Heat Stroke and Related Illness

Basics

Description

  • Heat stroke occurs during imbalance in heat production, absorption, and dissipation. It can result from excessive body heat generation and storage without appropriate dissipation, high ambient temperature, low radiation or convective heat loss, decreased evaporation, or inadequate fluid/electrolyte replacement in response to losses through sweat or GI disturbance.
  • Two forms of heat stroke exist:
    • Exertional heat stroke (EHS), which occurs during periods of intense exertion with exposure to high temperatures in otherwise healthy individuals
    • Nonexertional or classic heat stroke (NEHS), in which the body is unable to compensate for an increase in ambient temperature; more common in very young and elderly, chronic illness, and during heat waves

Epidemiology

  • In the United States, 658 deaths per year from heat illness; recognized as a leading cause of death in athletes, especially football early in the season
  • Recent heat waves associated with increase in heat related illness, EHS, NEHS, and deaths

Risk Factors

  • Environmental: high ambient temperature, humidity, lack of wind or shade, heat waves, overheated indoor environment, lack of air conditioning, social isolation, inability to care for self, or entrapment in closed space (i.e., car, trunk; internal automobile temperature in sunlight with poor ventilation can reach 131–172°F; the sharpest temperature increase occurs within first 15 minutes)
  • Medical: obesity, low fitness level, cardiac disease, previous episode of heat illness, lack of sleep, concurrent febrile illness, diabetes mellitus or insipidus, diarrhea, hyperthyroidism, dehydration, vascular disease, sweat gland dysfunction, sunburn, viral illness, sickle cell, history of malignant hyperthermia
  • Drugs/medications:
    • Anticholinergics
    • Antihistamines
    • Stimulants
    • β-Blockers
    • Calcium channel blockers
    • Diuretics
    • Psychiatric medications
    • Recreational drugs and alcohol
  • Behaviors:
    • Lack of recognition of risk factors or warning signs
    • Overexertion with inadequate or majority hypotonic fluid intake
    • Inappropriate clothing; heavy, dark, tight-fitting, overbundling
    • Lack of acclimatization and conditioning (early in athletic season)
    • Children left in vehicles

General Prevention

  • Avoid enclosed spaces; never leave a child in a car.
  • In high ambient temperatures: Reduce activity levels, keep cool, frequent breaks, use shaded areas.
  • Allow adaptation to warmer climates which may take 8 to 10 exposures of 30 to 45 minutes each daily or every other day; promote gradual conditioning over 10 to 14 days.
  • Air conditioning or fans during hot weather
  • Cool or tepid baths
  • Increase fluid intake before, during, and after scheduled exercise or strenuous activity (up to 200 to 300 mL q10–20min); do not wait until thirsty.
  • Precooling using external (cold water immersion, cooling vests) or internal (drinking cold liquid/ice) may improve performance before endurance events in heat.
  • Loose, light-colored clothing, protective hat
  • Liberal dietary sodium:
    • Avoid NaCl tablets (possible hypernatremia, potassium depletion, gastric irritation, delayed gastric emptying).
  • Frequently flex leg muscles when standing.
  • Avoid prolonged standing in hot environments.
  • Avoid caffeine and alcohol.

Pathophysiology

  • Heat production increases by 10 to 20 times with strenuous exercise.
  • When environmental temperature is greater than body temperature, body gains heat by conduction and radiation and can only lose heat by evaporation and convection (limited by humidity and lack of air movement).
  • Children have greater body surface-to-mass ratio, higher metabolic rate, inability to increase cardiac output, decreased sweat production, and inability to independently change environments compared to adults.
  • Severe disease is a result of thermal injury to tissues which causes a systemic inflammatory response.
    • Dehydration results in loss of sweating, hence decreased evaporation.
    • >40°C, cell volume, membrane integrity, metabolism, acid–base balance is affected.
    • Extreme core temperatures >42°C can uncouple oxidative phosphorylation and allow enzyme systems to cease functioning.

Commonly Associated Conditions

Heat illness is on a continuum of severity, including the following:

  • Miliaria rubra (prickly heat): Heat rash, usually caused by obstruction of sweat glands by clothes or lotions, produces an erythematous papular rash; usually self-limited
  • Heat cramps/spasms: exercise-induced muscle spasms during or immediately after exercise; related to poor conditioning and water and sodium depletion
  • Heat tetany: progression of heat cramps into paresthesias and carpopedal spasm
  • Heat syncope: alteration of consciousness (i.e., dizziness, syncope) at end of strenuous or upright event
  • Heat edema: swollen feet and ankles due to peripheral vasodilation, vascular leak, and orthostatic pooling
  • Heat exhaustion: relatively insidious onset. Associated with water and/or salt depletion. Copious perspiration with headache, nausea, vomiting, malaise, myalgias, pallor, light-headedness, visual disturbances, syncope, temperature 38–40°C, dehydration, electrolyte imbalance, hemoconcentration; can persist or evolve into heat stroke
  • Heat stroke: core body temperature exceeding 40°C with altered mental status ranging from confusion, disorientation, and incoherent speech to delirium, decerebrate posturing, seizure, and coma. May have acute, sudden onset (80%) or slower onset (minutes to hours, 20%). Classic (NEHS) heat stroke is associated with dry skin and prolonged exposure to elevated temperatures at rest. EHS may present with anhidrosis or profuse sweating.

There's more to see -- the rest of this topic is available only to subscribers.