Formation of ice crystals in the intercellular space increases its hypertonicity drawing water from the cells. Experimentally it appears that the duration of extracellular hypertonicity is the primary determinant of tissue injury. As a consequence of this primary event, a secondary phenomenon of endothelial injury with thrombosis, hemo-concentration and increased viscosity then results. This secondary phenomenon further compromises the biochemical environment of the injured cells, impairs tissue perfusion, enhances local hypoxia and contributes to tissue edema on rewarming. While mild cases of frostbite may involve only an isolated area inadequately protected from cold exposure, severe cases involving the hands and feet tend to occur simultaneously with hypothermia.
Peripheral vasoconstriction occurs with a detected drop in tissue temperature.
This is a protective mechanism designed to maintain the body's core temperature. With continued cold exposure, periodic cold induced vasodilation will reperfuse and rewarm the tissue threatened by cold exposure. If, however, the body's core temperature becomes threatened, shunting will cease with a continued drop in tissue temperature and eventual freezing. Remembering the association between severe frostbite and hypothermia, it may also be necessary to simultaneously rewarm the entire patient. This may require the use of heating blankets, warmed intravenous solutions or even warm peritoneal lavage.