Heat Stroke


Article Author:
Andrew Morris


Article Editor:
Gaurav Patel


Editors In Chief:
William Gossman


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
1/29/2019 11:58:30 PM

Introduction

Heat-related illness is a spectrum of conditions progressing from heat exhaustion, heat injury, to life-threatening heat stroke. Heat stroke is a clinical constellation of symptoms that include a severe elevation in body temperature which typically, but not always, is greater than 40°C. Also, there must be clinical signs of central nervous system dysfunction that may include ataxia, delirium, or seizures, in the setting of exposure to hot weather or strenuous physical exertion.[1] Risk factors include environmental variables, medications, drug use, and other medical comorbidities.[2]

Etiology

It is important to differentiate where the patient is on the heat illness continuum. The signs and symptoms of heat exhaustion may present similarly include cramping, fatigue, dizziness, nausea, vomiting, headache. If progression to end organ damage occurs it then becomes heat injury. Finally, neurologic alteration distinguishes heat stroke from heat injury.

There are two forms of heat stroke, classic and exertional. Classic heat stroke typically affects elderly individuals with chronic medical conditions while exertional heat stroke affects otherwise healthy people who engage in strenuous exercise in hot or humid weather.[3]

Epidemiology

Estimating the public health impact of extreme heat is difficult because health care providers are not required to report heat-related illnesses. In the United States, from 2006 to 2010, there were at least 3332 deaths attributed to heat stroke.[4] However, these numbers are believed to be largely under-reported. Mortality correlates with the degree of body temperature elevation, time to initiation of cooling, and the number of organ systems affected.[5]

Pathophysiology

Normally, thermoregulation is an extremely efficient process, with a mere 1°C change in core temperature for every 25°C to 30°C change in ambient temperature.[2] In the adapted state, heat-shock proteins repair the damage caused by hyperthermia. The body’s ability to dissipate heat through increased cardiac output, vasoconstriction of splanchnic circulation, and sweating maintains the effective temperature range of these proteins. However, if environmental humidity is above 75%, evaporative cooling begins to become ineffective. The other methods of heat loss, including radiation, conduction, and convection, do not transfer heat well when the temperature outside the body exceeds the temperature of the skin.[6]

Subsequent inadequate water repletion may lead to substantial electrolyte abnormalities. Primarily, normonatremia or hypernatremia dehydration follows. If severe enough, it may lead to hemorrhage, brain edema, and permanent brain damage. Rarely, hyponatremia occurs following overcompensation with hypotonic fluid repletion seen in marathon runners and other exertional heat stroke populations.[2] Hyperkalemia has been associated with heat stroke, which occurs as potassium is released from muscle breakdown or acidosis causing a shift of potassium from cells to plasma. Potassium is a potent vasodilator in skeletal and cardiac muscle, and severe reductions in this electrolyte will lead to cardiovascular instability and reduced muscle blood flow that predisposes to rhabdomyolysis.[1] Sequelae from rhabdomyolysis can range from mild hypocalcemia to acute renal failure. Hyperkalemia and hypocalcemia together can lead to cardiac conduction abnormalities including QT interval prolongation, ST segment changes, and in rare instances may lead to fatal cardiac arrhythmias.[6]

There is also a range of coagulopathies associated with heat stroke, from simple activation of coagulation cascade and fibrinolysis to fatal hemorrhage or disseminated intravascular coagulation.  Endothelial damage from heat is thought to cause downstream effects that result in platelet aggregation and microvascular thrombosis predisposing to consumptive coagulation, which paradoxically causes bleeding when platelets get used quicker than the body's ability to produce them.[2]

History and Physical

Patients who present with heat stroke typically have vital sign abnormalities to include an elevated core body temperature, sinus tachycardia, tachypnea, a widened pulse pressure, and a quarter of patients will be hypotensive. Other associated presenting signs/symptoms may be weakness, lethargy, nausea, vomiting, dizziness, flushing, lung crackles, oliguria, excessive bleeding, and evidence of neurologic dysfunction.[1] Classic heat stroke patients often present with hot, dry skin because of a failure of the normal sweating response, also known as anhidrosis. Whereas in exertional heat stroke, anhidrosis is an uncommon finding. Instead, prolonged sweating occurs following the cessation of exercise.[6]

Evaluation

The workup of patients presenting with possible heat stroke should include frequent monitoring of vital signs, a rectal temperature, as well as laboratory studies CBC, CMP, PT/PTT, blood gasses, serum CPK, and urine myoglobin. Based on clinical judgment, some patients may also benefit from toxicology screening, a chest radiograph, and an EKG.[3] EKG changes may show ST depression, QT prolongation, and other T-wave changes consistent with ischemia. All patients with heat stroke will have tachypnea and tachycardia. The arterial C02 levels will often dip below 20 mmHg and a quarter of the patients will be hypotensive.[2] Medical reconciliation is crucial when evaluating suspected classic heat stroke patients with emphasis on the recognition of diuretic, beta-blocker, and anticholinergic medications.

