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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

Reference:

(1) McIntosh SE et al. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite: 2014 update. Wilderness Environ Med. 2014;25(4 Suppl):S43-54

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