Pediatric emergency medicine trisk 1964 1964
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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 do 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.
