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Pathophysiology of frostbite

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

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pathophysiology of frostbite

Injury caused by the freezing of tissue can be divided into 4 overlapping pathological pahses:

  • prefreeze
    • presence of tissue cooling with accompanying vasoconstriction and ischaemia
    • does not involve actual ice crystal formation
    • there is hyperesthesia and paresthesia due to neuronal cooling and ischaemia

  • freeze-thaw phase
    • formation of ice crystals intracellularly (during a more rapid-onset freezing injury) or extracellularly (during a slower freeze)
    • results in protein and lipid derangement, cellular electrolyte shifts, cellular dehydration, cell membrane lysis, and cell death
    • thawing process may initiate ischemia-reperfusion injury and the inflammatory response

  • vascular stasis phase
    • vessels may fluctuate between constriction and dilation
    • blood may leak from vessels or coagulate within them

  • late ischaemic phase
    • caused by progressive tissue ischemia and infarction from a cascade of event e.g. - inflammation mediated by thromboxane A2, prostaglandin F2α, bradykinins, and histamine; intermittent vasoconstriction of arterioles and venules; continued reperfusion injury; showers of emboli coursing through the microvessels; and thrombus formation in larger vessels
    • cell death is caused by destruction of the microcirculation


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