Heat Emergencies

 Introduction

Heat emergencies represent a spectrum of disorders caused by exposure to high environmental temperature and/or impaired heat dissipation mechanisms. They range from mild (heat cramps) to life-threatening (heat stroke).

In critical care and emergency medicine, heat illness is considered a true medical emergency when core temperature exceeds 40°C with central nervous system dysfunction.

Thermoregulation Overview

• The hypothalamus (preoptic area) acts as the body’s thermostat.
• Heat is produced by metabolism and muscle activity.
• Heat is lost via:
  • Radiation (60%)
  • Evaporation (25%) – dominant in hot environments
  • Conduction and convection (15%)
• In extreme heat or humidity, evaporation (sweating) becomes ineffective, leading to heat accumulation and cellular dysfunction.

 

 Spectrum of Heat-Related Illnesses

Disorder	Core Temp (°C)	Key Features
Heat edema	Normal	Dependent edema, elderly, due to vasodilation
Heat rash (miliaria)	Normal	Obstruction of sweat ducts, itchy papulovesicular rash
Heat cramps	Normal–mild ↑	Painful involuntary muscle spasms due to salt depletion
Heat syncope	Normal–mild ↑	Transient LOC from peripheral vasodilation & venous pooling
Heat exhaustion	37–40°C	Volume depletion, fatigue, dizziness, tachycardia, no CNS dysfunction
Heat stroke	≥40°C	CNS dysfunction + multiorgan failure, true emergency

 

1. Heat Edema

Core Temperature: Normal
Mechanism:

• Occurs due to peripheral vasodilation and venous pooling when the body is exposed to heat, especially in elderly or unacclimatized individuals.
• The capillary hydrostatic pressure increases, leading to transudation of fluid into interstitial tissue, typically in the lower limbs.

Clinical Features:

• Mild swelling of ankles, feet, or hands after standing in heat.
• No pain, redness, or systemic illness.
• Occurs in hot, humid climates or after travel to tropical regions (“tropical edema”).

Management:

• Reassurance; it resolves spontaneously.
• Leg elevation, compression stockings, and avoiding prolonged standing help.
• No diuretics required unless another cause (like heart failure) is suspected.

 

2. Heat Rash (Miliaria / Prickly Heat)

Core Temperature: Normal
Mechanism:

• Caused by obstruction of sweat ducts → sweat leaks into epidermis or dermis → inflammatory reaction.
• Common in hot, humid conditions and in people wearing occlusive clothing.

Types:

• Miliaria crystallina: superficial, clear vesicles without inflammation.
• Miliaria rubra (“prickly heat”): red, itchy papules due to deeper obstruction.
• Miliaria profunda: deeper dermal involvement, may cause heat intolerance due to reduced sweating.

Clinical Features:

• Itchy papulovesicular rash, mainly on neck, upper trunk, groin, and under breasts.
• Worse with sweating, resolves in cooler environments.

Management:

• Move to cool, dry environment.
• Loose cotton clothing.
• Calamine lotion, mild topical steroids if inflamed.
• Avoid heavy creams and occlusive ointments.

 

3. Heat Cramps

Core Temperature: Normal or mildly elevated
Mechanism:

• Due to loss of sodium and chloride in sweat without adequate replacement.
• Typically occurs during or after strenuous physical activity in hot environments.
• Results in hyponatremia of extracellular fluid, leading to painful muscle contractions.

Clinical Features:

• Painful, involuntary muscle spasms in calves, arms, or abdomen.
• Sweating may be profuse.
• Patient is alert, with normal mental status.
• Serum sodium may be low or normal.

Management:

• Rest and cooling.
• Oral or IV rehydration with electrolyte-containing fluids (not plain water).
• Normal saline (0.9%) if IV route is required.
• Educate on salt supplementation during heavy exertion in heat.

