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Electrical Burn Injuries

  • Author: Richard F Edlich, MD, PhD, FACS, FACEP; Chief Editor: Deepak Narayan, MD, FRCS  more...
 
Updated: Sep 17, 2013
 

Overview

Since its inception in 1849, commercial use of electricity has been one of the most potentially dangerous commodities in our society. According to statistical data, 0.8-1% of accidental deaths are caused by an electric injury, with approximately one quarter caused by natural lightning. Electric injury accounts for 1000 deaths each year in the United States, with a mortality rate of 3-15%.[1, 2]

As the widespread use of electricity and injuries from it increase, all health professionals involved in burn care must appreciate the physiologic and pathologic effects and management of electric current injury. As either the current or its arc causes these injuries, an understanding of some fundamental laws of physics is an essential prerequisite of proper management. This article describes the consequences of accidental contact with commercial electric current and delineates principles involved in burn care.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Electric Shock and Thermal (Heat or Fire) Burns.

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Physics of Electricity

Electricity is the flow of electrons from atom to atom.[3, 4] Movement of electrons is comparable to the way water is passed along in a bucket brigade. Electrons, which comprise the current, are passed along from atom to atom. Amperage is the term used for the rate of flow of electrons. Every time 6.242 x 1015 electrons pass a given point in 1 second, 1 ampere of current has passed. The current is what can kill or hurt a victim of an electric injury. One ampere is roughly equivalent to the amount of current flowing through a lighted 100-watt light bulb.

In most materials, a number of electrons are free to move about at random until a driving force termed voltage propels them to move in one direction. A large voltage exerts a greater force, which moves more electrons through the wire at a given rate of time. Electric voltage of 380 volts or less is considered low voltage and above 380 volts, high voltage. High voltage is generated at the power plant and is transformed down to approximately 120 volts for most wall outlets in homes.

Resistance

Resistance of the human body has been likened to that of a leather bag filled with an electrolyte fluid, with high resistance on the outside and lower inside.[5] Skin resistance also varies depending on moisture content, thickness, and cleanliness. Resistance offered by the callused palm may reach 1,000,000 ohms/cm2, while the average resistance of dry normal skin is 5000 ohms/cm2. This resistance may decrease to 1000 ohms/cm2 if hands are wet. Skin resistance is encountered primarily in the stratum corneum that serves as an insulator for the body. The voltage gradient in skin cannot be increased indefinitely and breaks down at low voltages. Exposure of the skin to 50 volts for 6-7 seconds results in blisters that have a considerably diminished resistance.

The dermis offers low resistance, as do almost all internal tissues except bone, which is a poor conductor of electricity. Other factors that affect the flow of electrons are the nature and size of the substance through which it passes. If the atomic structure of the material is such that the force of attraction between its nucleus and outer electrons is small, little force is required to cause electron loss. These substances (eg, copper, silver) in which electrons are loosely bound are termed conductors, because they readily permit the flow of electrons. Materials such as porcelain and glass are composed of atoms that have powerful bonds between their nuclei and the outer electrons. These materials are termed insulators because electron flow is restricted.

Resistance is a measure of how difficult it is for electrons to pass through a material and is expressed in a unit of measurement termed an ohm. The resistance offered to the flow of electricity by any material is directly proportional to its length and inversely proportional to its cross-sectional area. Electricity is transmitted by a high-voltage system, because it allows the same amount of energy to be carried at lower current, which reduces electrical loss through leakage and heating. The relationship between current flow (amperage), pressure (voltage), and resistance is described in Ohm's law, which states that the amount of current flowing through a conductor is directly proportional to voltage and inversely related to resistance.

Current (I) = Voltage (E)/Resistance (R)

Electrons set in motion by the current force (voltage) may collide with each other and generate heat. The amount of heat developed by a conductor varies directly with its resistance. Power (watts) lost as a result of the current's passage through a material provides a measure of the amount of heat generated and can be determined by Joule's law.

Power (P) = Voltage (E) x Current (I)

Because E = I x R (resistance), the above equation becomes P = I(squared) R. Consequently, the heat produced is proportional to the resistance and the square of the current. Commercial electric currents usually are generated with a cyclic reversal of the direction of electric pressure (voltage). Pressure in the line first pushes and then pulls electrons, resulting in alternating current. Frequency of current in hertz (Hz) or cycles per second is the number of complete cycles of positive and negative pressure in 1 second. The usual wall outlet (120 volts) provides a current with 120 reversals of the direction of flow occurring each second and is termed 60-cycle current. Frequency of alternating current can be increased to a range of millions of cycles per second. In direct current, electron travel is always in the same direction.

