Abstract. The present study attempts to better understand the mechanism of injuries associated with direct lightning strikes. We reviewed the records of 256 individuals struck by lightning between 1965 and 1999, including 56 people who were killed. Basal skull fracture, intracranial haemorrhage, pulmo nary haemorrhage, or solid organ rupture was suspected in three men who died. Generally these lesions have been attributed to current flow or falling after being struck. However, examination of surface injuries sustained suggested that the true cause was concussion secondary to blast injury resulting from vaporization of water on the body surface by a surface flashover spark. To investigate this hypothesis, an experimental model of a lightning strike was created in the rat. Saline-soaked blot ting paper was used to simulate wet clothing or skin, and an artificial lightning impulse was applied. The resultant lesions were consistent with our hypothesis that the blast was reinforced by the con cussive effect of water vaporization. The concordance between the clinical and experimental evidence argues strongly for blast injury as an important source of morbidity and mortality in lightning strikes.
Necrosis due to an electrical injury extends by progressive obstruction of blood vessels. Means of inhibiting expansion of necrosis and predicting early the demarcation line after an electric injury were studied in the local electric injury of a rabbit ear produced by application of an electric current of 50 Hz, 1800 V for 1 sec between the right ear and the right posterior leg. Although no effective method of inhibiting expansion of necrosis was obtained, a method of predicting a demarcation line of necrosis was obtained by inducing ischemia of the ear early after the application of an electric current. From three hours to three days after the application of the electric current, ischemia of the ear was induced by compressing it between a pair of blood pressure cuffs at a pressure of 300 mmHg. As a result, the area proximal to the expected demarcation line of necrosis became white by ischemia, while the peripheral part remained dark red because of thrombi, and the expected demarcation line was clearly observed. Two to three weeks after the application of the electric current, the ear almost invariably fell off at this expected line. Therefore, in the electric injury of the hand, it can be distinguished clinically whether or not the area will become necrotic by inducing ischemia from the tips of the fingers to the upper arm early after the electric injury.
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