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Heat Stroke
Kingdom of Saudi ArabiaMinistry of HealthDirectorate of Health Affairs in GurayatGurayat General Hospital
Dr.Hisham Abid AldabaghMSc. Internal Medicine
Definition
•Heatstroke is defined typically as hyperthermiaexceeding 41°C (106 °F) and anhidrosis associatedwith an altered sensorium.
Forms
1- Classic, or nonexertional, heatstroke (NEHS)
• Classic heatstroke, which occurs during environmental heatwaves, is more common in the very young and the elderlyand should be suspected in children, elderly persons, andchronically ill individuals who present with an alteredsensorium.
Classic heatstroke occurs because of failure of the body's heat dissipating mechanisms
2- Exertional heatstroke (EHS). • EHS affects young, healthy individuals who engage in
strenuous physical activity, and EHS should be suspected inall such individuals who exhibit bizarre, irrational behavioror experience syncope.
•
• Both types of heatstroke are associated with high morbidityand mortality, especially when cooling therapy is delayed.
EHS results from increased heat production, which overwhelms the body's ability to dissipate heat.
Exertional heatstroke• EHS is characterized by hyperthermia, diaphoresis, and an
altered sensorium, which may manifest suddenly duringextreme physical exertion in a hot environment.
• A number of symptoms (eg, abdominal and muscularcramping, nausea, vomiting, diarrhea, headache, dizziness,dyspnea, weakness) commonly precede the heatstroke andmay remain unrecognized.
• Syncope and loss of consciousness also are observedcommonly before the development of EHS.
• EHS commonly is observed in young, healthy individuals(eg, athletes, firefighters, military personnel).
• Because their ability to sweat remains intact, patients withEHS are able to cool down after cessation of physicalactivity and may present for medical attention withtemperatures well below 41°C.
• Despite education and preventive measures, EHS is still aleading cause of disability and death in high school athletes,particularly football players.
Risk factors
• A preceding viral infection, dehydration, fatigue, obesity,lack of sleep, poor physical fitness, and lack ofacclimatization.
• EHS also may occur because of increased motor activity dueto drug use, such as cocaine and amphetamines, and as acomplication of status epilepticus.
Non exertional heatstroke
• NEHS is characterized by hyperthermia, anhidrosis, and analtered sensorium, which develop suddenly after a periodof prolonged elevations in ambient temperatures (ie, heatwaves).
• Core body temperatures greater than 41°C are diagnostic,although heatstroke may occur with lower core bodytemperatures.
• Classic heatstroke most commonly occurs during episodesof prolonged elevations in ambient temperatures.
• It affects people who are unable to control theirenvironment and water intake (eg, infants, elderly persons,individuals who are chronically ill), people with reducedcardiovascular reserve, and people with impaired sweating(e.g., from skin disease or ingestion of anticholinergic orpsychiatric drugs).
Epidemiology• Frequency
• Overall incidence studies in the US shows that the incidence ofheat stroke is between 17.6 to 26.5 cases per 100,000population.
• In Saudi Arabia, the incidence of heat stroke varies seasonally,from 22 to 250 cases per 100,000 population.
• According to the Centers for Disease Control and Prevention,8,015 deaths were attributed to excessive heat exposure from1979-2003, or an average of approximately 334 deaths per yearin United States
Racial and sexual disparities in incidence
• Heatstroke affects all races equally. However, because ofdifferences in social advantages, the annual death rate dueto environmental conditions is more than 3 times higher inblacks than in whites.
• Heatstroke affects both genders equally. However, becauseof gender differences in the workforce, the annual deathrate due to environmental conditions is 2 times higher inmen than in women.
Age-related disparities in incidence
• Infants, children, and elderly persons have a higherincidence of heatstroke than young, healthy adults.
• Exertional heat stroke (EHS) is a leading cause of injury anddeath in high school athletes; approximately two-thirds ofsuch cases occur in August and involve football players,often those who are obese or overweight.
With the influence of global warming, it is predicted that the incidence of heatstroke cases and fatalities will also become more prevalent.
Behavioral responses are important in the management oftemperature elevations and may provide clues to preventingthe development of heatstroke.
Pathophysiology
• Excessive heat denatures proteins, destabilizes phospholipids andlipoproteins, and liquefies membrane lipids, leading to cardiovascularcollapse, multiorgan failure, and, ultimately, death.
