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MD Consult: Books: Goldman: Cecil Medicine: Chapter 112 – ELECTRIC INJURY

Goldman: Cecil Medicine, 23rd ed.

Copyright © 2007 Saunders, An Imprint of Elsevier


Basil A. Pruitt Jr.



The tissue damage caused by electric current ranges from a transient increase in cell membrane permeability to immediate coagulation necrosis of large volumes of tissue. The clinical consequences include disturbances in the physiologic electrical conduction systems, a process that may cause cardiopulmonary arrest; tetanic muscle contractions, with resulting compression fractures of vertebrae; and delayed tissue damage, such as cataract formation.


As the use of electricity has increased worldwide, the number of electric injuries has increased. The precise incidence of electric injury is unknown, but the National Centers for Health/Centers for Disease Control and Prevention have estimated that 52,000 trauma admissions take place in the United States each year for electric injuries. Four percent of patients admitted to the U.S. Army Burn Center during a recent 20-year period had high-voltage electric injury; at other burn centers, the percentage of admissions related to electric injury has ranged from 0.04 to 6.7%.


Environmental conditions, duration of contact, pathway of the current, type of current (and if alternating current, the frequency of the current), and voltage all influence the effects of electricity on tissue. Voltage greater than 40 is potentially dangerous, and the likelihood of sudden death and remote tissue injury increases as voltage increases to 1000. Voltages greater than 1000 are considered to be high tension and are associated with immediate severe tissue damage. Alternating current is more dangerous than direct current because of its likelihood of producing cardiac arrest or cessation of respiration and its tetanic effect, which may prevent the patient from breaking contact with the source of electricity. As the frequency of alternating current increases to greater than 60 cps, tissue injury decreases. The path of the current through the body between the points of contact is important in determining tissue damage; a course through the heart or the respiratory center of the brain is especially dangerous. Ventricular fibrillation can be produced by current flow of only 100 mA from a hand to the feet. Rapid separation of a patient from the source of electricity is crucial because tissue damage increases in proportion to the duration of contact. Resistance to current flow at the point of contact is influenced by environmental conditions; dry and thickened palmar or plantar skin is more resistant to the passage of current than is skin moistened by perspiration or other liquid.

Heat is the principal mediator of tissue damage in electric injury, the severity of which is related to voltage and duration of contact. Tissue-specific differences in resistance to the flow of current (neural tissue least; blood vessels, muscle, and skin intermediate; and bone greatest) may explain differences in tissue injury caused by low-voltage current. Because all body tissues and fluids are conductive, the soft tissues between bone and skin can be viewed as a volume conductor. Heat is produced in tissues as a function of voltage drop and current flow per unit of cross-sectional area (i.e., density of the current). The inverse relationship between the density of the current and the tissue’s cross-sectional area accounts for the frequency of severe injury to the digits and extremities and the rarity of major injury to the trunk in patients with high-tension electric injury ( Fig. 112-1 ). Contact with less than 1000 V causes injuries that are self-limited because at contact points, where the density of the current is greatest, the skin is severely injured and chars, which results in a rapid increase in resistance and reduction of the passage of current. When the source is greater than 1000 V, arcing is so intense that tissue destruction is increased markedly as relatively constant levels of current are maintained. Arcing, which may occur across the flexor surfaces of joints, can char the skin in these areas and ignite the patient’s clothing. After cessation of the flow of current, the heated tissue acts like a volume radiator and cools unevenly, with the superficial portions cooling more rapidly than the deeper portions; deeper tissues are therefore more prone to severe injury.

FIGURE 112-1  Charring at the contact site in the first web space and at the site of arcing in the antecubital space (black arrows) of a victim of electric injury. The fixed flexion deformity of the thumb and other digits is characteristic of severe high-voltage injury to the hand and forearm. The severity of injury is indexed by the marked edema of the forearm muscles bulging above the cut edges of the fasciotomy incision and by the patchy dark discoloration of the muscles of the arm and the forearm, particularly the deeper muscle exposed in the central portion of the forearm incision (white arrow).

Tissue damage can also be caused by low-voltage direct current (i.e., contact with automobile battery terminals or with defective or inappropriately used medical equipment, such as electrosurgical devices, external pacing devices, or defibrillators). Direct current injuries have been reported to be particularly common during laparoscopy with high-voltage coagulation.