In classical heat stroke, respiratory alkalosis predominates, whereas exertional heat stroke may also have concomitant lactic acidosis. Electrolyte derangements are variable between the two etiologies, but commonly in exertional heat stroke hypocalcemia, hyperphosphatemia, and hyperkalemia reflect muscle breakdown that occurs. Rhabdomyolysis is more common in exertional than cloassical heat stroke, with a higher elevation of CPK markers reported. In classic heat stroke, AST and ALT elevations are the most common lab abnormalities reported.[2] Associated kidney injury, liver manifestations, and other end-organ damage may also occur in either presentation.[1]

Treatment / Management

Management of heat stroke includes ensuring adequate airway protection, breathing, and circulation.  After ABC’s, rapid cooling becomes the mainstay of treatment with ancillary management in response to other end-organ damage. Intubation for profound unconsciousness is rarely needed, as rapid cooling quickly improves the Glasgow coma scale.[6] Adequate rehydration is essential without over correcting the sodium if derangements exist. It is mandatory to measure core temperature with a rectal or esophageal probe continually and cooling measures should be stopped once the temperature is 38 to 39 degrees Celsius. No definitive studies support any cooling method over another.[7] Ice bath immersion is the timeliest to reduce core body temperature, however, in older populations, it may not be realistic as cardiac monitoring may not be feasible and extreme agitation may hinder compliance.[8] Other common methods include ice pack applications to the groin or axilla and evaporative cooling using a fan with cool saline on the skin of patients.

Several pharmacologic adjuncts also merit consideration in the treatment of heat stroke. Dantrolene is a skeletal muscle relaxer, shown to reduce heat production in sustained muscle contracture and is useful for the treatment of malignant hyperthermia. However, it has been shown to have no effect on patient outcomes with heat stroke.[9] A small study suggested that high dose benzodiazepine may blunt the shivering reflex and decrease oxygen consumption, therefore providing a theoretical benefit to patients. The problem is that heat stroke patients may be unable to compensate through mechanisms such as shivering.[10] Therefore the universal use of benzodiazepines is not the current recommendation but could be tailored to the shivering, agitated patient. There is no role for antipyretics for the treatment of heatstroke patients and may be toxic to the liver.[1]

Differential Diagnosis

The common differentials include polypharmacy, toxic ingestions, meningitis, sepsis, neuroleptic malignant syndrome, serotonin syndrome, and malaria. Detailed medication review can exclude several of these disease processes. Except for heat cramps, neither muscle rigidity nor muscle clonus are signs of heat stroke and can distinguish neuroleptic malignancy and serotonin syndrome. Travel history should be questioned, evaluating exposure to malaria endemic environments and the particular malaria species in that area. However, malaria, sepsis, or meningitis will not be commonly present with the same elevations in core body temperature.

Prognosis

Patients presenting with heat stroke have high mortality depending on the etiology of the presentation. However, the death rate from exertional heat stroke is relatively low (3 to 5%) compared to classic heat stroke (10 to 65%).[5][4] 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.[4]

Complications

The sequelae of the insult may persist beyond the initial CNS dysfunction, involving injury to the gut, kidney, skeletal muscle, or other organ systems. Complications of heat stroke include acute respiratory distress syndrome, disseminated intravascular coagulation, acute kidney injury, hepatic injury, hypoglycemia, rhabdomyolysis, and seizures.[5] Despite normalization of core temperature with cooling, many patients continue to display core temperature disturbances and multi-organ dysfunction. Research has shown that even reversible complications following heat stroke may take longer than 7 weeks to resolve.[11]

Deterrence and Patient Education

Prevention is the definitive treatment for heat stroke. It is essential to check on the elderly frequently, especially individuals who do not have access to air-conditioning. Wear appropriate clothing, avoid leaving children unattended in cars, and reschedule strenuous activity if there is hot, humid weather. [6] Individuals should seek shade if experiencing the signs and symptoms of heat stroke. Once the clinician has diagnosed heat stroke, rapid cooling should initiate immediately with careful monitoring and reassessment.  After treatment for exertional heat stroke, the patient must abstain from exercise for 7 days minimum. Follow-up in all cases should occur a week after presentation to screen for signs of end-organ damage.[12][6]

