Pathophysiology of frostbite

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