Heat-Related Illnesses¶

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Chapter 478 | Part 15: Disorders Associated with Environmental Exposures · Parts 15-16 – Genetics, Genomics & Precision Medicine · Chapter 478

Key Clinical Points¶

Heatstroke is defined by a total loss of thermoregulatory function, core temperature >40.5°C (104.9°F), and CNS dysfunction.
Classic heatstroke (CHS) typically affects older patients with chronic diseases during heat waves; Exertional heatstroke (EHS) affects young, healthy athletes/laborers.
Rapid cooling is essential; target temperature for stopping active cooling is 38°–39°C (100.4°F–102.2°F) to avoid hypothermic afterdrop.
Antipyretics (salicylates, acetaminophen) have no therapeutic role and may exacerbate coagulopathies or hepatic stress.
Avoid anticholinergic medications (e.g., atropine) as they inhibit sweating.
Wet-bulb globe temperature (WBGT) is superior to heat index as it incorporates radiant heat and wind speed.
Heat exhaustion is a diagnosis of exclusion; if signs of heatstroke are present, rapid cooling and resuscitation are indicated.
EHS patients are often profusely diaphoretic despite dehydration; CHS patients often have anhidrosis and dry skin.
Prognosis worsens if initial core temperature exceeds 42°C (107.6°F) or if prolonged hyperthermia occurs.
Mortality correlates directly with the number of dysfunctional organ systems.

DEFINITION & OVERVIEW¶

• Core Definition:

Definition (Harrison's 22e): the clinical manifestations of heatstroke reflect a total loss of thermoregulatory function. • Thermoregulation Mechanism: ◦ Central thermostat: Located in the preoptic nucleus of the anterior hypothalamus. ◦ Efferent signals: Trigger cutaneous vasodilation and diaphoresis to facilitate heat loss. ◦ Skin surface: Primary site of heat loss; skin blood flow can increase 25–30 times over the basal rate. • Heat-Related Spectrum: ◦ Range: Includes heat syncope, muscle cramps, and heat exhaustion to medical emergencies like heatstroke. ◦ Distinction: Fever reflects intact thermoregulatory function; heatstroke reflects a total loss of that function.

Thermoregulation Mechanisms¶

• Heat Dissipation: ◦ Evaporation: Single most efficient mechanism, but becomes progressively ineffective as relative humidity rises to >70%. ◦ Radiation: Continuous loss of infrared electromagnetic energy into the environment. ◦ Conduction & Convection: Direct transfer to cooler objects or air currents; both become ineffective when environmental temperature exceeds skin temperature. • Environmental Assessment: ◦ Wet-bulb globe temperature (WBGT): Superior to heat index as it incorporates radiant heat and wind speed.

Acclimatization¶

• Physiologic Adaptations: ◦ Duration: Requires 1 to several weeks of exposure/work in a hot environment. ◦ Thermoregulatory set point: Altered during acclimatization. ◦ Sweating: Lowered threshold for initiation; increased volume (1–2 L/h); lower salt concentration. ◦ Cardiovascular: Plasma volume expansion → improved cutaneous vascular flow; heart rate lowers with higher stroke volume. • Persistence: ◦ Adaptation dissipates rapidly once the individual leaves the hot environment; plasma volume decreases and acclimatization is lost within weeks.

EPIDEMIOLOGY¶

• Environmental Impact: Climate change is globally increasing heat-related morbidity and mortality due to more frequent/widespread extreme heat events. • High-Risk Groups: ◦ Elderly: Especially those with poor nutrition or lack of access to air-conditioned environments. ◦ Children & Adolescents: Preadolescents and teenagers are at risk due to potential poor judgment during vigorous exercise in high humidity/heat. • Clinical Risks: ◦ Cardiovascular events (CVA, MI) occur ≥ 10 times more often in conditions of extreme severity. ◦ Risk factors: Obesity, poor conditioning, lack of acclimatization, and mild dehydration.