• In a simplified model, thermosensors located in the skin, muscles, andspinal cord send information regarding the core body temperature to theanterior hypothalamus, where the information is processed andappropriate physiologic and behavioral responses are generated.Physiologic responses to heat include an increase in cardiac output andblood flow to the skin (as much as 8 L/min), which is the major heat-dissipating organ; dilatation of the peripheral venous system; andstimulation of the eccrine sweat glands to produce more sweat.
• iHypothalamic dysfunction may alter temperature regulation and mayresult in an unchecked rise n temperature and heat illness.
Physical Examination
• Vital signs
• Temperature: Typically, temperature exceeds 41°C.
• Pulse: Tachycardia, exceeding 130 beats per minute is common.
• Blood pressure: Patients commonly are normotensive, with awide pulse pressure; however, hypotension is common andmay result from a number of factors, including vasodilation ofthe cutaneous vessels, pooling of the blood in the venoussystem, and dehydration.
Central nervous system• Symptoms may range from irritability to coma.
• Patients may present with delirium, confusion, delusions, convulsions,hallucinations, ataxia, tremors, dysarthria, and other cerebellar findings,as well as cranial nerve abnormalities and tonic and dystonic contractionsof the muscles. Patients also may exhibit decerebrate posturing,decorticate posturing, or they may be limp.
• Coma also may be caused by electrolyte abnormalities, hypoglycemia,hepatic encephalopathy, uremic encephalopathy, and acute structuralabnormalities, such as intracerebral hemorrhage due to trauma orcoagulation disorders.
• Cerebral edema and herniation also may occur
• Eyes
• Examination of the eyes may reveal nystagmus andoculogyric episodes due to cerebellar injury. The pupils maybe fixed, dilated, pinpoint, or normal.
Cardiovascular
• Heat stress places a tremendous burden on the heart. Patients withpreexisting myocardial dysfunction do not tolerate heat stress forprolonged periods.
• Patients commonly exhibit a hyperdynamic state, with tachycardia,low systemic vascular resistance, and a high cardiac index.
• Hypodynamic state, with a high systemic vascular resistance and alow cardiac index, may occur in patients with preexistingcardiovascular disease and low intravascular volume.
• A hypodynamic state also may signal cardiovascular collapse.
Pulmonary
• Patients with heatstroke commonly exhibit tachypnea andhyperventilation caused by direct CNS stimulation, acidosis,or hypoxia.
• Hypoxia and cyanosis may be due to a number of processes,including atelectasis, pulmonary infarction, aspirationpneumonia, and pulmonary edema.
• ARDS develop because of multiple insults, including heat-induced pulmonary damage, aspiration pneumonia, and asa complication of liver failure.
Digestive• Gastrointestinal hemorrhage occurs frequently in heatstroke patients.• Patients commonly exhibit evidence of hepatic injury, including
jaundice and elevated liver enzymes. Hypoglycemia, abnormalcoagulation, cerebral edema, and death can occur
• Rarely, fulminant hepatic failure occurs, accompanied byencephalopathy, hypoglycemia, and disseminated intravascularcoagulation (DIC) and bleeding.
• Prolonged coagulation times also may signal the development of DIC,which, when present, carries a poor patient prognosis. DIC also maypredispose patients to development of acute respiratory distresssyndrome (ARDS), which also increases mortality.
• Musculoskeletal
• Muscle tenderness and cramping are common;rhabdomyolysis is a common complication of EHS. Thepatient's muscles may be rigid or limp.
• Renal
• Acute kidney injury is a common complication of heatstrokeand may be due to hypovolemia, low cardiac output, andmyoglobinuria (from rhabdomyolysis). Patients may exhibitoliguria and a change in the color of urine.
Causes
• The etiology of heatstroke may involve any of the following:
• Increased heat production
• Decreased heat loss
• Reduced ability to acclimatize
• Reduced behavioral responsiveness
Increased heat production
Increased muscular activity may involve any of the following:
Increased metabolism can result from any of the following:
ExerciseInfections
ConvulsionsSepsis
TetanusEncephalitis
Strychnine poisoningStimulant drugs
SympathomimeticsThyroid storm
Drug withdrawalDrug withdrawal
Thyroid storm
• Moderate physical exercise, convulsions, and shivering candouble heat production and result in temperatureelevations that generally are self-limited and resolve withdiscontinuation of the activity.
