Hospitalized electrocution victims can show evidence of myocardial ischemia and arrhythmias (139,141,145,147,149,152,158). Because of the onset of arrhythmia can be delayed, these patients are monitored for 24 h after admission, particularly when there is a history of heart disease, loss of consciousness at the scene, or apparent current flow through the heart (139,141,142,145,232,233). The heart can be normal at autopsy (181). Petechiae may be found in the myocardium, and larger hemorrhages have been described in the pericardium and endomyocardium (181). Petechiae on eyelids, conjunctiva, visceral pleura, and epicardium are a sign of vitality in an electrocution death (197,234). Their presence does not depend on voltage or current pathway (197). The development of petechiae may be a combination of venous congestion owing to cardiac
arrest and elevated blood pressure caused by muscle contractions (197). Widespread or focal necrosis with variable hemorrhage and acute contraction bands in the myocardium and conduction system are seen, and these changes are responsible for delayed arrhythmias (Fig. 36; refs. 139, 142, 232, 235, and 236). Myocardial infarction does occur in the absence of coronary atherosclerosis, and coronary spasm is likely (236-238). Vascular spasm has also been attributed to lightning (167). Coronary thrombosis is a rare cause of myocardial infarct in an electrocution victim (142).
High- and low-voltage electrical current flowing along vessels causes damage to the intima and media (contraction band necrosis), leading to immediate or delayed thrombosis and consequent ischemia (38,139-142,144,145,147,151,152,157,158,161,235). Major limb arteries are patent because of better heat dissipation because of greater blood flow, but small intramuscular arteries necrose from thermal damage and occlude, even under viable skin (139,149,154,168,172). Medial damage can lead to aneurysm formation (149). Elevated blood pressure due to contraction of skeletal muscles and vasoconstriction from electrical current can lead to rupture of pre-existent cerebral aneurysms (149,234).
Muscle damage is caused by heat, electrical current, ischemia, and trauma (145). High-voltage current causes considerable muscle, vessel, and nerve damage (38,150, 152). The extent of cutaneous burns in a low-voltage electrocution does not predict the amount of muscle necrosis (139,141,144,145,147,150,152,157,158,172). Muscle compartment syndromes develop secondary to edema and vascular ischemia (139,141,147,152). Myoglobinuria leads to renal failure (see Chapter 8, Section 13. and refs. 38, 141, 142, 144, 145, 147, 152, 157, and 158). There is no significant correlation
of postmortem blood myoglobin levels and death by electric current (239,240). Myoglobin increases after death resulting from autolysis (239). Hyperkalemia also occurs (147). Electrical damage of skeletal muscle cell membranes is not immediately apparent as grossly visible necrosis (147,168). Ischemic effects can be delayed (141, 146,150). Electrically injured tissue can be irregular in distribution and be found at sites distant from the visible entry and exit sites (141,146,148). Although the muscle initially appears normal, irreversible electroporaton and thermal denaturation changes have already occurred (146). Later discovery of more extensive muscle necrosis indicates progression of these changes (147). Extensive muscle damage from high-voltage burns may require amputation (148,149,189,193,210,230). Gas gangrene has been described (241).
Damage to lungs is rare in electrocution (157). Blunt pulmonary trauma (e.g., contusion) is more common (157,167). ARDS is a sequela (145).
Cases of high-voltage and, rarely, low-voltage electrocution causing direct rupture of an abdominal viscus (e.g., stomach, intestine, gallbladder, esophagus) have been observed and likened to blast effects (145,176,242,243). A urinary bladder fistula has been described (244). Coagulation necrosis of small vessels can cause ischemic changes in the bowel (154,242). Paralytic ileus has been observed (154). Solid organ necrosis is usually a consequence of blunt trauma or the direct effects of burns (e.g., liver, pancreas; see refs. 157, 167, 210, 242, and 245). Some cases of solid organ damage have been attributed to electrical current (246).
DC (e.g., lightning) and high-voltage AC can either throw an individual or result in a fall owing to an intense muscular contraction (38,141,142,145,147,150,152,157,182). In a lightning strike, there is no prolonged duration of contact from tetanic muscle contractions as seen in AC electrocution (153,164,165,174). The high temperature of an arc flash rapidly heats air, causing a blast effect that throws the victim (147,209).
Head injury occurs (147,166,209,210). Central nervous system sequelae occur irrespective of whether the head was in the apparent pathway of the electric current (38,147,166,247). Cerebral anoxic injury results from cardiorespiratory arrest (139,147,152,174). Cerebral vein thrombosis has been observed (247). Long-term
neurological and psychiatric sequelae occur without central nervous system tissue injury (38,147,247). Long-term spinal cord damage has been attributed to low- and high-voltage electrocution (38,178,248). Following a lightning strike, the victim loses consciousness because of cardiorespiratory arrest, which is transient and responds to resuscitation (147). Subsequent behavioral changes and amnesia have been observed (143).
Muscle spasm from AC causes cervical spine and long bone fractures and dislocations (e.g., shoulder [38,144,145,147,152,157,161,210,249,250]). Bony injury also results from falls (152,158).
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