Heat Emergencies

Quick Reference

Critical Alerts

• Heat stroke is life-threatening: Core temp ≥40°C (104°F) + CNS dysfunction
• Rapid cooling is essential: Target less than 39°C within 30 minutes
• Classic vs Exertional heat stroke: Different populations, same emergency
• Cold water immersion is gold standard: For exertional heat stroke
• Antipyretics do NOT work: Hypothalamic setpoint is normal
• Multiorgan failure can develop: DIC, rhabdo, renal failure, hepatic failure
• Mortality 10-65%: Depends on cooling rapidity and organ failure extent
• Time to cooling determines outcome: Every minute counts

Heat Exhaustion vs Heat Stroke

Emergency Treatments

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Definition

Overview

Heat emergencies represent a spectrum of illnesses caused by failure of thermoregulation during heat exposure, ranging from benign heat cramps to life-threatening heat stroke. [1] Heat stroke is defined as core body temperature ≥40°C (104°F) with central nervous system dysfunction manifesting as confusion, altered mental status, seizures, or coma. [2] It is a true medical emergency requiring immediate recognition and aggressive cooling, as delayed treatment leads to irreversible multiorgan failure and death. [1,2]

Heat stroke differs fundamentally from fever in that the hypothalamic temperature setpoint remains normal; the elevated temperature results from an imbalance between heat production/absorption and heat dissipation. [3] This distinction explains why antipyretic medications are ineffective in heat stroke.

Classification

Heat Illness Spectrum:

Heat Stroke Types:

Classic heat stroke typically affects vulnerable populations during heat waves when environmental heat stress overwhelms diminished physiologic reserve. [4] Exertional heat stroke occurs in otherwise healthy individuals during strenuous physical activity, particularly in hot, humid conditions. [5]

Epidemiology

Burden of Disease:

• Heat-related deaths have increased globally due to climate change, with over 70,000 excess deaths during the 2003 European heat wave. [6]
• In the United States, heat-related illness causes approximately 600-1,500 deaths annually. [7]
• Classic heat stroke predominantly affects elderly individuals (65 years) during heat waves. [4]
• Exertional heat stroke most commonly affects young athletes, military recruits, and occupational workers (construction, agriculture). [5]
• Athletes have an incidence of 0.2-1.0 cases per 1,000 participants in high-risk sports. [8]
• Military populations show incidence rates of 2.5-3.5 cases per 1,000 recruits during basic training. [9]

Mortality:

• Overall mortality for heat stroke ranges from 10-65%, depending on severity, time to cooling, and organ failure extent. [2,10]
• Mortality without treatment approaches 80%. [1]
• Mortality with rapid cooling (achieving normothermia less than 30 minutes) is 10-15%. [11]
• Delayed cooling beyond 2 hours is associated with mortality ≥60%. [12]
• Presence of multiorgan failure increases mortality to ≥50%. [13]

Seasonal and Geographic Variation:

• Heat stroke incidence peaks during summer months (June-August in Northern Hemisphere). [14]
• Urban heat islands amplify risk in densely populated areas. [6]
• Populations without air conditioning are at 2-3 fold increased risk. [14]
• First heat wave of season carries higher risk due to lack of acclimatization. [15]

Etiology and Risk Factors

Environmental Risk Factors:

Individual Risk Factors:

Occupational and Recreational Risk:

• Military training (forced marches, obstacle courses in heat). [9]
• Athletics (American football, soccer, long-distance running, tennis). [8]
• Occupational exposure (construction workers, agricultural workers, firefighters). [16]
• Religious practices (Hajj pilgrimage – heat exposure in large crowds). [17]

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Pathophysiology

Normal Thermoregulation

Heat Balance Equation: Heat storage = Metabolic heat production + Environmental heat gain - Heat loss

Heat Dissipation Mechanisms:

Hypothalamic Control: The preoptic anterior hypothalamus integrates thermal input from peripheral and central thermoreceptors, maintaining core temperature at 37°C (±0.5°C). [3] Heat exposure triggers:

1. Peripheral vasodilation (mediated by nitric oxide and vasoactive peptides)
2. Sweating (cholinergic sympathetic activation of eccrine glands)
3. Behavioral responses (seeking shade, reducing activity)