Alternating current

Alternating current has almost entirely superseded direct current, since it is cheaper and can be transformed easily into any required voltage. Most machines in industry and appliances in the home use alternating currents; therefore, workers and consumers are mainly at risk from this current. Direct current usage is primarily restricted to the chemical and metallurgical industries, ships, streetcar systems, and some underground train systems.[6, 7]

Electric arc

Contact with high-voltage current may be associated with an arc or light flash.[8] An electric arc is formed between two bodies of sufficiently different potential (high-voltage power source and the body, which is grounded). The arc has an intense, pale-violet light and consists of ionized particles that are driven by the voltage pressure between the two bodies and are present in the space between them. Temperature of the ionized particles and immediately surrounding gases of the arc can be as high as 4000°C (7232°F) and can melt bone and volatilize metal. As a general guide, arcing amounts to several centimeters for each 10,000 volts. Burns occur where portions of the arc strike the patient. The electric arc remains the cause of most high-voltage electrical burn injuries. Because of its high frequency, the electric arc has become the basis for many standard safety precautions.

Flash burns are caused by head from a nearby electric arc that can have temperatures of 5000°C. These hot flashes can pass over the surface of the body, usually resulting in superficial partial-thickness burns. Flash burns have no internal electrical component.

Effects of electricity on the body

Effects of electricity on the body are determined by 7 factors: (1) type of current, (2) amount of current, (3) pathway of current, (4) duration of contact, (5) area of contact, (6) resistance of the body, and (7) voltage.[9] Low-voltage electric currents that pass through the body have well-defined physiologic effects that are usually reversible. For a 1-second contact time, a current of 1 milliampere (mA) is the threshold of perception, a current of 10-15 mA causes sustained muscular contraction, a current of 50-100 mA results in respiratory paralysis and ventricular fibrillation, and a current of more than 1000 mA leads to sustained myocardial contractions.

Humans are sensitive to very small electric currents because of their highly developed nervous system. The tongue is the most sensitive part of the body. Using pure direct current and 60-cycle alternating current, the first sensations are those of taste, which are detected at 45 microamperes. When subjected to 60-cycle alternating current, the threshold of perception in the hands of men and women, which is usually a tingling sensation, is approximately 1.1 mA. Using pure direct current applied to hands, the first sensations are those of warmth in contrast to tingling, detected at 5.2 mA.

Skin offers greater resistance to direct current than alternating current, thus 3-4 times more direct current is required to produce the same biologic effect elicited by alternating current. With increasing alternating current, sensations of tingling give way to contractions of muscles. The magnitude of the muscular contractions enhances as the current is increased. Finally, a level of alternating current is reached for which the subject cannot release the grasp of the conductor. The maximum current a person can tolerate when holding a conductor in one hand and still let go of the conductor using the muscles directly stimulated by the current is termed the "let-go" current. This tetanizing effect on voluntary muscles is most pronounced in the frequency range of 15-150 Hz.

Such strong muscular reactions may cause fractures and/or dislocations. Numerous reports of bilateral scapular fractures and shoulder dislocations and fractures in electric accidents attest to this occurrence. As the frequency increases above 150 Hz, the potential for this sustained contraction is lessened. At frequencies from 0.5-1 megacycle, these high-frequency currents do not elicit sustained contractions of the skeletal muscles. For 60-cycle alternating current, the let-go threshold for men and women is 15.87 mA and 10.5 mA, respectively. The lower value for women may result from their generally somewhat poorer muscular development compared to men.

Electrical accidents involving power frequency (50-60 Hz) and a relatively low voltage (150 V/cm) occasionally can result in massive trauma to the victim. Skeletal muscle and peripheral nerve tissue are especially susceptible to injury. Historically, Joule heating, or heating by electrical current, was viewed as the only mechanism of tissue damage in electrical trauma. Yet in some instances, Joule heating does not adequately describe the pattern of injury observed distant to the sites of contact with the electrical source. These victims exhibit minimal external signs of thermal damage to the skin, while demonstrating extensive muscle and nerve injury.

Recently, electroporation of skeletal muscle and nerve cells was suggested as an additional mechanism of injury in electrical burns. This mechanism is different from Joule heating, even though it is influenced by temperature. It is the enlargement of cellular-membrane molecular-scale defects that results when electrical forces drive polar water molecules into such defects. Experimental studies have documented that electroporation effects can mediate significant skeletal muscle necrosis without visible thermal changes.

