Freezing In frostbite, cooling of the body causes narrowing of the blood vessels (vasoconstriction). Temperatures below are required to form ice crystals in the tissues. The process of freezing causes ice crystals to form in the tissue, which in turn causes damage at the cellular level. Ice crystals can damage cell membranes directly. In addition, ice crystals can damage small blood vessels at the site of injury. Scar tissue forms when fibroblasts replace the dead cells. Rewarming Rewarming causes tissue damage through reperfusion injury, which involves vasodilation, swelling (edema), and poor blood flow (stasis). Platelet aggregation is another possible mechanism of injury. Blisters and spasm of blood vessels (vasospasm) can develop after rewarming. Non-freezing cold injury The process of frostbite differs from the process of non-freezing cold injury (NFCI). In NFCI, temperature in the tissue decreases gradually. This slower temperature decrease allows the body to try to compensate through alternating cycles of closing and opening blood vessels (vasoconstriction and vasodilation). If this process continues, inflammatory mast cells act in the area. Small clots (microthrombi) form and can cut off blood to the affected area (known as ischemia) and damage nerve fibers. Rewarming causes a series of inflammatory chemicals such as prostaglandins to increase localized clotting. Pathophysiology The pathological mechanism by which frostbite causes body tissue injury can be characterized by four stages: Prefreeze, freeze-thaw, vascular stasis, and the late ischemic stage. # Prefreeze phase: involves the cooling of tissues without ice crystal formation. # Freeze-thaw phase: ice-crystals form, resulting in cellular damage and death. # Vascular stasis phase: marked by blood coagulation or the leaking of blood out of the vessels. # Late ischemic phase: characterized by inflammatory events, ischemia and tissue death.
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