Acclimatization (7-14 days):

• Increased plasma volume (10-20%)
• Earlier onset of sweating at lower core temperature
• Increased maximum sweat rate (1.5-2.5 L/hr)
• Reduced salt loss in sweat
• Enhanced cardiovascular efficiency

Heat Stroke Pathogenesis

Phase 1: Thermoregulatory Failure When environmental heat stress and/or metabolic heat production exceed dissipation capacity, core temperature rises. [1] Contributing factors:

• Extreme environmental conditions (high temperature + humidity)
• Excessive exertion
• Impaired heat loss (medications, dehydration, skin disease)
• Excessive heat production (stimulants, infection, thyrotoxicosis)

Phase 2: Direct Cellular Injury At core temperatures \≥40-41°C, direct thermal injury occurs: [18]

• Protein denaturation and unfolding
• Loss of cell membrane integrity
• Mitochondrial dysfunction
• Endoplasmic reticulum stress
• Apoptosis and necrosis

Particularly vulnerable organs:

• Brain: Purkinje cells, hippocampus (explains ataxia, memory deficits)
• Intestinal mucosa: Barrier dysfunction, endotoxemia
• Liver: Hepatocyte necrosis
• Kidney: Acute tubular necrosis
• Skeletal muscle: Rhabdomyolysis (especially exertional)

Phase 3: Systemic Inflammatory Response Cellular injury and intestinal barrier failure trigger a systemic inflammatory cascade resembling sepsis: [19]

Cytokine Storm:

• Release of IL-1β, IL-6, TNF-α, IL-8
• Activation of complement cascade
• Production of acute phase reactants

Endotoxemia:

• Gut barrier failure allows translocation of endotoxin (LPS)
• Toll-like receptor 4 (TLR4) activation
• Amplification of inflammatory response

Endothelial Activation:

• Increased vascular permeability (capillary leak)
• Expression of adhesion molecules (ICAM-1, VCAM-1)
• Microvascular thrombosis
• Disseminated intravascular coagulation (DIC)

Phase 4: Multiorgan Dysfunction The combination of direct thermal injury, inflammatory response, and microvascular thrombosis leads to progressive multiorgan failure: [13]

Central Nervous System:

• Cerebral edema
• Cerebellar damage (Purkinje cell loss → persistent ataxia)
• Seizures (excitotoxicity, cerebral edema)
• Coma (global cerebral dysfunction)

Cardiovascular:

• Initial hyperkinetic state (high cardiac output, low SVR)
• Myocardial dysfunction (troponin elevation, reduced ejection fraction)
• Distributive shock → hypotension
• Arrhythmias (electrolyte disturbances, direct thermal injury)

Hepatic:

• Centrilobular necrosis
• Transaminase elevation (often \≥1,000 U/L)
• Coagulopathy (reduced synthesis of clotting factors)
• Acute liver failure (jaundice, encephalopathy)

Renal:

• Acute tubular necrosis (ATN)
• Prerenal azotemia (volume depletion)
• Pigment nephropathy (myoglobin from rhabdomyolysis)
• Acute kidney injury requiring dialysis in 25-30% of severe cases [20]

Hematologic:

• Thrombocytopenia (consumption, sequestration)
• Disseminated intravascular coagulation (DIC) in 30-45% [21]
• Prolonged PT/aPTT, elevated D-dimer, low fibrinogen
• Microangiopathic hemolytic anemia (schistocytes)

Respiratory:

• Acute respiratory distress syndrome (ARDS) from capillary leak
• Hyperventilation (initial respiratory alkalosis)
• Metabolic acidosis (lactate accumulation)

Gastrointestinal:

• Intestinal ischemia
• Nausea, vomiting, diarrhea
• Hemorrhage (stress ulceration, coagulopathy)

Metabolic:

• Hypoglycemia or hyperglycemia
• Hypocalcemia
• Hyperkalemia (rhabdomyolysis)
• Hyperphosphatemia (rhabdomyolysis)
• Lactic acidosis

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Clinical Presentation

Heat Exhaustion

Heat exhaustion represents a milder form of heat illness where thermoregulation is still partially effective but failing. [1] Core temperature is elevated but less than 40°C, and CNS function remains intact.

