Heat-Related Illnesses¶
Chapter 478 | Part 15: Disorders Associated with Environmental Exposures
KEY CLINICAL POINTS¶
- Heat-related illnesses range from mild (heat syncope, cramps) to life-threatening (heatstroke) and are increasingly prevalent due to climate change.
- Heatstroke is defined by core temperature >40.5°C (104.9°F) and CNS dysfunction, requiring immediate cooling and resuscitation.
- Frostbite treatment involves rapid rewarming with 37–40°C water, avoiding hot air, and managing complications like neuropathy and infection.
- Key risk factors include dehydration, anticholinergic medications, cardiovascular disease, and lack of acclimatization to heat.
- Cooling strategies (e.g., immersion, cold packs) and IV fluid resuscitation are critical for heatstroke management.
1. DEFINITION & OVERVIEW¶
Heat-related illnesses encompass a spectrum of disorders from heat syncope and cramps to life-threatening heatstroke. Frostbite, though distinct, is also discussed as an environmental injury. Heatstroke is characterized by loss of thermoregulatory control, leading to hyperthermia and multiorgan failure.
Table 477-4 Treatment for Frostbite¶
| 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. |
| Stabilize core temperature and treat hypothermia. | Immerse part in 37°–39°C (99°–102.2°F) circulating water containing antiseptic soap until distal flush (10–45 min). | Leave hemorrhagic vesicles intact to prevent desiccation and infection. |
| 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). |
1.1 Heat-Related Illness Spectrum¶
Heat syncope, cramps, exhaustion, and heatstroke represent a continuum of severity. Frostbite is a separate but related environmental injury involving cold exposure.
1.2 Thermoregulation Mechanisms¶
The body dissipates heat via evaporation, radiation, conduction, and convection. Impairment of these mechanisms leads to heat accumulation.
2. EPIDEMIOLOGY¶
Climate change has increased heat-related morbidity and mortality. Extreme heat events are more frequent and affect diverse populations. Vulnerable groups include the elderly, those with limited access to cooling, and individuals with cardiovascular or metabolic disorders.
Table 478-1 Heat-Related Illness: Predisposing Factors and Differential Diagnosis¶
| 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 |
| Endocrine and immune-related illness | Diabetic ketoacidosis, Multiple-organ dysfunction syndrome, Pheochromocytoma |
2.1 Risk Factors¶
Age extremes, cardiovascular inefficiency, dehydration, anticholinergic medications, and lack of heat acclimatization increase risk. Obesity and poor physical fitness also contribute.
2.2 Demographics¶
Heatstroke mortality is highest in the elderly and those with comorbidities. Heat exhaustion is more common in laborers, athletes, and military personnel.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Heat-related illnesses arise from impaired thermoregulation. Environmental heat stress, combined with factors like dehydration, anticholinergic drugs, or cardiovascular disease, overwhelms the body's cooling mechanisms. Heatstroke results from loss of thermoregulatory control, leading to hyperthermia and systemic inflammation.
3.1 Thermoregulatory Failure¶
Evaporation is the primary heat loss mechanism, but humidity and clothing reduce its efficacy. Heatstroke occurs when core temperature exceeds 40.5°C, causing cellular injury and multiorgan dysfunction.
3.2 Pathophysiology of Heatstroke¶
Thermosensitive enzymes become dysfunctional, leading to oxidative phosphorylation uncoupling. Systemic inflammation, coagulopathy, and rhabdomyolysis develop due to cellular damage.
4. CLINICAL FEATURES¶
Symptoms vary by severity. Heat syncope presents with dizziness and fainting, while heat exhaustion includes headache, nausea, and tachycardia. Heatstroke is marked by CNS dysfunction, hyperthermia, and multiorgan failure.
4.1 Heat Cramps¶
Intermittent muscle spasms due to electrolyte imbalance (hypokalemia, hyponatremia). Common in unacclimated individuals after exertion.
5. DIFFERENTIAL DIAGNOSIS¶
Conditions mimicking heatstroke include neuroleptic malignant syndrome, serotonin syndrome, and infections. Other differentials include metabolic encephalopathy, stroke, and toxicologic agents.
5.1 Non-Heat-Related Mimics¶
Neuroleptic malignant syndrome (NMS), serotonin syndrome, and cerebral abscesses can present with CNS dysfunction and hyperthermia.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis of heatstroke requires core temperature >40.5°C and CNS dysfunction. Laboratory findings include hyperkalemia, elevated creatine kinase, and coagulopathy. Differential diagnosis excludes infections, drug toxicity, and other metabolic causes.
Table 478-2 Typical Manifestations of Heatstroke¶
| CLASSIC | EXERTIONAL |
|---|---|
| Older patient | Younger patient |
| Anhidrosis (possible) | Diaphoresis (common) |
| Central nervous system dysfunction | Myocardial/hepatic injury |
| Oliguria | Acute renal failure |
| Coagulopathy (mild) | Disseminated intravascular coagulation |
| Mild lactic acidosis | Marked lactic acidosis |
6.1 Diagnostic Criteria¶
Core temperature >40.5°C, CNS dysfunction, and exclusion of other causes of hyperthermia. Laboratory tests include electrolytes, creatine kinase, and coagulation studies.
7. MANAGEMENT & TREATMENT¶
Immediate cooling is critical for heatstroke. IV fluids, monitoring, and supportive care are essential. Frostbite requires rapid rewarming and prevention of complications like infection and neuropathy.
7.1 Cooling Strategies¶
Cool water (15°C) spray, cold packs, and immersion in ice-cold water are effective. Avoid antipyretics and anticholinergics. Aggressive IV resuscitation with isotonic fluids is required.
7.2 Frostbite Management¶
Rapid rewarming with 37–40°C water, avoiding hot air. Thrombolytics may reduce amputation risk. Monitor for infection and compartment syndrome.
8. PROGNOSIS & COMPLICATIONS¶
Mortality increases with core temperatures >42°C and prolonged hyperthermia. Complications include renal failure, coagulopathy, rhabdomyolysis, and multiorgan failure. Early cooling improves outcomes.
8.1 Prognostic Factors¶
Core temperature >42°C, duration of hyperthermia, and presence of rhabdomyolysis or coagulopathy correlate with poor outcomes.
9. SPECIAL CONSIDERATIONS¶
Elderly patients and those with comorbidities require close monitoring. Pediatric patients may present with heat edema or syncope. Heat-related illnesses during pregnancy require careful fluid management.
9.1 Vulnerable Populations¶
Elderly, immunocompromised, and those with cardiovascular disease are at higher risk. Heat exhaustion in athletes and laborers often requires inpatient care.
10. KEY POINTS & CLINICAL PEARLS¶
- Immediate cooling is critical for heatstroke. 2. IV fluids and monitoring are essential for stabilization. 3. Frostbite requires rapid rewarming and prevention of infection. 4. Recognize heatstroke early to prevent multiorgan failure. 5. Avoid antipyretics and anticholinergics in heatstroke.