Abstract
Observations on early pathophysiology of burning suggests that the release of prostaglandins and thromboxanes plays a role in dermal ischemia. Because of the similarities of the early-phase frostbite wound, blister fluids were aspirated from 10 patients with frostbite, and routine biochemical analysis, immunoelectrophoresis, immunodiffusion, and evaluation of prostaglandins E2, F2 alpha, and thromboxane B2 were performed. Potassium, serum glutamic-oxaloacetic transaminase (SGOT), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) levels exceeded normal serum values. All blisters were found to have IgM, IgG, IgA, C3a, and opsonin. PgE2 was present in levels less than normal, but PgF2 alpha and TxB2 were markedly elevated. Since the vasoconstricting metabolites of arachidonic acid, PgF2 alpha and TxB2, are known to mediate dermal ischemia in burns and pedicle flaps, it is suggested they may play a role in the pathogenesis of frostbite.
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