• Strenuous exercise and status epilepticus can increase heatproduction 10-fold and, when uninterrupted, canoverwhelm the body's heat-dissipating mechanisms,leading to dangerous rises in body temperature.
• Stimulant drugs, including cocaine and amphetamines, cangenerate excessive amounts of heat by increasingmetabolism and motor activity through the stimulatoryeffects of dopamine, serotonin, and norepinephrine.
• Neuroleptic agents also may elevate body temperature byincreasing muscle activity, but, occasionally, these agents maycause neuroleptic malignant syndrome(NMS). NMS is anidiosyncratic reaction characterized by hyperthermia, alteredmental status, muscle rigidity, and autonomic instability andappears to be due to excessive contraction of muscles.
• Certain drugs, such as inhaled volatile anesthetics andsuccinylcholine, may result in malignant hyperthermia.
• In contrast to heatstroke, malignant hyperthermia is believed to beinduced by a decreased ability of the sarcoplasmic reticulum toretain calcium, resulting in sustained muscle contraction.
Decreased heat loss
• Reduced sweating can result from any of the following:
• Dermatologic diseases
• Drugs
• Burns
• Reduced central nervous system (CNS) responses may result from the following:
• Advanced age
• Young age (toddlers and infants)
• Alcohol
• Barbiturates
• Other sedatives
• Reduced cardiovascular reserve may result from thefollowing:
• Advanced age
• Beta-blockers
• Calcium channel blockers
• Diuretics
• Cardiovascular drugs - Interfere with the cardiovascularresponses to heat and, therefore, can interfere with heatloss
• Drugs that can result in decreased heat loss include thefollowing:
• Anticholinergics
• Neuroleptics
• Antihistamines
• Exogenous factors that can decrease heat loss include thefollowing:
• High ambient temperatures
• High ambient humidity
• Reduced ability to acclimatize
• Persons at the extremes of age (ie, toddlers and youngchildren, the elderly) may be less able to generate adequatephysiologic responses to heat stress.
• Reduced behavioral responsiveness
• Infants, patients who are bedridden, and patients who arechronically ill are at risk for heatstroke because they areunable to control their environment and water intake.
Complications
• The central nervous system (CNS) is especially sensitive tothe damaging effects of hyperthermia. Widespread celldeath occurs but is more evident in the region of thecerebellum (Purkinje cells).
• Heatstroke–related long-term CNS sequelae includecerebellar deficits, dementia, hemiplegia, quadriparesis,and personality changes.
• Rhabdomyolysis was observed in almost all patients with EHS and in as many as 86% of patients with NEHS.
• Compartment syndrome is observed most commonly in patients with severe rhabdomyolysis and in patients who are immobilized.
• Acute kidney injury may occur in as many as 25-30% of patients who have heatstroke (especially EHS).
• Acute liver failure due to centrilobular hepatic necrosis and cholestasis generally occurs in the first 48 hours, but it can peak as long as 2 weeks after the onset of heatstroke.
• DIC is a rare complication and caries a poor prognosis when it occurs.
• ARDS may be due to direct thermal injury to the lung, or it may complicate liver failure, infection, or aspiration
• Arterial blood gas analysis may reveal respiratory alkalosis due todirect central nervous system (CNS) stimulation and metabolicacidosis due to lactic acidosis. Hypoxia may be due to pulmonaryatelectasis, aspiration pneumonitis, or pulmonary edema.
• Lactic acidosis commonly occurs following exertional heatstroke(EHS) but may signal a poor prognosis in patients with classicheatstroke.
• Blood glucose,Hypoglycemia may occur in patients with EHS and inpatients with fulminant hepatic failure.
Electrolytes
• Hypernatremia due to reduced fluid intake and dehydrationcommonly is observed early in the course of disease but may be dueto diabetes insipidus.
• Hyponatremiais observed in patients using hypotonic solutions, suchas free water, and in patients using diuretics. It also may be due toexcessive sweat sodium losses.
• Hypokalemia is common in the early phases of heatstroke, anddeficits of 500 mEq are not unusual. However, with increasing muscledamage
• Hyperkalemia may be observed commonly.
