What is the role of reperfusion and ischemia in the pathogenesis of frostbite?

Updated: Jul 29, 2019
  • Author: Bobak Zonnoor , MD; Chief Editor: Dirk M Elston, MD  more...
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Answer

As tissue is rewarmed, reperfusion injury becomes prominent. Progressive edema of the frostbitten area develops over the first 48-72 hours, followed by bleb formation and necrosis of devitalized tissue. Demarcation of necrotic tissue occurs in the next 60-90 days.

Microscopically, reperfusion results in intracellular swelling, tissue edema with increased compartment pressure, platelet aggregation and thrombosis, and inflammatory leukocyte infiltration with release of free oxygen radicals, prostaglandins, and thromboxane. To date, however, agents that block these mediators have had only marginal clinical success.

Zook et al, in a study of a live gracilis muscle preparation, found that time to reperfusion of muscle after freezing varied but that almost all circulation was restored 10 minutes after rewarming. [22] Blood flow in the microcirculation resumed at near-normal levels after rewarming, suggesting that the vascular structures were not damaged by freezing. The most significant damage was created by white clots and fibrin formation with associated microvascular thrombosis, beginning at 5 minutes after rewarming and continuing for as long as 1 hour after rewarming).

Zook et al noted that platelet abnormalities and fibrin formation resulted in the greatest early and late tissue damage and that classic reperfusion injury did not seem to be as important a factor as was previously believed. [22] This may explain the varied results noted in the literature after attempts to modify mediators of ischemia-reperfusion injury, which do not affect platelets or fibrin formation.

The true effect of chemical mediators remains controversial. However, ischemia-reperfusion injury may still occur because of delayed microvascular thrombosis, compounding the mechanical effects of ice formation and the chemical effects of platelet abnormalities and fibrin microvascular clot formation.


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