High-voltage accidents

The national electric code defines high-voltage exposure as greater than 600 volts. In the medical literature, high-voltage exposure is judged as greater than 1,000 volts. In high-voltage accidents, the victim usually does not continue to grasp the conductor. Often, he or she is thrown away from the electric circuit, which leads to traumatic injuries (eg, fracture, brain hemorrhage). The infrequency with which sustained muscular contractions occur with high-voltage injury apparently occurs because the circuit is completed by arcing before the victim touches the contact. Currents that cause subjects to "freeze" to the circuit despite their struggle to be free are frightening, painful, and hard to endure, even for a short time.

Turning off power source

Consequently, a witness of the accident must turn off the power source as soon as possible. If this is not possible, the victim must be disengaged from the electric current. Wearing lineman's gloves, trained electricians must separate the victim from the circuit by a specially insulated pole. Looping a polydacron rope around the injured patient is another method of pulling him or her from the electric power source. Ideally, the first responder should stand on a dry surface during the rescue.

Muscular contractions

Tests using gradually increasing amounts of direct current produce sensations of internal heating rather than severe muscular contractions; however, sudden changes in the magnitude of direct current produce powerful muscular contractions. At the instant of interruption of the direct current, the subject occasionally falls back a considerable distance; the impact of the fall may cause a fracture. As the alternating current strength increases above 20 mA, a sustained contraction of muscles of respiration of the chest occurs.

Normal respiration returns after the current has been turned off, provided that the duration of current flow is less than 4 minutes. If sustained contractions last longer than this time interval, death from asphyxiation occurs, unless the current is stopped and mouth-to-mouth ventilation on the breathless patient is started. The pathway of current flow, involved in tetanic contractions of the muscles of respiration, is usually arm to arm or arm to leg and does not pass through the respiratory center located in the medulla of the brainstem. This center is injured in executions in the electric chair, leading to permanent respiratory arrest.

Treatment at the scene

When current flow increases above 30-40 mA, ventricular fibrillation may be induced. Numerous factors can influence the magnitude of electric current required to produce ventricular fibrillation.[10, 11, 12, 13] Factors found to be of primary importance are duration of current flow and body weight. The threshold for ventricular fibrillation is inversely proportional to the square root of the shock duration and directly proportional to body weight.[14]

When the heart is exposed to currents of increasing strength, its susceptibility to fibrillation first increases and then decreases with even stronger currents. At relatively high currents (1-5 amps), the likelihood of ventricular fibrillation is negligible with the heart in sustained contraction. If this high current is terminated soon after electric shock, the heart reverts to normal sinus rhythm. In cardiac defibrillation, these same high currents are applied to the chest to depolarize the entire heart.

If disconnecting the victim from the electric circuit does not restore pulses, the first responder must start cardiopulmonary resuscitation to restore breathing and circulation. Ideally, when they arrive at the scene of the accident, paramedics will continue this resuscitation. Field intervention should include advanced life support treatments delivered under the direction of a physician at the hospital base station using telemetered communication. Telemetered monitoring of these patients is recommended throughout transport to the advanced life support hospital facility.

These life-threatening consequences of low-voltage electric burns usually occur without any lesions of the skin at entrance and exit points of the current. An absence of local lesions indicates that the surface area of contact (current density) is large and that the heat is insufficient to produce a thermal injury; however, the smaller the surface area of the contact, the greater the density of the current and the more energy is transformed into heat that can cause local burn injury.

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Low-Voltage Electric Burns

Low-voltage electric burns almost exclusively involve either the hands or oral cavity.[15] In either injury, hospitalization is recommended to treat the local burn injury and monitor for systemic sequelae. The most common cause of low-voltage electric burns of the hand is contact with an extension cord where the insulating material has worn off either from wear or misuse. Most of these patients are children aged 5 years or younger. A low-voltage burn of the hand usually consists of a small deep burn that may involve vessels, tendons, and nerves. These burns involve a small area in the hand, yet they may be severe enough to require amputation of a finger.

Initial treatment of hand burn wound

The hand burn wound is first cleansed with poloxamer 188 and then treated with poloxamer 188 gel impregnated with polymyxin (10,000 U/g), nystatin (4000 U/g), and nitrofurantoin (0.3%) twice daily. Immobilize the patient's hand in a splint and maintain it in an elevated position above his or her heart. At 48-72 hours after injury, a time in which acute edema has subsided, patients with full-thickness burns are taken to the operating room for debridement of devitalized tissue and coverage with viable tissue.

Surgical treatment

Surgical treatment varies with the severity of the injury. If the injury involves only skin loss, coverage is accomplished by autogenous skin grafts. If bone, tendon, or joint is exposed, pedicle flaps accomplish coverage. This coverage prevents the development of septic necrosis of these specialized structures, a normal consequence of conservative treatment; however, when the electric injury results in damage to the skin, tendon, nerves, and all blood vessels, amputation of the devitalized portion of the finger is necessary.

