Frostbite

Basics

Description

  • Tissue damage caused by cold temperature exposure
  • Mechanism:
    • Tissue damage results from:
      • Direct cell damage: Intracellular ice crystal formation
      • Indirect cell damage: Extracellular ice crystal formation leads to intracellular dehydration and enzymatic disruption
      • Reperfusion injury: Occurs upon rewarming. Fluid rich in inflammatory mediators (prostaglandin and thromboxane) extravasates through damaged endothelium promoting vasoconstriction and platelet aggregation
      • Clear blisters from extracellular exudation of fluid
      • Hemorrhagic blisters occur when deeper subdermal vessels are disrupted, indicating more severe tissue injury
      • The end result is arterial thrombosis, ischemia, and ultimately, necrosis
    • Devitalized tissue demarcates as the injury evolves over weeks to months, hence the phrase “frostbite in January, amputate in July”

Etiology

  • Cold exposure: Duration of exposure, wind chill, humidity, and wet skin and clothing all increase the likelihood of frostbite
  • Predisposing factors:
    • Extremes of age
    • Altered mental status (intoxication or psychiatric illness)
    • Poor circulatory status

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