Frostbite injuries: a rational approach based on the pathophysiology

Abstract

The breakdown products of arachidonic acid have been implicated as mediators of progressive dermal ischemia in both cold and thermal injuries. Increased tissue survival can be demonstrated experimentally with the preservation of the dermal microcirculation by using antiprostaglandin agents and thromboxane inhibitors. Thirty-eight consecutive patients (28 males and 10 females aged 2 mo to 46 yr) with frostbite injuries were treated at the University of Chicago's Burn Center in January 1982 with a protocol designed to decrease the production of thromboxane locally and prostaglandins systemically. All patients recovered without significant tissue loss. The average hospital stay was 5.6 days for acute injuries and 6.9 days for subacute injuries.