Symptoms:

Signs:

Key Distinction: Mental status remains intact. If confusion, ataxia, or other CNS dysfunction is present, consider heat stroke.

Heat Stroke

Heat stroke is defined by the triad: [2]

1. Core body temperature ≥40°C (104°F)
2. Central nervous system dysfunction
3. History of heat exposure

Note: Some patients may present with core temperature less than 40°C if measured after initial cooling or if rapidly progressing. Clinical judgment is essential.

Central Nervous System Manifestations (defining feature):

Cardiovascular:

Respiratory:

Skin:

Important: Presence of sweating does NOT exclude heat stroke. The classic teaching of "hot and dry" applies primarily to classic heat stroke; exertional heat stroke typically presents with ongoing sweating. [5]

Gastrointestinal:

• Nausea, vomiting (common)
• Diarrhea (may be bloody if intestinal ischemia)
• Abdominal pain

Renal:

• Oliguria, anuria (acute kidney injury)
• Dark urine (myoglobinuria if rhabdomyolysis)

History

Key Questions:

Environmental Exposure:

• When did symptoms begin?
• What was the ambient temperature and humidity?
• Indoor or outdoor setting?
• Access to shade, water, air conditioning?
• Duration of exposure?

Activity:

• What were you doing? (exercise, work, rest)
• Intensity and duration of activity?
• Wearing protective equipment or heavy clothing?

Hydration:

• Fluid intake during and before exposure?
• Urine output and color?

Medical History:

• Prior episodes of heat illness?
• Chronic medical conditions (cardiac, diabetes, kidney, psychiatric)?
• Recent illness (especially febrile illness, diarrhea)?

Medications and Substances:

• Current medications (especially anticholinergics, diuretics, beta-blockers, antipsychotics)?
• Recreational drug use (stimulants, MDMA, alcohol)?

Acclimatization:

• Recent arrival to hot climate?
• Usual level of heat exposure and activity?

Social History:

• Living conditions (air conditioning, housing)?
• Occupational exposure?
• Support system (check on elderly during heat wave)?

Physical Examination

Vital Signs:

Core Temperature Measurement:

• Rectal temperature is GOLD STANDARD for core temperature assessment [22]
• Oral temperature underestimates by 0.5-1.5°C (tachypnea, mouth breathing)
• Axillary temperature underestimates by 1-2°C
• Tympanic temperature unreliable (affected by ambient temperature, cerumen)
• Temporal artery scanners underestimate
• Bladder and esophageal probes accurate (ICU setting)

Neurologic Examination:

Skin Examination:

Cardiovascular Examination:

• Assess perfusion (capillary refill, peripheral pulses)
• Jugular venous pressure (volume status)
• Heart sounds (murmur, gallop)

Respiratory Examination:

• Work of breathing
• Crackles (pulmonary edema, ARDS, aspiration)

Abdominal Examination:

• Tenderness (intestinal ischemia, hepatic congestion)
• Hepatomegaly (hepatic congestion, acute hepatitis)

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Red Flags

Immediate Life-Threatening Signs

High-Risk Features for Poor Outcome

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Differential Diagnosis

Other Causes of Hyperthermia + Altered Mental Status

Key Differentiating Point: Heat stroke requires environmental heat exposure or exertion. If hyperthermia occurs without heat exposure, consider other diagnoses.

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Diagnostic Approach

Clinical Diagnosis

Heat stroke is primarily a clinical diagnosis based on: [2]

1. Core body temperature ≥40°C (104°F) (rectal measurement)
2. Central nervous system dysfunction (confusion, ataxia, seizures, coma)
3. History of environmental heat exposure or exertion

No laboratory test confirms or excludes heat stroke. Do not delay treatment awaiting laboratory results.