Oral cavity damage

Low-voltage electricity also can damage the oral cavity, leaving a permanent scar. These injuries occur most frequently in those aged 1-2 years and generally (60%) in boys. Most of these children are injured by sucking an extension cord socket (53.7%). Biting an electrical cord accounts for 29.9% of these burns and sucking an electric outlet, 1.8%.

Two types of low-voltage electric burns of the lips and mouth occur. The most common type occurs when an electric arc is formed between 2 wires of opposite polarity and passes external to the body surface via the child's electrolyte-rich saliva. Heat generated may be greater than 1371°C (2500°F), resulting in severe destruction of the mouth and contiguous tissue. Low-voltage electricity also can cause a contact burn when current enters the mouth and passes throughout the body, exiting through a ground source (eg, wet diaper touching a metal pipe). Contact electrical burns can cause death from ventricular fibrillation; fortunately, this type of burn is uncommon.

A 5% incidence of cardiac and/or respiratory arrest occurs in patients with electric burns of the oral cavity. Initially, the center of the wound resulting from an oral cavity burn is grayish-white and depressed, surrounded by a slightly elevated margin. Histologically, the central portion of the wound exhibits protein coagulation, fat liquefaction, and necrosis of collagen. A narrow zone of hyperemic tissue surrounds this central area and fades into adjacent tissue.

Electric burns of the oral cavity do not disturb the arterial system beyond the margin of central necrosis, but almost all veins are occluded or thrombosed for some distance beyond the burn. Immediately after injury, tissue is soft to palpation and painless from sensory neural damage. Within a few hours, intense swelling appears in the surrounding tissues. As these burned tissues become more protuberant because of developing edema, labial competence decreases, making control of saliva difficult.

Healing of oral cavity

Edema subsides from 5-12 days after injury, when demarcation of nonviable tissue becomes apparent. Over the next 2 weeks, nonviable tissue separates from viable tissue. As devitalized tissue sloughs, bleeding from the labial artery may complicate its separation. Necrotic tissue soon replaces granulation tissue, and wound repair occurs by epithelial migration, collagen synthesis, and contraction. This healing distorts the appearance of the tissue considerably, and induration of the wound occurs for 3-5 months before spontaneous softening takes place.

Sites of involvement

Electric burns of the oral cavity can involve the lip, tongue, mucous membranes, and underlying bone.[15] The most frequent site of involvement is the upper and lower lips with the intervening commissure. This injury to the lip may be associated with damage to the orbicularis oris muscle as well as mucous membranes. As muscles heal, microstomia may develop, and repair of the injured mucous membranes may result in labial, alveolar, and tongue adhesions. Obliteration of the buccal sulcus may cause drooling. Injury to the tongue is common (26%) but usually not severe; however, adhesions can develop, resulting in ankyloglossia, which impairs speech.

Severity of bony injury

Severity of bony injury from a low-voltage electric burn may vary considerably. Injury may be isolated to a single tooth or involve many orofacial structures. Composite dysplasia involving both dentine and enamel of a tooth may be evident. The injured tooth has a vital pulp, a shorter root than crown, and a wrinkled, pitted, brownish labial surface. Abnormal growth of the orofacial structures causes dental changes, such as crossbite, crowding, and retrusion of the bite. Severity of electric burns of the mouth can be categorized into 3 groups: minor, moderate, and severe.

  1. Minor injury involves less than one third of either the upper and lower lip without commissure injury or less than one sixth of both lips with commissure injury.
  2. Moderate injury affects more than one third of either lip without commissure injury or more than one sixth of each lip with commissure injury. Moderate injuries are limited to skin around the lips with minimal mucosal loss and do not involve the buccal sulcus.
  3. Severe injury includes a significant loss of skin and muscle and mucosal involvement of buccal sulcus.

Treatment of oral cavity electric burns

Cleanse an electric burn wound of the oral cavity with poloxamer 188 and then treat with a petroleum base antibiotic ointment 4 times a day. Usually, the application of arm splints is advisable to keep the child's hands away from his or her mouth. Administer feedings through a catheter bulb syringe to limit trauma to the injured area.

Tetanus immunoprophylaxis is mandatory for patients with a tetanus-prone wound.[16] Systemic antibiotic therapy has no apparent therapeutic benefit. Delayed hemorrhage from the labial artery is noted in as many as 24% of patients. Bleeding can occur at any time from the day of injury to 221 days later. In most cases, bleeding can be controlled easily with manual pressure; however, ligation of the bleeding vessel is occasionally required. When these patients are discharged from the hospital, instruct their parents on how to manage delayed bleeding by direct application of pressure.