ETIOLOGY & PATHOPHYYSICOLOGY¶

• Impairment Factors: ◦ Anticholinergics: Impair sweating and blunt the normal cardiovascular response to heat. ◦ Phenothiazines & Heterocyclic antidepressants: Cause central depletion of dopamine → interfere with preoptic nucleus function. ◦ Beta-blockers & Calcium channel blockers: Inhibit sweating by reducing peripheral blood flow. • Systemic Response: ◦ Heat-induced SIRS: Reflects responses of both innate and adaptive immune systems. ◦ Endothelial Damage: Injury to the vascular endothelium activates the coagulation cascade. ◦ Splanchnic Ischemia: Significant shunting away from splanchnic circulation leads to endotoxemia. • Cellular Injury: ◦ Hepatocytes: Highly sensitive to heat; AST is routinely elevated, and ALT may exceed 100 times normal values. ◦ Threshold: Above 42°C (107.6°F) → rapid direct cellular injury, nonfunctional enzymes, and irreversible uncoupling of oxidative phosphorylation.

CLINICAL FEATURES¶

• General Presentation: ◦ Symptoms: Weakness, dizziness, disorientation, ataxia, gastrointestinal or psychiatric symptoms. ◦ Vital Signs: Tachypnea, tachycardia, hypotension, and widened pulse pressure. • Progression to Heatstroke: ◦ Sudden onset occurs when maintenance of adequate perfusion requires peripheral vasoconstriction → cutaneous radiation ceases → core temperature rises dramatically.

Minor Heat-Emergency Syndromes¶

• Heat Edema: Mild swelling of hands, feet, and ankles; caused by cutaneous vasodilation and increased secretion of ADH and aldosterone. • Prickly Heat (miliaria rubra): Maculopapular, pruritic, erythematous rash. Treatment: 1% salicylic acid TID (caution for salicylate toxicity) or chlorhexidine cream. • Heat Syncope: Postural hypotension due to volume depletion, decreased vasomotor tone, and peripheral vasodilation. • Hyperventilation Tetany: Respiratory alkalosis → paresthesia and carpopedal spasm. Treatment: Reassurance and addressing hyperventilation. • Heat Cramps: ◦ Cause: Relative deficiency of Na, K, and fluid at the intracellular level; often from high sweat salt content + consumption of hypotonic fluids. ◦ Treatment: Oral electrolyte solutions (e.g., 2x 650-mg salt tablets dissolved in 1 quart water → 0.1% saline).

Heat Exhaustion¶

• Definition: Maintenance of thermoregulatory control and CNS function. • Clinical Status: Core temperature elevated but generally <40.5^oC. • Management: Observation/IV rehydration for healthy patients; inpatient monitoring for elderly or those with comorbidities.

Heatstroke¶

• Core Features: Total loss of thermoregulatory function and CNS dysfunction. • Clinical Presentation: Often preceded by non-specific prodromal symptoms (weakness, dizziness). • Cardiac/Pulmonary: Potential for troponin elevation; may present with noncardiogenic pulmonary edema and basilar rales despite hypovolemia. • Laboratory Findings: ◦ Liver: AST routinely elevated; ALT often >100x normal. ◦ Coagulation: Decreased platelets, fibrinogen, and prothrombin. ◦ Metabolic: Hypernatremia (secondary to dehydration in CHS); stress leukocytosis. • Comparison of Manifestations (Table 3): ◦ Classic Heatstroke (CHS): Older patient; sedentary; anhidrosis; mild lactic acidosis; normonatremia. ◦ Exertional Heatstroke (EHS): Younger patient; active/exercising; diaphoresis; marked lactic acidosis; hyponatremia.

DIFFERENTIAL DIAGNOSIS¶

• Clinical Mimics: ◦ Malignant hyperthermia (post-anesthesia). ◦ Neuroleptic malignant syndrome (antipsychotics, SSRIs). ◦ Infections: Meningitis, encephalitis, malaria, sepsis. ◦ Toxidromes: Serotonin syndrome, strychnine, sympathomimetics. • Predisposing Factors & Differential Categories (Table 2): ◦ Cardiovascular: Age extremes, Beta/calcium block, CHF, Dehydration, Diuresis, Obesity, Poor fitness. ◦ Impaired Heat Loss: Antihistamines, Phenothiazines, Occlusive clothing, Skin abnormalities. ◦ Excessive Load: Environmental conditions, Exertion, Fever, Hypermetabolic state, Lack of acclimatization. ◦ Toxicologic: Amphetamines, Anticholinergic toxidrome, Cocaine, Dietary supplements, Hallucinogens, Salicylates, Withdrawal syndromes.