• Hypophosphatemia secondary to phosphaturia
• Hyperphosphatemia secondary to rhabdomyolysis
• Hypocalcemia secondary to increased calcium binding indamaged muscle
• Hypomagnesemia also are observed
Hepatic function tests
• Aminotransferase (aspartate aminotransferase [AST] andalanine aminotransferase [ALT]) levels commonly rise to thetens of thousands during the early phases of heatstroke andpeak at 48 hours, but they may take as long as 2 weeks to peak.
• Jaundice may be striking and may be noted 36-72 hours afterthe onset of liver failure.
Muscle function tests
• Creatinine kinase (CK), lactate dehydrogenase (LDH), aldolase,and myoglobin commonly are released from muscles whenmuscle necrosis occurs.
• CK levels exceeding 100,000 IU/mL are common in EHS.
• Elevations in myoglobin may not be noted despite musclenecrosis because myoglobin is metabolized rapidly by the liverand excreted rapidly by the kidneys.
• Complete blood cell count
• Elevated white blood cell counts commonly are observed in patientswith heatstroke, and levels as high as 40,000/μ L have beenreported. Platelet levels may be low.
• Renal function tests
• Elevations in serum uric acid levels, blood urea nitrogen, and serumcreatinine are common in patients whose course is complicated byrenal failure.
• Urinalysis
• Presence of red blood cells, and proteinuria are common.
• Cerebrospinal fluid analysis
• Cerebrospinal fluid (CSF) cell counts may show anonspecific pleocytosis, and CSF protein levels may beelevated as high as 150 mg/dL.
• Other
• Myoglobin causes a reddish brown discoloration of theurine but does not affect the color of plasma. This is incontrast to hemoglobin, which causes discoloration of bothplasma and urine.
Diagnostic Considerations
• Other problems to be considered include the following:• Sepsis• Diabetic ketoacidosis• Closed head trauma• Malignant hyperthermia• Encephalitis• Cerebral malaria• Cerebral hemorrhage• Amphetamine and cocaine toxicity• Strychnine poisoning
Differential Diagnoses
• Cocaine Toxicity• Delirium• Delirium Tremens (DTs)• Hepatic Encephalopathy• Hyperthyroidism• Meningitis• Neuroleptic Malignant Syndrome• Salicylate Toxicity• Tetanus• Uremic Encephalopathy
Medical Care
• Heatstroke is a medical emergency and continues to be one of theleading causes of preventable death in sports.
• Rapid reduction of the core body temperature is the cornerstone oftreatment because the duration of hyperthermia is the primarydeterminant of outcome.
• Except for the mildest cases, patients diagnosed with exertionalheatstroke (EHS) or nonexertional heatstroke (NEHS) should beadmitted to the hospital for at least 48 hours to monitor forcomplications.
• Once heatstroke is suspected, cooling must begin immediately andmust be continued during the patient's resuscitation.
• The American College of Sports Medicine recommends that coolingbe initiated at the scene, before transporting the patient to anemergency department for further evaluation and treatment.
• The basic premise of rapidly lowering the core temperature by atleast 0.2°C/min to approximately 39°C (to avoid overshooting andrebound hyperthermia) remain the primary goal.
• Removal of restrictive clothing and spraying water on thebody, covering the patient with ice water–soaked sheets, orplacing ice packs in the axillae and groin may reduce thepatient's temperature significantly.
• Patients who are unable to protect their airway should beintubated.
• Patients who are awake and responsive should receivesupplemental oxygen.
• Intravenous lines may be placed in anticipation of fluidresuscitation and for the infusion of dextrose and thiamineif indicated.
• Hypoglycemia is a common occurrence in patients with EHSand may be a manifestation of liver failure; therefore,infusion of dextrose 50% in water solution (D50W) shouldbe considered in all patients with heatstroke
• Interventions to enable intensive monitoring include thefollowing:
• Insert a thermistor probe or temperature-sensing Foleycatheter to monitor temperature continuously
• Insert a nasogastric tube to monitor for gastrointestinalbleeding and fluid losses
• Place a Foley catheter to monitor urine output and/ormonitor body temperature
Methods for cooling
• The optimal method of rapidly cooling patients has been amatter of debate for some time.
• A 2013 guideline from the Wilderness Medical Societyrecommends ice-water immersion as a superior method forrapidly lowering core body temperature below the criticallevels normally found in heatstroke patients.
