Pediatric emergency medicine trisk 491

Children who have sustained minor household electrical injuries and
are asymptomatic usually do not require laboratory evaluation, cardiac
evaluation, or hospitalization.
In more severe injuries, entry and exit wounds and arc burns are poor
predictors of internal damage. Tissue that appears viable initially may
become ischemic over several days.

Current Evidence
An electrical injury occurs when a person comes into contact with the current
produced by a human-made or natural source. The spectrum of electrical injury is
enormous, ranging from low-voltage household accidents to million-volt
lightning strikes ( Table 90.8 ). Appropriate management requires an
understanding of the basic physical aspects of electricity, the physiologic
responses to injury, and the potential for immediate and delayed damage.
Lightning that strikes individuals carries a 30% risk of mortality and claims
approximately 100 lives annually in the United States. The death rate is highest
among children ranging from 15 to 19 years of age. The majority of struck-bylightning injuries in the United States originate in the South and the Midwest.
Harnessed electrical power is responsible for approximately 700 deaths/year, of
which 10% are children. Household electrical cords are the major cause of
electrocution in children 12 years of age and younger, with an estimated 1,000
ED visits for oral electrical burns from 1997 to 2012. High-tension electrical
injuries dominate in older children who climb on trees, buildings, or utility
structures. Tasers and stun guns, which are high-voltage, low-current stimulators,
cause pain due to involuntary muscle contractions.
The severity of electrical injury depends on six factors: (i) The resistance of
skin, mucosa, and internal structures; (ii) the type of current (alternating or
direct); (iii) the frequency of the current; (iv) the intensity; (v) the duration of
contact; and (vi) the pathway taken by the current. Precise separation of the effect
of these factors, which are interrelated, is impossible. Together, they produce
either heat or current, and a variety of injuries result.

TABLE 90.8
LIGHTNING VERSUS HIGH-VOLTAGE ELECTRICAL INJURY
Factor

Lightning

High voltage

Duration
Energy level

Prolonged
Much lower

Type of current
Shock wave
Cardiac arrhythmia
Burns

Brief
100,000,000 V
200,000 A
Direct
Present
Asystole
Superficial, minor

Renal failures

Rare

Fasciotomy and
amputation

Rare

Usually alternating
Absent
Ventricular fibrillation
Deep, frequently
obscured
Common secondary to
myoglobinuria
Common, early, extensive

Resistance is a major factor determining the amount of current flow through
tissue. The intensity of the electrical shock produced by a certain voltage can vary
with gender and age. Tissue injury is inversely related to resistance. Dry skin
provides resistance of approximately 40,000 ohms, whereas thick, callused palms
may provide up to 1 × 106 ohms. Thin, moist, or soiled skin lowers resistance to
the 300 to 1,000 ohm range. The highly vascular, moist oral mucosa has even
lower resistance.
The type of current is another important determinant of injury. Alternating
current (AC) at low voltage is able to induce tetanic muscle contraction and is,
therefore, more dangerous than direct current (DC). Normal household 60-Hz
current changes direction 120 times per second, a frequency that induces an
indefinite refractory state at neuromuscular junctions. The resultant muscle
contractions prevent the victim from releasing his grip (“locking-on”), thus
extending the duration of contact.

DC is used in medical settings for cardiac defibrillation, countershock, and
pacing. Currents as low as 1 mA may trigger ventricular fibrillation, and high
currents may damage the heart and conducting tissues directly. Lightning is
another example of DC, discharged in a single, massive bolt that lasts 1/10,000 to
1/1,000 second. The brevity of exposure makes deep thermal injury unlikely.


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


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.