Pediatric emergency medicine trisk 1963 1963
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In general, high-voltage injury is more dangerous than low-voltage injury. A
higher voltage is more likely to cause “locking-on” and associated deep tissue
injury, although its tendency to throw victims from the source of current may
mitigate this effect. The possibility of head and cervical spine injuries must be
considered in these cases. The value of the current, or amperage, is of even
greater importance than the voltage. Flow as low as 1 to 10 mA may be perceived
as a tingling sensation. Progressively higher flows may paralyze muscles and
ventilation, precipitate ventricular fibrillation, and cause deep tissue burns.
Clinical Recognition
Electrical injury may produce a variety of clinical sequelae, ranging from local
damage to widespread multisystem disturbances. Victims of the most severe
accidents are commonly pulseless, apneic, and unresponsive. Current that passes
directly through the heart may induce necrosis and ventricular fibrillation.
Brainstem (medullary) paralysis or tetanic contractions of thoracic muscles may
result in cardiopulmonary collapse. Lightning injury is capable of inducing
asystole, from which the heart may recover spontaneously, but the accompanying
respiratory failure is commonly prolonged. Unless ventilation is initiated
promptly, hypoxia leads to secondary ventricular fibrillation and death.
Other cardiac disorders, including arrhythmias and conduction defects, are
common among survivors. Supraventricular tachycardia, atrial and ventricular
extrasystoles, right bundle branch block, complete heart block, and prolongation
of the QT interval are most common. Complaints of crushing or stabbing
precordial pain may accompany nonspecific ST–T wave changes. Some patients
sustain myocardial damage or even ventricular wall perforation. Despite evidence
of important cardiac injuries, patients without secondary hypoxic–ischemic injury
usually regain good myocardial function.
Nervous system injury is also common and may involve the brain, spinal cord,
peripheral motor and sensory nerves, and sympathetic fibers. Loss of
consciousness, seizures, amnesia, disorientation, deafness, visual disturbances,
sensory deficits, hemiplegia, and quadriparesis occur acutely but may be
transient. Vascular damage may produce subdural, epidural, or intraventricular
hemorrhage, and patients with brain hemorrhage or ischemic injury may become
comatose. Additional problems develop within hours to days after injury. The
syndrome of inappropriate antidiuretic hormone secretion may precipitate
cerebral edema. Electroencephalograms reveal diffuse slowing, epileptiform
discharges, or burst suppression patterns, but these may not have prognostic
significance. Spinal cord dysfunction more often results in motor than sensory
deficit. Peripheral neuropathies with patchy distribution may reflect direct
