Treatment of freezing injury

Abstract

Report on therapeutic procedures in patients with second and third degree congelations (frostbite) on the feet. Two mechanisms of tissue damage caused by exposure to cold temperature will be discussed pathophysiologically: direct freezing injuries and cell death through intra and extracellular ice crystal formation as well as transient and finally irreversible tissue damage due to decreased perfusion. The condition of decreased perfusion results from persistent vaso-constriction induced by cold temperature, increased blood viscosity, sludge phenomenon and occlusion by platelet thrombi in the microvasculature. Frostbite beyond the erythematous stage should be treated primarily with a parenteral therapy in order to improve the hemorrheologic parameters, in particular within the micro-vascular compartment. Colloidal plasma volume expander such as 10% dextran solution is used to increase the intravascular volume. This solution (with its coating effect) and pentoxifyllin lowers the aggregation of erythrocytes and platelets. The latter will also be favourably influenced by the use of iloprost or acetylsalicylic acid. Iloprost as a stable metabolite of prostacyclin is a powerful vasodilator which attenuates the peripheral vascular resistance and activates fribrinolysis. Pentoxifyllin is considered to lower pathologically increased levels of fibrinogen. Both drugs may protect against damage of the vascular endothelium. Based on their pharmacological effects the above-mentioned drugs may improve tissue perfusion and therefore tissue damage caused by frostbite can be limited. However, an important factor is to strictly avoid bacterial infections in the cold-damaged tissue.