Definitive treatment of electric burns

Definitive treatment of electric burns of the lips and mouth remains controversial.[15] Four different treatment plans have been proposed to either prevent or correct the deformity. Immediate excision within 12 hours after injury has been recommended to shorten the period of wound repair and to permit restoration with minimal reconstructive procedures. Delayed primary reconstruction, 4-7 days after injury when the extent of tissue necrosis is known, has also been suggested. Delayed reconstruction following complete healing of the wound is another approach. Finally, immediate postburn splinting to avoid surgical reconstruction has also been advocated.

Consensus on fundamental principles

Definitive care of electric burns of the oral cavity remains controversial, yet consensus has been reached on several fundamental principles. Without treatment, the injury heals with an almost invisible scar in a considerable number of patients (20%). Most surgeons also agree that delineating the extent of damage soon after injury is difficult and that early excision may sacrifice normal tissue. Finally, immediate prosthetic splinting reduces the need to reconstruct the oral cavity after the injury.

On the basis of these principles, immediate treatment of electric burns of the oral cavity should include splinting of the mouth after acute edema resolves, often 5-12 days after injury. Splinting should continue until the scar softens and loses its contractile potential, which usually takes 6-12 months. Surgical revision should then be performed to correct residual deformity.

Adequate function and aesthetic appearance

Prosthetic treatment of electric burns of the oral cavity attempts to provide physical resistance to contraction of the injured tissue. Maintain symmetric width of the oral stoma to attain adequate functional and aesthetic appearance of the injured mouth. Position each commissure laterally equidistant to the midline of the lips, and maintain the orbicularis oris muscle at a 2-point fixation. This prosthetic treatment can be accomplished either intraorally or extraorally, depending on the patient's dentition and ability to cooperate. Because these patients are often aged only 1-2 years, parents must participate and cooperate in the treatment plan.

Perform intraoral commissure splinting using a fixed, semifixed, or removable appliance. Intraoral prostheses have posts at the oral commissures that apply static traction to the injured healing tissue. Bilateral posts oppose the sphincterlike action of the orbicularis oris muscle as well as the forces of wound contraction. Unfortunately, many children with electric burns of the oral cavity are not referred to regional burn centers soon after their injury and do not benefit from these prostheses. Without these appliances, the burn wound is allowed to heal by contraction, and the contracting scar often causes severe deformities. In such cases, final reconstruction is best achieved after the scars are allowed to soften, usually 6-12 months after the injury. Reconstructive procedures undertaken when the scars are hypertrophic tend to produce additional hypertrophic scarring.

Two types of deformity

Two principal types of deformity that result from oral cavity electric burns are those that are limited to the corner of the mouth and those that involve loss of a section of lower lip. When the corner of the lip is destroyed, parts of the upper and lower lips adhere and interfere with full opening of the mouth. The corner of the mouth can be reconstructed by separating the adherent portions of the upper and lower lips and excising the scar. In most cases, skin loss is negligible and only mucous membrane is required to establish the normal outline of the mouth.

Restoring the mucous membrane

One of two procedures can be used to restore the mucous membrane, depending on the amount of mucosa missing at the vermilion border. If the raw areas of the corners of the upper and lower lips are shorter than 1.5 cm, use an advancing flap from adjacent mucous membrane. More extensive loss requires transfer of mucous membrane flaps from the cheek.

  • Tongue flaps also have been used to restore the commissure defect. A laterally or anteriorly based tongue flap taken from the ventral surface of the tongue is preferable to avoid placing gustatory papillae on the lips. However, tongue flaps have several disadvantages. Tongue tissue often is too bulky and retains its papillary appearance. Furthermore, the junction at the vermilion border may be indistinct, and a color disparity may exist between the lips and flap in patients with dark skin tones. If the median section of the lip mucous membrane is lost, the lip retracts and adheres to the alveolar process. Adhesions of the lower lip must be divided. Either a skin graft or a local mucous membrane flap covers the resulting defect.
  • V-Y advancement procedure: Because skin grafts tend to contract significantly, use normal mucous membrane from the bordering regions, if possible. A V-Y advancement procedure can be used to advance the mucous membrane to replace the deficiency. In this procedure, first excise the scar to allow the lip to assume its normal position. Then make an incision along the inner surface of the lip close to the alveolar processes. The buccal incision is extended toward the molar region and then vertically over the mucous membrane of the cheek. The resulting 2 rectangular-shaped flaps are then sutured together to form a V-Y advancement flap. The raw area on the alveolar process is covered with a split-thickness skin graft that enhances the depth of the buccal sulcus.
  • Other procedures: Various procedures have been described to repair median losses of muscle and skin of the lower lip.
    • A triangular wedge excision or the Hagedorn rectangular flap technique can repair small-to-moderate losses.
    • A step bilateral rectangular flap advancement is another approach that utilizes the line of the chin crease to mask the scar.
    • The Stein procedure, use of an Abbé flap from the central portion of the upper lip, or modified Stein operation that rotates flaps from each side of the philtrum to restore contour to the lower lip are not recommended because they result in noticeable deformity of the upper lip.