Core Temperature Measurement

Preferred Method: Rectal thermometer

• Most accurate reflection of core temperature
• Standard of care in emergency department
• Continuous rectal probe for monitoring during cooling

Alternative Methods (ICU/intraoperative):

• Esophageal probe
• Bladder catheter with temperature sensor
• Pulmonary artery catheter

Inadequate Methods:

• Oral (underestimates by 0.5-1.5°C)
• Axillary (underestimates by 1-2°C)
• Tympanic (unreliable, variable)
• Temporal artery (underestimates)

Laboratory Evaluation

Purpose: Assess severity, identify complications, guide management

Initial Laboratory Tests:

Additional Tests Based on Clinical Scenario:

Imaging

Not routinely required for diagnosis but may be indicated for complications or alternative diagnoses.

CT Head (Non-contrast):

• Indications: Persistent coma after cooling, focal neurologic deficits, concern for intracranial hemorrhage
• Findings: Cerebral edema, hemorrhage (rare)

Chest X-ray:

• Indications: Dyspnea, hypoxia, abnormal lung exam
• Findings: Aspiration pneumonitis, ARDS, pulmonary edema

ECG:

• Routine: All heat stroke patients
• Findings: Sinus tachycardia, nonspecific ST-T changes, arrhythmias, QTc prolongation, conduction abnormalities

Echocardiography:

• Indications: Hemodynamic instability, troponin elevation, concern for myocardial dysfunction
• Findings: Reduced ejection fraction, wall motion abnormalities

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Treatment

Principles of Management

1. ABCs: Airway, Breathing, Circulation
2. Remove from heat immediately
3. Initiate rapid cooling IMMEDIATELY: Do not delay for laboratory confirmation
4. Goal: Reduce core temperature to less than 39°C (102.2°F) within 30 minutes [11]
5. Aggressive IV fluid resuscitation
6. Monitor for and treat complications (rhabdomyolysis, DIC, seizures, arrhythmias)
7. ICU admission for all heat stroke patients

Critical Concept: Time to normothermia is the strongest predictor of outcome. Every minute of delay increases mortality and morbidity. [12] Cooling takes precedence over diagnostic workup.

Heat Cramps

Presentation: Painful skeletal muscle cramps during or after exertion in heat, without hyperthermia or CNS dysfunction.

Treatment:

• Rest in cool environment
• Oral rehydration with electrolyte-containing fluids (sports drinks, oral rehydration solution)
• Passive muscle stretching
• Salt supplementation if prolonged exertion and large sweat losses
• IV fluids: Normal saline 1-2 L if unable to tolerate PO

Disposition: Discharge with return precautions

Heat Exhaustion

Presentation: Core temp less than 40°C, weakness, fatigue, headache, nausea, intact or mildly impaired mentation.

Treatment:

Disposition:

• Observe 4-6 hours minimum
• Discharge criteria: Symptoms resolved, tolerating PO, normal vital signs, reliable follow-up
• Admit if: Progression to heat stroke, persistent symptoms, unable to tolerate PO, significant comorbidities, unsafe home environment

Heat Stroke (MEDICAL EMERGENCY)

Immediate Resuscitation (First 10 Minutes)

Airway and Breathing:

• Assess and secure airway
• Intubation indications: GCS \≥8, inability to protect airway, respiratory failure, refractory seizures
• High-flow oxygen to maintain SpO2 greater than 92%

Circulation:

• Large-bore IV access (18-gauge or larger, two lines)
• Aggressive IV fluid resuscitation:
  • Normal saline 1-2 L rapid bolus (over 15-30 minutes)
  • Reassess hemodynamics (BP, HR, UOP, lactate)
  • Continue fluids at 200-500 mL/hr titrated to urine output goal 0.5-1 mL/kg/hr
  • Monitor carefully for fluid overload (crackles, elevated JVP, pulmonary edema)
  • Cold IV fluids (4°C) provide adjunctive cooling [23]
• Vasopressors if hypotension persists despite adequate fluid resuscitation (norepinephrine preferred)

Disability (Neurologic):

• Assess GCS, pupillary response
• Rapid glucose check (treat hypoglycemia if present)

Exposure:

• Remove all clothing
• Begin cooling IMMEDIATELY (see below)

Cooling Strategies

Goal: Core temperature less than 39°C (102.2°F) within 30 minutes [11]

Method Selection:

Cold Water Immersion (CWI): [24]