INVESTIGATIONS & DIAGNOSIS¶

Initial Assessment: Identify clinical triad of exposure to heat stress, CNS dysfunction, and core temperature >40.5^oC (104.9°F).
Laboratory Workup:
Cardiac: Troponins, CK, LDH.
Liver: AST, ALT.
Coagulation: Platelets, fibrinogen, prothrombin.
Metabolic: Glucose, Calcium, Sodium.
Advanced Diagnostics (if mental status persists):
Toxicologic screening.
Cranial CT and spinal fluid analysis.

MANAGEMENT & TREATMENT¶

Rapid Cooling:
Primary goal: Immediate reduction of core temperature.
Methods: Spray cool water with fans; Ice-water immersion (preferred for EHS); Ice-water bags or cooling body bags; Cold packs to neck, axillae, and groin.
Cooling Termination:
Stop active cooling when core temperature reaches 38°–39°C (100.4°F–102.2°F) to avoid hypothermic afterdrop.
Resuscitation & Fluid Management:
Crystalloid for volume expansion.
Monitor electrolytes and acid-base status.
Monitoring:
Continuous core temperature monitoring.
CVP, Troponins, CK, LDH, and Urinalysis (to monitor for myoglobinuria/hematuria).

PROGNOSIS & COMPLICATIONS¶

• Impact of Delay: Delayed cooling → severe hepatic dysfunction, renal failure, DIC, and fulminant multi-organ failure. • Direct Injury: Temperatures >42^oC (107.6°F) cause rapid direct cellular injury and enzyme nonfunction. • Mortality: Directly correlates with the number of dysfunctional organ systems.

KEY PEARLS & CLINICAL TRAPS¶

• Antipyretics: No therapeutic role; may exacerbate coagulopathy or hepatic stress. • Anticholinergics: Avoid (e.g., atropine) as they inhibit sweating. • Cooling Priority: Rapid cooling is the priority over initial administration of antiarrhythmics. • EHS vs CHS: EHS patients are often diaphoretic; CHS patients may have anhidrosis and dry skin.

Reference Tables¶

TABLE 477-4 Treatment for Frostbite¶

Harrison's 22e, p.3772

BEFORE THAWING	DURING THAWING	AFTER THAWING
Remove from environment.	Consider parenteral analgesia and ketorolac.	Gently dry and protect part; elevate; place pledgets between toes, if macerated.
	Administer ibuprofen (400 mg PO).
Stabilize core temperature and treat hypothermia.	Immerse part in 37°–39°C (99°–102.2°F) (thermometer-monitored) circulating water containing an antiseptic soap until distal flush (10–45 min).	Leave hemorrhagic vesicles intact to prevent desiccation and infection.
	Encourage patient to gently move part.
Address medical or surgical conditions.	If pain is refractory, reduce water temperature to 35°–37°C (95°–99°F) and administer parenteral narcotics.	Consider tetanus prophylaxis; elevate part. Administer hydrotherapy at 37°C (99°F). Consider dextran or phenoxybenzamine or, in severe cases, thrombolysis rt-PA (IV or intraarterial).

Harrison's 22e, p.3773

ILLNESS	PREDISPOSING FACTORS
Cardiovascular inefficiency	Age extremes Beta/calcium channel blockade Congestive heart failure Dehydration Diuresis Obesity Poor physical fitness
Impaired heat loss	Antihistamines Heterocyclic antidepressants Occlusive clothing Skin abnormalities
Excessive heat load	Environmental conditions Exertion Fever Hypermetabolic state Lack of acclimatization
Toxicologic illness	Amphetamines Anticholinergic toxidrome Cocaine Dietary supplements Hallucinogens Malignant hyperthermia Neuroleptic malignant syndrome Salicylates Serotonin syndrome Strychnine Sympathomimetics Withdrawal syndromes (ethanol, hypnotics)

TABLE 478-2 Typical Manifestations of Heatstroke CLASSIC Older patient Predisposing health factors/ medications…¶

Harrison's 22e, p.3775

CLASSIC	EXERTIONAL
Older patient	Younger patient
Epidemiology (heat waves)	Sporadic cases
Anhidrosis (possible)	Diaphoresis (common)
Oliguria	Acute renal failure
Mild lactic acidosis	Marked lactic acidosis
Normoglycemia/calcemia	Hypoglycemia/calcemia
Normonatremia	Hyponatremia