 

4. Heat Syncope

Core Temperature: Normal or mildly elevated
Mechanism:

• Occurs from peripheral vasodilation and venous pooling, reducing cerebral perfusion.
• Often happens after prolonged standing or sudden change in posture in a hot environment.
• Volume depletion and lack of acclimatization increase risk.

Clinical Features:

• Transient loss of consciousness (LOC) or near-syncope.
• Skin warm and moist, pulse weak, blood pressure low.
• Rapid spontaneous recovery on lying down.

Management:

• Supine position, leg elevation.
• Oral rehydration and rest in a cool environment.
• Rule out cardiac syncope in elderly.

 

5. Heat Exhaustion

Core Temperature: 37–40°C
Mechanism:

• Represents failure of cardiovascular response to heat stress.
• Caused by salt and water depletion, leading to decreased effective circulating volume.
• Core temperature rises, but thermoregulatory mechanisms (sweating, vasodilation) are still intact.

Clinical Features:

• Symptoms: Fatigue, weakness, dizziness, headache, nausea, vomiting.
• Signs: Tachycardia, hypotension, profuse sweating, mild temperature elevation.
• No CNS dysfunction — patient remains oriented (key differentiator from heat stroke).

Management:

• Move to cool shaded environment.
• Rest and remove excess clothing.
• Oral or IV isotonic fluids (normal saline).
• Monitor vital signs and urine output.
• If untreated, may progress to heat stroke.

 

6. Heat Stroke

Core Temperature: ≥ 40°C
Mechanism:

• Thermoregulatory failure → uncontrolled rise in core temperature.
• Cellular injury, inflammatory cytokine surge, coagulopathy, and multiorgan failure.
• Two types:
  • Classic (non-exertional): Elderly, infants, chronic illness, during heat waves.
  • Exertional: Young healthy individuals during strenuous activity in heat.

Clinical Features:

• CNS dysfunction: Confusion, seizures, delirium, coma.
• Skin: Hot, flushed, may be dry (classic) or sweaty (exertional).
• Cardiovascular: Tachycardia, hypotension.
• Multiorgan involvement:
  • Rhabdomyolysis → AKI
  • DIC → bleeding
  • Hepatic failure
  • ARDS

Investigations:

• Core temp (rectal): ≥40°C
• ↑ CK, ↑ AST/ALT, ↑ creatinine, DIC profile abnormal, metabolic acidosis.

Management:

• Immediate cooling (goal ≤39°C within 30–60 min):
  • Evaporative method: Spray tepid water + fan
  • Cold water immersion (preferred in exertional)
  • Ice packs to axillae, groin, neck
• ABCs of resuscitation; airway protection if comatose
• IV isotonic fluids, avoid overhydration
• Treat complications: seizures, rhabdomyolysis, DIC, renal failure
• Avoid antipyretics (ineffective, may worsen hepatic injury).

Prognosis:

• Mortality 10–50% depending on delay in treatment.
• Neurological damage can be permanent if core temperature remains >42°C for >1 hour.

 

 Summary Table

Disorder	Core Temp (°C)	Key Mechanism	Main Features
Heat edema	Normal	Vasodilation & venous pooling	Ankle swelling
Heat rash	Normal	Sweat duct obstruction	Itchy rash
Heat cramps	Normal–mild ↑	Salt depletion	Painful muscle cramps
Heat syncope	Normal–mild ↑	Vasodilation & reduced cerebral perfusion	Transient LOC
Heat exhaustion	37–40°C	Volume depletion	Weakness, hypotension, no CNS dysfunction
Heat stroke	≥40°C	Thermoregulatory failure	CNS dysfunction, multiorgan failure

 

 References

1. Harrison’s Principles of Internal Medicine, 21st ed. — Chapter 480, Environmental Disorders: Heat Illness
2. UpToDate: Heat stroke and heat exhaustion (2024)
3. AHA Statement: Environmental Heat Exposure and Cardiovascular Health (Circulation, 2021)
4. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346(25):1978–88.
5. WHO Technical Report on Heat Health Action Plans, 2022.