• Gold standard for exertional heat stroke
• Technique:
  • Immerse patient to neck in cold water (1-15°C; colder is more effective)
  • Stir water to prevent warm layer around body
  • Continuous rectal temperature monitoring
  • Remove when core temp reaches 39°C to prevent overcooling
• Cooling rate: 0.15-0.35°C/min
• Advantages: Fastest cooling, well-tolerated by young patients
• Disadvantages: Limited access to patient for monitoring/procedures, risk of shivering (counterproductive), impractical in elderly or obese patients
• Contraindications: Hemodynamic instability (relative), need for ongoing resuscitation

Evaporative Cooling: [25]

• Technique:
  • Spray lukewarm water (15°C) continuously over entire body surface
  • Direct high-flow fans over patient to maximize evaporation
  • Remove when core temp reaches 39°C
• Cooling rate: 0.1-0.2°C/min
• Advantages: Maintains patient access, well-tolerated, effective, practical in ED
• Disadvantages: Slightly slower than CWI

Ice Pack Application:

• Technique:
  • Apply ice packs to groin, axillae, neck (areas of large superficial vessels)
  • Rotate ice packs frequently to maintain cold contact
• Cooling rate: 0.05-0.15°C/min
• Role: Adjunct to other methods; less effective as monotherapy

Cold IV Fluids:

• Technique: Infuse 4°C (refrigerated) normal saline rapidly
• Cooling rate: 0.05-0.1°C/min (limited)
• Role: Adjunct; provides volume resuscitation + modest cooling

Cooling Blankets/Pads:

• Cooling rate: 0.03-0.08°C/min
• Role: Adjunct only; too slow for initial management

Intravascular Cooling Catheters:

• Role: ICU setting for refractory hyperthermia
• Advantages: Precise temperature control
• Disadvantages: Invasive, requires ICU, slow initial cooling

Gastric/Bladder/Peritoneal Lavage with Iced Saline:

• Role: Historical; rarely used; invasive; limited efficacy
• Not recommended given superior alternatives

DO NOT USE:

• Antipyretics (acetaminophen, NSAIDs): INEFFECTIVE. The hypothalamic setpoint is normal in heat stroke; these agents work by resetting the hypothalamic setpoint and are therefore useless. [3]
• Dantrolene: NOT effective in heat stroke (only effective in malignant hyperthermia). [26]

Cooling Endpoints:

• Target: Core temperature less than 39°C (102.2°F)
• Stop active cooling when target reached to avoid iatrogenic hypothermia
• Overshoot phenomenon: Temperature may continue to decrease after cooling stopped
• Monitor temperature every 15 minutes after stopping cooling (risk of rebound hyperthermia, though uncommon)

Management of Shivering

Problem: Shivering increases metabolic heat production, counteracting cooling efforts.

Treatment:

Note: If neuromuscular blockade is used, patient MUST be adequately sedated as paralysis does not provide sedation or analgesia.

Seizure Management

Treatment:

Adjunct: Aggressive cooling (seizures often terminate with normothermia)

Rhabdomyolysis Management

Rhabdomyolysis occurs in 25-30% of heat stroke, especially exertional. [20]

Diagnosis: CK \≥1,000 U/L (often \≥15,000-20,000 U/L), myoglobinuria

Treatment:

Indications for Dialysis:

• Severe hyperkalemia (\≥6.5 mEq/L) refractory to medical management
• Severe metabolic acidosis (pH \≥7.1)
• Acute kidney injury with oliguria/anuria despite adequate volume resuscitation
• Volume overload unresponsive to diuretics
• Uremia (BUN \≥100 mg/dL)

DIC Management

DIC occurs in 30-45% of heat stroke patients. [21]

Diagnosis:

• Thrombocytopenia (platelets less than 100,000)
• Prolonged PT/INR and aPTT
• Decreased fibrinogen (less than 200 mg/dL)
• Elevated D-dimer (\≥500 ng/mL)
• Schistocytes on peripheral smear

Treatment:

Key Principle: Treat underlying cause (cooling, supportive care). Transfuse blood products only for active bleeding or severe deficiency.