Postpone surgery on the lower lip until the patient is aged at least 9 years, by which time permanent lower incisors have erupted and alveolar bone growth is not significantly influenced by the tightness of the lower lip. Surgery performed earlier results in a tight lower lip and either overbite occlusion or retrognathism from pressure on the growing mandible or lower anterior dentition. The earliest indication of these impending dental problems is forward protrusion of the upper lip beyond the reconstructed lower lip. Later, crowding or lingual deviation of lower deciduous teeth becomes evident. If these problems develop, orthodontic appliances are necessary to hold teeth in proper relationship.

Prevention

Prevention remains the best treatment of low-voltage electric burns. Educate parents regarding potential safety hazards and the need for close supervision of their children; this is important to decrease the incidence of childhood electric injuries. Use the following guidelines:

  1. Use extension cords on a limited and temporary basis only.
  2. Replace damaged electrical cords.
  3. Place plastic nonconductive dummy plugs in unused outlets.
  4. Do not use electric appliances near water, and keep them out of children's reach.
  5. Supervise children closely, especially when electric toys are in use. Such toys should bear the Underwriters' Laboratories label of safety, and damaged toys should be repaired or discarded.
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High-Voltage Electric Burns

Burns due to contact with high-voltage electric circuits conform to 2 general types.

Burns from an electric arc

In burns from an electric arc, the current courses external to the body from the contact point to the ground.[8] Circumscribed burns occur where the portions of the arc contact the patient. These contact points may be multiple, single, or diffuse and vary in their depths. The most common contact points for the current are the hands and skull, while the most common ground areas are the heels. Entry points on the flexor surfaces often produce "kissing" entry lesions, resulting from severe tetanic muscle contractions and causing extensive tissue damage. The most common of these lesions is the circumscribed deep wound on the volar surface of the forearm in association with contact wounds of the palm. A flame may complicate this burn injury if the flashes of an arc ignite the victim's clothing.

Burns from an electric current

The other burn injury is from an electric current that passes between the power source and the anatomic point of contact (entrance wound), and between the patient (exit wound) and the grounding mechanism, causing hidden destruction of deeper tissues. Such electrically conductive burns are simply thermal injuries occurring when the electric energy is converted to thermal energy. The extent of the electric burn is related to the magnitude, frequency, and duration of the current flow and the volume and resistance of the tissue.

Resistance

Resistance of living tissue changes as the current flows. Skin represents an initial barrier to flow of current and serves as insulation to the deeper tissues. Once an electric current contacts skin, the amperage rises slowly, followed by an abrupt and rapid climb. This change in flow coincides with a progressive decline in skin resistance. Once this skin resistance breaks down, current enters the underlying tissue whose internal tissue resistance, with the exception of bone, is negligible to current flow. Within seconds, electric current in tissue peaks and then falls precipitously to zero. Current ceases to flow when the heat-producing tissue carbonization (eschar) volatilizes tissue fluid. Termination of current flow is signaled by the appearance of an arc or flash.

Current pathways

Low-voltage current generally follows the path of least resistance (ie, nerves, blood vessels), yet high-voltage current takes a direct path between entrance and ground. The volume of soft tissue through which current flows behaves as a single uniform conductor, thus is a more important determinant of tissue injury than the internal resistance of the individual tissues. Current is concentrated at its entrance to the body, then diverges centrally, and finally converges before exiting. Consequently, the most severe damage to the tissue occurs at the sites of contact, which are commonly referred to as the entrance and exit wounds.

Entry and exit wounds

High-voltage electric entry wounds are charred, centrally depressed, and leathery in appearance, while exit wounds are more likely to "explode" as the charge exits. High-voltage electrical burns often leave a black metallic coating on the skin that is mistaken for eschar, from vaporization of the metal contacts and electroplating of the conductive skin surface. Cleansing of the coating usually reveals only superficial skin injury. Electric current chooses the shortest path between the contact points and involves the vital structures in its pathway. Fatalities are high (nearly 60%) in hand-to-hand current passages and are considerably lower (20%) in hand-to-foot current passages. Severity of damage to the tissue is greatest around the contact sites.

Consequently, anatomic locations of the contact sites are critical determinants of injury. Most of this underlying tissue damage, especially muscle, occurs at the time of initial insult and does not appear to be progressive. Microscopic studies of electric burns demonstrate that this initial destruction of tissues is not uniform. Areas of total thermal destruction are mixed with apparently viable tissue. Between the entrance and exit points of the electric current, widespread anatomic damage and destruction may be seen. An electric current can injure almost every organ system.