Clinical Manifestations

Cardiopulmonary arrest can be caused by low-voltage electric injury but is more common with high-voltage electric injury. Extensive tissue necrosis may also liberate enough potassium to cause cardiac dysfunction. Because cardiac arrhythmias may recur after resuscitation or develop 24 to 48 hours after injury, all patients who have sustained high-voltage electric injury should undergo continuous electrocardiogram (ECG) monitoring for at least 48 hours after the last ECG-documented arrhythmia. Renal failure may occur in patients with high-voltage electric injury if inapparent deep tissue injury with accompanying occult edema results in an underestimation of fluid requirements, inadequate resuscitation, and oliguria. Additionally, the destruction of muscle and red blood cells liberates hemochromes that may precipitate in the renal tubules unless adequate urinary output is maintained ( Chapter 121 ).

Muscle Damage

High-voltage electric injury commonly causes edema beneath the investing fascia of the involved muscle compartments, thereby compromising nutrient blood flow to muscles within the compartments and to distal unburned tissue. Clinical indications for surgical release of intracompartmental pressure by fasciotomy and surgical exploration of a limb include impaired capillary refilling of distal unburned skin or nails, cyanosis of distal unburned skin, stony hardness of a muscle compartment on palpation, and diminished or absent pulsatile flow in the distal arteries as assessed by Doppler ultrasound. Tissue pressures 30 mm Hg or higher above atmospheric pressure, as measured by a catheter placed in the compartment, indicate the need for immediate decompression. If clinical signs are consistent with deep tissue injury but large vessel pulses are intact, arteriography can determine the need for operative intervention, including amputation of the affected limb. “Pruning” of the arterial tree, with a decrease in the density of nutrient branches in the muscles of an involved limb, identifies the level of amputation needed to remove muscle that has been irreversibly damaged. Muscle blood flow of 1 mL/min/100 g of tissue, as determined by xenon 133 “washout,” has been proposed as the minimum level required for ultimate tissue viability. In patients with high-voltage electric injury, myoglobinemia and elevation of serum creatine phosphokinase reflect significant muscle damage, and myoglobinuria is a strong predictor of the need for fasciotomy in the first 24 hours after injury.

Neurologic Examination

On admission and at scheduled intervals thereafter, a detailed neurologic examination must be performed on all patients with high-voltage electric injury; all nerve deficits should be documented fully. Central nervous system or peripheral nerve dysfunction may be apparent immediately after electric injury or may appear later. Recovery of function after direct electrical nerve damage is rare. Conversely, spontaneous resolution of immediate and early functional deficits of nerves not injured directly (motor nerves are more sensitive to nondestructive injury than sensory nerves are) is common. A polyneuritic syndrome of relatively late onset can induce deficits in the function of peripheral nerves far removed from the points of electric contact. Direct nerve damage of the spinal cord causes immediate deficits, which are more often transient than deficits of later onset. Delayed-onset spinal cord deficits can be manifested as quadriplegia, hemiplegia, localized nerve deficits with signs of ascending paralysis, transverse myelitis, and even an amyotrophic lateral sclerosis–like syndrome. The cause of delayed paresthesias and nerve dysfunction after electric injury is unknown, but an increase in permeability of the cell membrane and associated loss of cell contents induced by exposure to a millivoltage electric field (electroporation) have been implicated. The greater improvement in neurologic function in children than in adults has been attributed to their greater neurologic plasticity.

Remote Organ Injury

Direct liver injury, focal pancreatic and gallbladder necrosis, and intestinal perforation have been reported after electric injury, but all are uncommon. Delayed hemorrhage from moderate to large blood vessels has been ascribed to an arteritis caused by the electric injury, but this hemorrhage seems to be most closely related to inadequate débridement of injured tissue or to vascular wall necrosis as a consequence of exposure after débridement.

Compression fractures of vertebral bodies may be produced by tetanic contractions of the paraspinous muscles. Fractures of the skull and the long bones of both the upper and lower extremities may be caused by falls after the electric shock.

Delayed Organ Damage

High-voltage electric injury has been associated with the subsequent formation of cataracts, most frequently in patients in whom the contact site was on the head or neck. Cataracts may form rapidly, but they more commonly develop 3 or more years after the injury. Rarely, exfoliative debris may be evident in the anterior chamber of the eye immediately after injury. Cholelithiasis and gastrointestinal dysfunction have been reported after high-voltage injury, but most centers have not noted an increased rate of either of these problems.


