thermal injury, vascular compromise, or current flow itself A variety of autonomic disturbances may resolve spontaneously or persist as reflex sympathetic dystrophy Transient paralysis (keraunoparalysis) has been described in electrical injury due to lightning possibly secondary to massive release of catecholamines Ocular damage is common, particularly after lightning strikes Direct thermal or electrical injury, intensive light, and confusion contribute to the presentation Findings include corneal lesions, hyphema, uveitis, iridocyclitis, and vitreous hemorrhage Choroidal rupture, retinal detachment, and chorioretinitis occur less often Autonomic disturbances in a lightning victim may cause fixed dilated pupils, which should not serve as a criterion for brain death without extensive investigation of other neurologic and ocular functions Cataracts and optic atrophy are possible late developments Electrical injury may induce direct or indirect complications in other organ systems Tetanic contractions may cause joint dislocations and fractures, especially of the upper extremity long bones and vertebrae Fractures of the skull and long bones may occur when high-tension shock throws the victim from the site of contact Early cardiopulmonary insufficiency, as well as direct renal effects, may cripple renal function Damaged muscle releases myoglobin and CPK As in crush injuries, myoglobin may induce renal tubular damage and kidney failure Pleural damage may cause large effusions, whereas primary lung injury or aspiration of gastric contents may lead to pneumonitis Gastric dilation, ileus, diffuse GI hemorrhage, and visceral perforation may occur immediately or later In addition to burns at the site of primary contact, burns are common where current has jumped across flexed joints Such burns are most common on the volar surface of the forearm and across the elbow and axilla Arcing current may also ignite clothing and produce thermal burns Entry and exit wounds and arc burns are poor predictors of internal damage Tissue that appears viable initially may become edematous and then ischemic or frankly gangrenous over several days Diminished peripheral pulses may provide immediate evidence of vascular damage, but strong pulses not guarantee vascular integrity Blood flow falls to a minimum at about 36 hours, but current or thermal damage may lead to vasospasm, delayed thrombosis, ischemic necrosis, or aneurysm formation and hemorrhage weeks after the injury Viable major arteries near occluded nutrient arteries may account for apparently adequate circulation and uneven destruction of surrounding tissues