Supportive Care

Electrolyte Management:

Acid-Base Management:

• Respiratory alkalosis (early): Supportive; resolves
• Metabolic acidosis (late): Treat underlying cause (cooling, fluids, perfusion); sodium bicarbonate if severe (pH less than 7.1) AND renal failure OR hyperkalemia

Organ Support:

Glucose Management:

• Hypoglycemia: D50W 25 g IV bolus, recheck
• Hyperglycemia: Usually resolves with treatment; insulin if severe (\≥300 mg/dL) and persistent

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Monitoring

Continuous Monitoring (all heat stroke patients):

• Core temperature (rectal probe or esophageal)
• Cardiac telemetry (arrhythmia detection)
• Blood pressure (arterial line if shock/vasopressor use)
• Oxygen saturation
• Urine output (Foley catheter)

Serial Assessments:

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Disposition

Heat Cramps

• Discharge if symptoms resolve, tolerating PO
• Return precautions: worsening symptoms, inability to tolerate PO, fever

Heat Exhaustion

• Observe minimum 4-6 hours in ED or observation unit
• Discharge criteria:
  • Symptoms resolved
  • Tolerating PO fluids
  • Normal vital signs
  • Core temperature normal
  • Reliable follow-up
  • Safe home environment (especially air conditioning if heat wave)
• Admit if:
  • Progression to heat stroke
  • Persistent symptoms despite treatment
  • Unable to tolerate PO
  • Significant comorbidities (cardiac, renal, elderly)
  • Unsafe home environment (no air conditioning during heat wave, homeless)

Heat Stroke

• ALL heat stroke patients require ICU admission [1,2]
• Continuous monitoring for delayed complications
• Multiorgan failure may evolve over 24-72 hours even after normothermia achieved
• Hepatic injury peaks at 48-72 hours
• Rhabdomyolysis and AKI may worsen for several days

ICU Management:

• Continuous core temperature monitoring
• Hemodynamic monitoring (arterial line, central venous pressure)
• Serial laboratory assessments (see Monitoring section)
• Organ support as needed (mechanical ventilation, vasopressors, dialysis)

ICU Duration: Typically 3-7 days; longer if multiorgan failure

Discharge Criteria from ICU:

• Hemodynamically stable off vasopressors
• Adequate oxygenation on room air or minimal supplemental O2
• Improving or stable organ function (renal, hepatic)
• Resolving neurologic dysfunction

Referrals and Consultations

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Prognosis and Outcomes

Mortality

• Overall mortality: 10-65% depending on severity, time to cooling, and organ failure [2,10]
• With rapid cooling (less than 30 min to normothermia): 10-15% [11]
• With delayed cooling (greater than 2 hours): greater than 60% [12]
• Prolonged hyperthermia (greater than 2 hours, or core temp greater than 42°C)
• Age greater than 65 years or less than 5 years
• Coma on presentation (GCS less than 8)
• Acute kidney injury requiring dialysis
• Hepatic failure (ALT greater than 1,000, INR greater than 2)
• Disseminated intravascular coagulation
• ARDS
• Persistent lactic acidosis (lactate greater than 4 mmol/L at 24 hours)
• Chronic comorbidities (cardiac, renal, diabetes)

Good Prognosis:

• Rapid cooling (less than 30 minutes)
• Young, previously healthy
• Exertional (vs classic)
• No multiorgan failure
• Early recognition and treatment

Long-Term Sequelae

Neurologic:

• Cerebellar dysfunction (ataxia, dysmetria): 10-20% of survivors; may be permanent due to Purkinje cell loss
• Cognitive impairment: Memory deficits, executive dysfunction (10-30%)
• Peripheral neuropathy (rare)
• Seizure disorder (rare; 2-5%)

Thermoregulatory:

• Persistent heat intolerance: 20-30% of survivors; may persist for months to years
• Impaired sweating: Anhidrosis or hypohidrosis

Renal:

• Chronic kidney disease: 5-15% if severe AKI occurred

Hepatic:

• Usually resolves completely; chronic liver dysfunction rare

Psychiatric:

• Post-traumatic stress disorder (PTSD): Rare

Return to Activity:

