Electrical burns.

Abstract

Electrical injury is unlike other burns because of extensive local destruction of tissue at the points of entrance and exit. Artz likened it to a severe muscle crush injury, whereas Hunt showed that the deep-tissue loss is secondary to extremely high temperatures from resistance of the tissues (skin and bone) to the passage of electric current. Although Joule's equivalent explains the heat exchange (often in thousands of degrees of centigrade) with many variables to be considered, it is usually the voltage that can be determined and probably is the most important factor. High tension (more than 1000 volts) and low tension (less than 1000 volts) and direct and indirect currents all exert differing effects. Arc burns can occur without the patient contacting the electrical source but can be quite destructive. Electrical injury can affect many organ systems, depending on the path of the current. The volume conductor theory explains why extremity burns are much worse than torso burns and why extensive débridement (particularly of periosseus muscle) is usually necessary. The progressive destruction of tissue is probably best explained by small vessel occlusion and possibly also by elevated levels of arachidonic acid in areas of greatest heat production. Antithromboxane agents have halted the progression in experimental animals; muscle biopsies and an increased uptake of technetium Tc 99m pyrophosphate help to determine nonviable tissue that must be débrided. Resuscitation must be aggressive to provide adequate circulatory volume. Normal vital signs should be maintained along with a urine output of 100 ml per hour to overcome the destructive renal tubular effect of myoglobin and hemoglobin products. Control of sepsis and its complications through aggressive wound management is critical for survival. Long-term problems from electrical injury are possible, and efforts at prevention may save life and limb.