Complications

Sequelae peculiar to this type of injury are important determinants in the choice of therapy. Various complications related to the damage to the various organ systems are now clearly identifiable.

  • Characteristic entry and exit wounds in extremities usually signal local destruction of deeper tissues, the magnitude of which often cannot be predicted.
  • Bone has a high resistance, thus readily transforms current to heat production, which may result in periosteal necrosis or even melting of the calcium phosphate matrix.

This injured underlying tissue has several consequences.

  • Necrosis of the entire limb is the most serious complication, necessitating amputation usually within 2-3 days after injury.
  • More commonly, the extent of underlying tissue injury involves a portion of the superficial and deep muscles of one or more compartments. Vessels within these electrically injured tissues exhibit increased vascular permeability. [17] This permeability change allows extravasation of fluids into the wounds, resulting in a reduction in intravascular volume that must be corrected by an intravenous (IV) infusion of Ringer lactate solution without glucose.

Treatment

See the list below:

  • The quantity of fluid sequestered in the injured tissue usually cannot be estimated using skin surface measurement, because the magnitude of damage to the underlying tissue often is grossly underestimated. Consequently, titrate the quantity of fluid administration to maintain an adequate urinary output.
  • In contrast to flame injury, completion of fluid resuscitation can be predicted by the patient's hematocrit and plasma volume. When extracellular fluid is restored, the hematocrit and plasma volume returns to normal, if significant hemolysis has not occurred.
  • In acute electric injuries in the adult with underlying devitalized tissue, administer Ringer lactate solution without glucose at a rate sufficient to maintain a urinary output of 50-100 mL/h.
  • In the presence of hemochromogens in the urine, the rate of fluid infused must be sufficient to maintain a minimum urinary output of 100 mL/h. This rate and volume of fluid administration is continued until the urine is free of pigment. Alkalization of the urine by adding sodium bicarbonate to the IV fluid increases the solubility and clearance rate of myoglobin in the urine.
  • Transfusions are unnecessary during the first 24 hours unless multiple escharotomies and/or fasciotomies result in significant blood loss. An almost immediate loss of intravascular fluid into an electrically burned extremity results in considerable swelling of the muscle lying within a relatively inelastic fascial compartment. [18] Such intense swelling of the injured muscle may cause noticeable changes in the circumference of the extremity. More frequently, fascial investments may limit the swelling to such a degree that minimal external enlargement of the limb occurs.

Postinjury physiologic events

Within a few hours after injury, rising interstitial pressure of the compartment exceeds the capillary perfusion pressure, resulting in muscle ischemia. Consequences of this reduced perfusion are a further increase in capillary permeability and extravasation of intravascular fluid, enhancing the interstitial pressure of the compartment. After 6-8 hours of ischemia, muscle damage is irreversible. This vicious cycle must be interrupted by fasciotomies, which limit ischemic injury to the muscle.

Muscle necrosis within a compartment has potentially severe systemic sequelae. It enhances local vascular permeability with extravasation of intravascular fluids into the injured site with resultant hypovolemia. Absorbed pigment from the damaged muscle cells and, to a lesser amount, hemoglobin from injured red blood cells are released into the circulation soon after burn injury and expose the kidney to significant pigment loads. This absorption of pigments into the intravascular space may lead to acute renal failure. The mechanism of acute myoglobinuric renal failure is obstruction of the collecting system in association with renal cortical ischemia.

Various modalities have been measured to elucidate the extent of muscle damage. The presence of myoglobin is always associated with underlying devitalized muscle, yet not all muscle damage is associated with myoglobinuria. Moreover, the presence of myoglobinuria does not identify either the extent or location of damaged or dead muscle.

Laboratory studies

Laboratory studies, such as elevation of serum enzymes, serum glutamic-oxaloacetic transaminase, or glutamic-pyruvic transaminase, are nonspecific, and levels are often elevated with only a cutaneous burn. Numerous procedures have been cited as valuable aids in the diagnosis of the extent and location of devitalized muscle. Escharotomies and fasciotomies are useful methods to identify and explore areas suspicious of containing devitalized tissue. These exploratory incisions permit assessment of the extent of muscle injury by visual and microscopic surveillance.

Microscopy as a guide to primary excision is the most accurate diagnostic procedure for muscle viability. In this method, frozen section histology is used to determine muscle damage. Because muscle cross striations may be preserved in dead or dying muscle, morphology of the muscle cell nuclei is the best indicator of viability. Muscle containing clumped nuclear chromatin or poor staining with hematoxylin indicates myonecrosis and should be excised.