• However, each method has its own theoretical advantagesand disadvantages.
• Ice-water immersion or an equivalent method has the advantage ofrapidly reducing core body temperature. Ice water can reduce corebody temperature to less than 39°C in approximately 20-40 minutes.
• The disadvantages of ice-water immersion include
- it may be extremely uncomfortable for patients who are awake.
- it can cause subcutaneous vasoconstriction, preventing the transferof heat via conduction.
- increases shivering, which in turn increases internal heatproduction.
- difficulty monitoring and resuscitating patients while using thismethod.
• Evaporative heat loss may be accomplished by removing all of the patient's clothes and intermittently spraying the patient's body with warm water while a powerful fan blows across the body, allowing the heat to evaporate.
• A number of other cooling techniques include peritoneal, thoracic, rectal, and gastric lavage with ice water; cold intravenous fluids; cold humidified oxygen; cooling blankets; and wet towels.
• Cardiopulmonary bypass has been suggested for use in the most severe cases. However, this requires highly trained personnel and sophisticated equipment.
Intravascular Temperature Management
• Intravascular Temperature Management (IVTM™) methodhas been recognized recently as a safe and effectivemethod for controlling core body temperature. Superior, infact, to other cooling methods for achieving andmaintaining target temperature
How Intravascular Temperature Management Works
• IVTM technology gets to the core of the temperature issue bymanaging patient temperature from the inside out. A catheter isinserted into the central venous system of a critically ill or surgicalpatient (femoral, subclavian, or internal jugular insertion). TheThermogard Temperature Managament System controls thetemperature of the saline circulating through the catheter balloonsvia remote sensing of the patient’s temperature. The patient iscooled or warmed as venous blood passes over each balloon –exchanging heat without infusing saline into the patient.
Pharmacologic measures
• Antipyretics (e.g., acetaminophen, aspirin, othernonsteroidal anti-inflammatory drugs) have no role in thetreatment of heatstroke
• Antipyretics actually may be harmful in patients whodevelop hepatic, hematologic, and renal complicationsbecause they may aggravate bleeding tendencies.
• Dantrolene in not effective in the treatment of heatstroke
• Immediate administration of benzodiazepines is indicatedin patients with agitation, shivering, or convulsions to stopexcessive production of heat.
• In addition, benzodiazepines are the sedatives of choice inpatients with sympathomimetic-induced delirium as well asalcohol and sedative drug withdrawals.
• Barbiturates may be used to stop convulsions despite theirtheoretical impedance of sweat production.
• Phenytoin is not effective in controlling convulsions in thissituation. Patients whose convulsions are refractory tobenzodiazepines and barbiturates should be paralyzed andprovided mechanical ventilation.
Fluid resuscitation
• Recommendations on the administration of intravenous fluids forcirculatory support differ among patient populations and depend onthe presence of hypovolemia, preexisting medical conditions, andpreexisting cardiovascular disease.
• While patients with heatstroke invariably are volume depleted,cooling alone may improve hypotension and cardiac function byallowing blood to redistribute centrally.
• Aggressive fluid resuscitation generally is not recommendedbecause it may lead to pulmonary edema.
• When pulse rate, blood pressure, and urine output do not provideadequate hemodynamic information, fluid administration should beguided by more invasive hemodynamic parameters, such as centralvenous pressure (CVP), pulmonary capillary wedge pressure,systemic vascular resistance index (SVRI), and cardiac index (CI)measurements.
• Patients who exhibit a hyperdynamic state (ie, high CI, low SVRI)generally respond to cooling and do not require large amounts ofintravenous crystalloid infusions.
• In hypotensive patients who exhibit a hypodynamic response (ie,high CVP, low CI), dobutamine may be the inotrope of choice inthese patients.
• Alpha-adrenergic drugs generally are contraindicated because theycause vasoconstriction and may interfere with heat loss.
• Treatment of rhabdomyolysis involves infusion of large amounts ofintravenous fluids (fluid requirements may be as high as 10 L),alkalinization of the urine, and infusion of mannitol. Fluid administrationis best guided by invasive hemodynamic parameters, and urine outputshould be maintained at 3 mL/kg/h to minimize the risk of renal failure.