Cardiopulmonary arrest must be treated by immediate institution of cardiopulmonary resuscitation ( Chapter 62 ). In patients with high urinary hemochrome concentrations, a urinary output of 75 to 100 mL/hr should be maintained ( Chapter 114 ). If the hemochromes do not clear promptly or the patient remains oliguric despite the administration of resuscitation fluids at more than twice the required rate as estimated on the basis of the extent of the burn and the patient’s weight ( Chapter 113 ), 25 g of mannitol should be given as an intravenous bolus and 12.5 g of mannitol should be added to each liter of intravenous fluid until the pigment has cleared from the urine. Hyperkalemia is treated as in any other patient ( Chapter 118 ).

If the electric injury is limited to the skin and subcutaneous tissue, an antibacterial cream such as Sulfamylon burn cream should be applied twice daily to the burned tissue until débridement is performed. The antimicrobial (mafenide acetate) in Sulfamylon readily diffuses into the nonviable tissue to limit microbial proliferation. As soon as resuscitation has restored hemodynamic stability, severely damaged limbs or other areas of tissue necrosis should be surgically explored. The viability of vital structures and the extent of deep tissue damage are assessed to determine the need for amputation. If amputation is not required, all necrotic tissue should be débrided to eliminate the source of hyperkalemia and reduce the risk for infection. It is imperative to examine the periosseous muscles, which may be necrotic because of delayed heat dissipation yet be overlain by more superficial viable muscles. After débridement or amputation, the operative wound should be dressed but not surgically closed, and the patient should be scheduled for re-exploration of the wound 24 to 72 hours later. At that time, residual necrotic tissue is débrided, and the wound is closed by skin grafts, tissue transfer, or the use of biologic dressings, depending on the condition, extent, and site of the wound. Overall, current treatment is associated with a 96% survival rate.


An estimated 300 to 350 persons are struck by lightning each year, and about 30% of these patients die. The duration of a lightning bolt is 1/100 to 1/1000 of a second, but it may have a voltage of approximately 1 billion V and induce currents ranging from 12,000 to 200,000 A. The temperature in a lightning bolt, which may be 30,000 K, dissipates in a few microseconds.

Clinical Manifestations

Cardiopulmonary arrest, which can be secondary to either asystole or ventricular fibrillation, is common in patients struck by lightning. Cardiopulmonary resuscitation must be instituted immediately; recovery has been reported in some patients who were apparently without life signs for 15 minutes or longer. Although signs of acute myocardial damage may become evident later, persistent or recurrent ECG abnormalities are uncommon. Coma is common immediately after injury and typically resolves in a few hours. Abdominal signs of peritonitis with free air in the peritoneal cavity of a patient struck by lightning should alert one to the possibility of intestinal perforation, which if present must be treated by prompt primary closure. Keraunoparalysis (lightning paralysis), which is characterized by paresthesias and paralysis, usually involves the lower limbs, often develops over a period of several days after lightning injury, is typically associated with vasomotor disorders, and is usually transient. Myoglobinuria is uncommon; when present, it is treated as described earlier for other electric injuries. Tympanic membrane rupture and hearing loss may also be caused by lightning injury. Cutaneous burns of the trunk and proximal areas of the limbs caused by lightning injury typically have a “splashed on” arborescent and spidery appearance and are generally superficial ( Fig. 112-2 ). Small, circular, full-thickness burns of the tips of the toes are also common and have been termed the tiptoe sign. Mottling of the skin and other signs of vasoconstriction previously considered to be specific to lightning injury generally resolve with adequate resuscitation.

FIGURE 112-2  The arborescent current markings shown on the face, neck, and anterior aspect of the trunk of this young patient, which are characteristic of lightning injury, healed without need for grafting. Note the focal lesions on the right arm indicating spread of the current that produced the markings on the right anterolateral aspect of the chest wall.


Current treatment, which emphasizes immediate cardiopulmonary resuscitation, has decreased mortality significantly to the point at which two thirds of lightning-injured patients now survive. Persistent nerve deficits and long-term problems are relatively uncommon in survivors.


Cardiopulmonary and fluid resuscitation combined with monitoring of limb tissue pressure and wound care has maximized tissue salvage, reduced renal failure, and increased survival of patients with lightning and high-voltage electric injuries. In a 10-year period, only 28 (22%) of 127 patients admitted to the U.S. Army Burn Center with high-voltage electric injury had permanent neurologic deficits at discharge.

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