• Gradual return over weeks to months
• Heat acclimatization protocol essential for athletes/military
• Increased risk of recurrence: Heat stroke survivors have 2-3× risk of repeat heat stroke [27]
• Some athletes/military may never be able to return to full activity in heat

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Prevention

Individual-Level Strategies

Acclimatization:

• Gradual exposure to heat over 7-14 days
• Progressive increase in exercise intensity and duration
• Heat acclimatization increases sweat rate, decreases sweat sodium, improves cardiovascular efficiency

Hydration:

• Maintain euhydration (urine pale yellow)
• Drink 500 mL (16 oz) water 2 hours before activity
• During activity: 200-300 mL (7-10 oz) every 15-20 minutes
• Electrolyte-containing beverages for prolonged activity (\≥1 hour)
• Avoid overhydration (hyponatremia risk)

Activity Modification:

• Schedule outdoor activity during cooler parts of day (early morning, evening)
• Take frequent breaks in shade or air conditioning
• Reduce intensity and duration during heat waves or high wet-bulb globe temperature (WBGT greater than 28°C)

Clothing:

• Light-colored, loose-fitting, breathable fabrics
• Hats for sun protection
• Avoid heavy or impermeable clothing/gear

Vulnerable Populations:

• Elderly: Check on regularly during heat waves, ensure air conditioning access
• Infants: Never leave in parked cars; ensure adequate hydration
• Chronic illness: Extra precautions, medication review
• Homeless: Access to cooling centers

Occupational and Athletic Strategies

Work/Practice Modification:

• Wet-Bulb Globe Temperature (WBGT) monitoring: Integrates temperature, humidity, solar radiation, wind
  • "WBGT less than 27°C: Normal activity"
  • "WBGT 27-31°C: Increase rest breaks, monitor athletes"
  • "WBGT greater than 31°C: Reduce/cancel strenuous activity"
• Work-to-rest ratios: Increase rest periods during extreme heat
• Buddy system: Monitor coworkers/teammates for symptoms

Medical Screening:

• Pre-participation physical examinations
• Identify high-risk individuals (prior heat illness, medications, chronic illness)
• Acclimatization status assessment

Onsite Resources:

• Cold water immersion tubs available at athletic events [24]
• Trained medical personnel
• Rectal thermometers for core temperature assessment
• Emergency action plans

Education:

• Recognize early symptoms
• Emphasize hydration
• Avoid stimulants (caffeine, energy drinks in excess)

Public Health Strategies

Heat Wave Response:

• Heat warning systems: Public alerts when dangerous heat forecast
• Cooling centers: Air-conditioned public spaces (libraries, community centers)
• Vulnerable population outreach: Check on elderly, homeless, chronically ill
• Electricity assistance: Subsidize air conditioning costs for low-income

Urban Planning:

• Increase green spaces and tree canopy (reduce urban heat island effect)
• Cool roofs and pavements
• Accessible water fountains

Climate Adaptation:

• Infrastructure improvements (air conditioning in public housing)
• Building codes (require cooling systems)
• Public education campaigns

Medication Review: Healthcare providers should review medications in at-risk patients during summer months, considering:

• Diuretics (volume depletion)
• Beta-blockers (impaired cardiovascular response)
• Anticholinergics (impaired sweating)
• Antipsychotics (impaired thermoregulation, NMS risk)

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Special Populations

Elderly

Increased Risk:

• Impaired thermoregulation (reduced sweating, blunted thirst)
• Chronic comorbidities (cardiovascular, renal, diabetes)
• Polypharmacy (anticholinergics, diuretics, beta-blockers)
• Social isolation (delayed recognition)
• Lack of air conditioning

Presentation:

• Classic heat stroke (non-exertional)
• Often dry skin (anhidrosis)
• Mortality higher (30-50%)

Management:

• Evaporative cooling preferred over cold water immersion (practical considerations)
• Careful fluid management (risk of fluid overload due to cardiac/renal dysfunction)
• High index of suspicion for complications

Athletes and Military

Increased Risk:

• Exertional heat stroke
• High metabolic heat production during intense activity
• Pressure to perform despite symptoms

Presentation:

• Rapid onset (minutes to hours)
• Usually sweating present
• High incidence of rhabdomyolysis

