pathophysiology of frostbite

Last reviewed 02/2021

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