• Alkalinization of the urine (to a pH of 7.5-8.0) prevents the precipitationof myoglobin in the renal tubules and may control acidosis andhyperkalemia in acute massive muscle necrosis. Mannitol may improverenal blood flow and glomerular filtration rate, increase urine output,and prevent fluid accumulation in the interstitial compartment (throughits osmotic action). Once renal failure occurs, dialysis is the only effectivetherapeutic modality for rhabdomyolysis.
• Metabolic support
• Muscle necrosis may occur so rapidly that hyperkalemia,hypocalcemia, and hyperphosphatemia become significant enoughto cause cardiac arrhythmias and require immediate therapy. In thepresence of renal failure, hemodialysis may be necessary.
• Hypertonic dextrose and sodium bicarbonate may be used to shiftpotassium into the intracellular environment while more definitivemeasures (e.g., intestinal potassium binding, dialysis) are prepared.
• Hepatic failure is treated conservatively; liver transplantation shouldbe considered in severe resistant cases:
• Early recognition and treatment of DIC, with replacement of clottingfactors, fresh frozen plasma, platelets, and blood
• ARDS should be treated aggressively, with early mechanicalventilation and positive end-expiratory pressure (PEEP).
• Renal injury
• AKI initially is treated with intravenous fluids, diuretics, andcorrection of associated acid-base and electrolyte abnormalities. Inthe setting of rhabdomyolysis, mannitol may be the diuretic ofchoice because it does not interfere with the acid-base status of theurine, and it may have antioxidant activity. Furosemide may causetubular acidosis and, therefore, may promote myoglobin depositionwithin the renal tubules. Once renal failure has set in, hemodialysisis the most effective therapy.
Proceduresmay include the following:• Endotracheal intubation• Pulmonary artery catheter insertion• Central venous line insertion• Nasogastric tube insertion• Lumbar puncture• Compartment pressure measurements• Fasciotomy• Thoracostomy• Peritoneal lavage• Hemodialysis
•
• Surgical Care
• Compartment syndrome must be suspected in all patients whoexhibit rhabdomyolysis and muscle edema and tenderness.Intramuscular compartment pressure measurements must beperformed when compartment syndrome is suspected, andfasciotomy must be performed when the intramuscular pressureexceeds 50 mm Hg.
• Fasciotomy also should be considered when intracompartmentalpressures are 30-50 mm Hg, especially when they show no tendencyto decrease in 6 hours and in patients who are hypotensive.
Prevention
• Heatstroke is a preventable illness, and education is thesingle most important tool for its prevention.
• Recognition of host risk factors and modification ofbehavior (e.g., limiting alcohol and drug intake, avoidinguse of medications and drugs that interfere with heatdissipation) and physical activity also can preventheatstroke.
• Cooling during exercise offers a similar benefit to exerciseperformance in hot environments as does the application ofprecooling, and both methods improve exerciseperformance with and without physiological alterations.
Prognosis
• Indicators of poor prognosis include the following:
- Initial temperature measurement higher than 41°C (106°F) or atemperature higher than 42°C (108°F) or a temperature persisting above39°C (102°F) despite aggressive cooling measures
- Coma duration longer than 2 hours
- Severe pulmonary edema
- Delayed or prolonged hypotension
- Lactic acidosis in patients with classic heatstroke
- Acute kidney injury and hyperkalemia
- Aminotransferase levels greater than 1000 IU/L during the first 24 hours
• Morbidity and mortality from heatstroke are related to theduration of the temperature elevation.
• When therapy is delayed, the mortality rate may be as highas 80%; however, with early diagnosis and immediatecooling, the mortality rate can be reduced to 10%.
• Mortality is highest among the elderly population, patientswith preexisting disease, those confined to a bed, and thosewho are socially isolated.
Patient Education• Education is the single most important tool for the prevention of
heatstroke. The media, public education, public health programs,and athlete safety programs can play a pivotal role in increasing thepublic's awareness of the dangers of heat during heat waves andadvising the public on methods of remaining cool.
• Similarly, drinking fluids on schedule (and not based only on thirst),frequent cooling breaks, and frequent visits to air-conditionedplaces are very important because even short stays in an air-conditioned environment may drastically reduce the incidence ofheatstroke.
• Recognition of host risk factors and modification of behavior (eg, limiting alcohol and drug intake and the use of medications and drugs that interfere with heat dissipation) and physical activity also will prevent heatstroke.