Enhancing Healthcare Team Outcomes

Optimal treatment in heatstroke patients relies on early recognition and expedition of rapid cooling. If expecting a heatwave, a designated area with equipment for multiple patients should be available in the emergency department. The physician should understand what resources are available for cooling patients, as each facility may use evaporative, ice-bath, or other methodology depending on its protocol. Careful coordination with nursing staff is necessary as close monitoring of patients with either a continuous rectal or esophageal temperature probe is necessary with careful communication to stop cooling measures at the desired 38 to 39°C. The physician should identify patients requiring cardiac monitoring and additional consultants, including intensivists, should be contacted early in the management if other end-organ damage has occurred. The use of dantrolene has been shown in several small trials to be ineffective and is not a reocmmendation in the treatment of heat stroke (Class 1).[9] The use of benzodiazepines in heat stroke may have merit for the appropriate patient that is agitated and shivering; however empiric treatment is inadvisable until further studies are undertaken (Class II).[10][8] Finally, expedited rapid cooling has been shown in several RCT both directly and indirectly to be the most effective treatment to limit mortality in heatstroke (Class 1).[8]


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Heat Stroke - Questions

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A 78-year-old female was found unresponsive in her apartment during a heat wave. She has shallow respirations and rigid muscles, and her skin is warm and dry. Which of the following is an inaccurate statement about the known complications of her condition?



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Which of the following is the best initial treatment for heat stroke?



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Which of the following is the best way to prevent heat illnesses in high school athletes?



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Which of the following people is at lowest risk for heat-related illness?



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A patient was doing yard work in 100-degree weather. He is confused with a temperature of 104 degrees F. What is the most likely diagnosis?



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How long should a patient recovering from heat stroke avoid heat exposure?



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What is the most severe of the heat-related illnesses?



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Out of the following, who would be at highest risk for a heat-related injury?



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A patient presents with a rectal temperature of 106 F, muscle cramps, headache, and confusion. What is the most likely diagnosis?



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You are lecturing the local soccer team about the dangers of heat-related injuries that occur when practicing outside in Florida. Of the following, which is the most dangerous form of heat-injury?



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Of the following, what puts patients at the largest risk for heat illness?



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Heat stroke is a serious condition that can have a wide variety of complications. Which of the following is not a complication of heat stroke?



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A 10-year-old, 30 kg female presents with dizziness, vomiting, and fatigue after spending the day at a soccer tournament. She opens her eyes only to speech, follows simple commands, and answers with confusing, inappropriate responses. Her vitals are BP 105/70 mmHg, HR 125 bpm, RR 25/minute, T 41 C rectally. What is the initial management?



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Out of the following, who would be at highest risk for a heat-related emergency?



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A 17-year-old female collapses at the finish line of a marathon. It is 95 F. After establishing that the patient's airway is intact, she is breathing, and has a pulse, what vital sign should be obtained?



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A 17-year-old male is brought to the emergency department. His friend says they were biking all morning, and it was very sunny. His friend began to act weird and was unable to ride his bike. The patient is hot, dry, vomiting, and unsteady on his feet. He has no medical history, and was in his usual state of health this morning, and has not ingested any substances. What is the most likely diagnosis?



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Heat Stroke - References

References

Heat stroke., Leon LR,Bouchama A,, Comprehensive Physiology, 2015 Apr     [PubMed]
Heat-related deaths--Chicago, Illinois, 1996-2001, and United States, 1979-1999.,, MMWR. Morbidity and mortality weekly report, 2003 Jul 4     [PubMed]
Misdiagnosis of exertional heat stroke and improper medical treatment., Druyan A,Janovich R,Heled Y,, Military medicine, 2011 Nov     [PubMed]
Early organ dysfunction course, cooling time and outcome in classic heatstroke., Pease S,Bouadma L,Kermarrec N,Schortgen F,Régnier B,Wolff M,, Intensive care medicine, 2009 Aug     [PubMed]
Cold water immersion: the gold standard for exertional heatstroke treatment., Casa DJ,McDermott BP,Lee EC,Yeargin SW,Armstrong LE,Maresh CM,, Exercise and sport sciences reviews, 2007 Jul     [PubMed]
Bouchama A,Knochel JP, Heat stroke. The New England journal of medicine. 2002 Jun 20;     [PubMed]
Wexler RK, Evaluation and treatment of heat-related illnesses. American family physician. 2002 Jun 1;     [PubMed]
Gaudio FG,Grissom CK, Cooling Methods in Heat Stroke. The Journal of emergency medicine. 2016 Apr;     [PubMed]
Adams T,Stacey E,Stacey S,Martin D, Exertional heat stroke. British journal of hospital medicine (London, England : 2005). 2012 Feb;     [PubMed]
Rashad FM,Fathy HM,El-Zayat AS,Elghonaimy AM, Isolation and characterization of multifunctional Streptomyces species with antimicrobial, nematicidal and phytohormone activities from marine environments in Egypt. Microbiological research. 2015 Jun;     [PubMed]
Bouchama A,Cafege A,Devol EB,Labdi O,el-Assil K,Seraj M, Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Critical care medicine. 1991 Feb;     [PubMed]
Hostler D,Northington WE,Callaway CW, High-dose diazepam facilitates core cooling during cold saline infusion in healthy volunteers. Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme. 2009 Aug;     [PubMed]

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