heat stroke.

Screening

There is insufficient evidence to recommend routine screening for heat stroke. However, close monitoring of athletes, runners, and military forces during hot weather is logical.

References

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Usama Talib, BSc, MD [3]

Overview

If heat stroke left untreated it may result in severe complications and even death. its complications include: multiple organ failure, acute renal failure, myocardial injury and even DIC. Timely resuscitation and fluid replacement decreases the mortality and can prevent sustained brain injury, which is the most important prognostic factor.

Natural History

Heat stroke presents with altered mental status and signs of dehydration. Its symptoms develop in a susceptible person who did excessive exercise in hot weather. If left untreated it may result in severe complications and eventually death.

Complications

The complications of heat stroke include:[1][2]

Life Threatening complications

Common Complications

Rare Complications

The rare complications include:[1][2]

Prognosis

The revival of the functioning of the central nervous system is a positive prognostic sign. It is usually seen following aggressive therapy. 20% patients face residual damage of the brain and a higher mortality is associated with this.[3][4]

References

  1. ↑ 1.0 1.1 Masood U, Sharma A, Syed W, Manocha D (2016). “Bowel Ischemia from Heat Stroke: A Rare Presentation of an Uncommon Complication”. Case Rep Med. 2016: 5217690. doi:10.1155/2016/5217690. PMC 5093235. PMID 27840645.
  2. ↑ 2.0 2.1 al-Mashhadani SA, Gader AG, al Harthi SS, Kangav D, Shaheen FA, Bogus F (1994). “The coagulopathy of heat stroke: alterations in coagulation and fibrinolysis in heat stroke patients during the pilgrimage (Haj) to Makkah”. Blood Coagul Fibrinolysis. 5 (5): 731–6. PMID 7865679.
  3. ↑ Hart GR, Anderson RJ, Crumpler CP, Shulkin A, Reed G, Knochel JP (1982). “Epidemic classical heat stroke: clinical characteristics and course of 28 patients”. Medicine (Baltimore). 61 (3): 189–97. PMID 7078400.
  4. ↑ Dematte JE, O’Mara K, Buescher J, Whitney CG, Forsythe S, McNamee T; et al. (1998). “Near-fatal heat stroke during the 1995 heat wave in Chicago”. Ann Intern Med. 129 (3): 173–81. PMID 9696724.
Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Chest X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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