Heat stroke overview
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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
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Buono MJ, Sjoholm NT (1988). "Effect of physical training on peripheral sweat production". J. Appl. Physiol. 65 (2): 811–4. PMID 3170430.
- ↑ NELSON N, EICHNA LW (1947). "Thermal exchanges of man at high temperatures". Am. J. Physiol. 151 (2): 626–52. PMID 18901907.
- ↑ 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.
- ↑ 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.
- ↑ Bouchama A, Knochel JP (2002). "Heat stroke". N. Engl. J. Med. 346 (25): 1978–88. doi:10.1056/NEJMra011089. PMID 12075060.
- ↑ 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.
- ↑ 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.
- ↑ Carbone JR (2000). "The neuroleptic malignant and serotonin syndromes". Emerg. Med. Clin. North Am. 18 (2): 317–25, x. PMID 10767887.
- ↑ Bodner RA, Lynch T, Lewis L, Kahn D (1995). "Serotonin syndrome". Neurology. 45 (2): 219–23. PMID 7854515.
- ↑ Ener RA, Meglathery SB, Van Decker WA, Gallagher RM (2003). "Serotonin syndrome and other serotonergic disorders". Pain Med. 4 (1): 63–74. PMID 12873279.
- ↑ 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.
- ↑ Bricknell MC (1994). "Heat illness in Cyprus". J R Army Med Corps. 140 (2): 67–9. PMID 8907832.
- ↑ 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.
- ↑ "Heat illness among high school athletes --- United States, 2005-2009". MMWR Morb. Mortal. Wkly. Rep. 59 (32): 1009–13. 2010. PMID 20724966.
- ↑ 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.
- ↑ Armstrong LE, Casa DJ, Watson G (2006). "Exertional hyponatremia". Curr Sports Med Rep. 5 (5): 221–2. PMID 16934202.
- ↑ Simon HB (1994). "Hyperthermia and heatstroke". Hosp Pract (Off Ed). 29 (8): 65–8, 73, 78–80. PMID 7914522.
- ↑ Bricknell MC (1994). "Heat illness in Cyprus". J R Army Med Corps. 140 (2): 67–9. PMID 8907832.
- ↑ Leon LR, Bouchama A (2015). "Heat stroke". Compr Physiol. 5 (2): 611–47. doi:10.1002/cphy.c140017. PMID 25880507.
- ↑ Tek D, Olshaker JS (1992). "Heat illness". Emerg Med Clin North Am. 10 (2): 299–310. PMID 1559470.
- ↑ 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.
- ↑ 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.
- ↑ Tek D, Olshaker JS (1992). "Heat illness". Emerg Med Clin North Am. 10 (2): 299–310. PMID 1559470.
- ↑ 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.
- ↑ 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.
- ↑ Leon LR, Bouchama A (2015). "Heat stroke". Compr Physiol. 5 (2): 611–47. doi:10.1002/cphy.c140017. PMID 25880507.
- ↑ Leon LR, Bouchama A (2015). "Heat stroke". Compr Physiol. 5 (2): 611–47. doi:10.1002/cphy.c140017. PMID 25880507.
- ↑ Bouchama A, Knochel JP (2002). "Heat stroke". N Engl J Med. 346 (25): 1978–88. doi:10.1056/NEJMra011089. PMID 12075060.