Management:

• Cold water immersion is gold standard [24]
• Aggressive fluid resuscitation for rhabdomyolysis
• Early return to play protocols must emphasize acclimatization

Prevention:

• Heat acclimatization protocols
• WBGT monitoring
• Mandatory rest breaks
• Onsite cold water immersion tubs and medical staff

Pregnancy

Considerations:

• Increased metabolic rate and heat production
• Fetal risk from maternal hyperthermia (neural tube defects if early pregnancy, fetal distress)
• Treatment same as non-pregnant patients (cooling is priority)
• Monitor fetal heart rate
• Obstetrics consultation

Pediatrics

Increased Risk:

• Higher surface area to body mass ratio (heat absorption)
• Immature thermoregulation
• Dependence on caregivers for hydration and heat avoidance
• Never leave children in parked cars (temperature can reach 50°C [122°F] in minutes)

Management:

• Same principles as adults (cooling, fluids, supportive care)
• Weight-based dosing for medications and fluids

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Quality Metrics and Performance Indicators

Process Measures

Outcome Measures

Documentation Requirements

History:

• Environmental conditions (temperature, humidity, duration of exposure)
• Activity level at time of onset
• Fluid intake
• Medications and substance use
• Time of symptom onset
• Time from symptom onset to cooling initiation

Physical Examination:

• Core temperature (rectal) with time documented
• Neurologic examination (GCS, mental status, cerebellar signs)
• Vital signs (including pulse, BP, RR, SpO2)

Treatment:

• Cooling method used
• Time cooling initiated
• Serial temperatures during cooling
• Time to reach target temperature (less than 39°C)
• Complications and management

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Key Clinical Pearls

Diagnostic Pearls

1. Heat stroke = core temp ≥40°C + CNS dysfunction + heat exposure – this is the diagnostic triad
2. Rectal temperature is mandatory – oral, axillary, tympanic all underestimate; if you don't measure rectal temp, you may miss the diagnosis
3. Sweating does NOT exclude heat stroke – exertional heat stroke typically has ongoing sweating; only classic heat stroke presents with dry skin
4. Check for "the big 4" complications: Rhabdomyolysis (CK, myoglobinuria), DIC (coags, platelets), AKI (Cr, UOP), hepatic injury (AST/ALT)
5. Heat stroke can mimic stroke – focal neurologic deficits can occur; don't get distracted by thrombolytics when the treatment is cooling
6. Differential includes drug-induced hyperthermia – NMS (antipsychotics), serotonin syndrome (SSRIs + other serotonergic drugs), anticholinergic toxicity, sympathomimetics (cocaine, amphetamines)

Treatment Pearls

7. Cool FIRST, ask questions later – do not delay cooling for laboratory confirmation or imaging; every minute counts
8. Cold water immersion is GOLD STANDARD for exertional heat stroke – fastest cooling rate (0.15-0.35°C/min)
9. Evaporative cooling is effective and practical – spray water + fans; nearly as effective as immersion, better access to patient
10. Target less than 39°C within 30 minutes – this is evidence-based and associated with survival benefit [11]
11. Stop cooling at 39°C – prevent overshoot hypothermia; temperature will continue to drift down
12. Antipyretics do NOT work – do not waste time – acetaminophen and NSAIDs are useless; hypothalamic setpoint is normal
13. Dantrolene does NOT work – only effective in malignant hyperthermia, not heat stroke [26]
14. Shivering counteracts cooling – treat with benzodiazepines (midazolam, lorazepam)
15. Aggressive fluids for rhabdomyolysis – target UOP 200-300 mL/hr to flush myoglobin

Disposition Pearls

16. ALL heat stroke patients go to ICU – even if they look better after cooling, multiorgan failure can develop over 24-72 hours
17. Hepatic injury peaks at 48-72 hours – don't be falsely reassured by normal initial LFTs
18. Heat exhaustion can go home after 4-6 hours observation – if symptoms resolve, tolerating PO, safe environment
19. Recurrence risk is high – counsel survivors on prevention; some may never be able to return to strenuous activity in heat
20. Document time to cooling – medicolegal and quality improvement; this is the single most important intervention

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References

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