Diagnostic tests

See the list below:

  • Early exploration of the burn wound remains the criterion standard for determining the severity of injury. If no detectable viability of an electrically injured extremity is observed, amputation is mandatory because it dramatically reduces life-threatening myoglobinuria.
  • MRI
    • MRI can be used to detect edema of the torso and extremities if the patient is medically stable enough to tolerate an imaging procedure.[19] Tissue edema is a manifestation of cell membrane damage that begins to accumulate minutes after electric injury from increased vascular permeability and extravasation of intracellular contents.
    • The presence of edema on MRI can direct attention to areas with substantial muscle cell damage. These edematous areas are at risk for compartment syndrome and compression neuropathies, and compartment pressures should be measured.
    • Compartment pressures exceeding 30 mm Hg compromise fluid and gas exchange between the blood and tissue and necessitate fasciotomy. The only reliable indicator of compartment pressures is a direct intramuscular pressure measurement. Digital pressure manometers are available for larger compartments. For smaller compartments, such as the hand or foot, manometers may cause infection of the perimuscular fluid, resulting in iatrogenic compartment syndrome. Absence of edema on MRI indicates either that the muscle is not injured or that severe heat exposure caused intravascular thrombosis with loss of muscle perfusion.
  • Nuclear medicine studies
    • No consistent correlation exists between MRI data and tissue survival or clinical outcome; therefore, nuclear medicine studies are a useful adjunct to MRI.[20, 21] Technetium Tc 99m stannous pyrophosphate (99m Tc-PYP) muscle scan is a sensitive and reliable diagnostic tool to define the extent and location of muscle injury. This test can be performed in most hospitals with a nuclear medicine department. An isotope is infused intravenously, and the scan is performed 2 hours later. Several characteristic scintigraphic imaging patterns indicate muscle damage. An increased cellular uptake of 99m Tc-PYP (hot spot) identifies an area of muscle damage consisting of 20-80% viable muscle, which should be followed clinically.
    • Conversely, areas with no uptake of this radioactive material (cold spot) are devoid of blood supply and obviously necrotic. Variations of this can occur, with a central cold spot surrounded by a perfused but injured area of muscle. Uneven distribution of muscle necrosis characteristic of high-voltage electric injuries is confirmed by this technique. This early identification of injured muscle by muscle scan is helpful in planning the operative approach and predicting the approximate level of debridement and/or amputation required. The short half-life (6 h) of 99m Tc-PYP allows this study to be repeated in 24 hours if extension of the injury is possible.
    • The major drawback to this technique is that the scan is excessively sensitive and may occasionally incorrectly identify areas of muscle injury. These false-positive tests appear related to the developing edema that occurs in the first 24 hours.
    • A newer isotope, technetium Tc 99m methoxy-isobutyl-isonitrile, shows decreased uptake in electrically injured tissues and better sensitivity in localization of muscle injury.
    • Newer strategies to detect muscle injury include measurement of tissue electrical impedance. Electrical resistance of electrically injured muscle decreases in proportion to the amount of cell membrane lysis.
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Neurologic Complications

Neurologic complications are the most common complications of electric injury.[22, 23, 24] Both acute and delayed central and peripheral nervous system sequelae have been described. Approximately 70% of patients were rendered unconscious in high-voltage electric injures, including all those in whom the current passed through the head and several patients in whom the current had not traversed the head. All unconscious patients, except those fatally injured, recovered within a few hours, most in 5-10 minutes. Transient agitation and confusion were seen in a few patients. With regard to their social rehabilitation, a follow-up study detected some mild changes in personality and mental capacity. Less-frequent complications of intracerebral injury include hemiplegia, aphasia, striatal symptoms, epilepsy, headaches, and memory and concentration deficits.

Peripheral nerve injury

Peripheral nerve injury may be involved by direct injury at the site of entrance or exit or in polyneuritic syndrome involving nerves far removed from the points of contact.[23] Typical symptoms include numbness (anesthesia) and "pins and needles" sensation (paresthesia). Loss of function in a peripheral nerve is usually transient, and complete recovery may be expected if the nerve is not involved in local tissue injury; however, permanent damage to peripheral nerves in electric injuries is limited to the area of local tissue contact.

Median, ulnar, and radial nerves have the highest incidence of persistent dysfunction. Heat released by current flow causes total or partial loss of nerve function. In deep burns involving nerve trunks, prognosis for recovery is unfavorable. In these severe injuries, usually total loss of nerve function occurs. Whenever a nerve deficit is discovered, perform surgical exploration to exclude contributing factors, such as the compartmental syndrome. A late cause of reversible peripheral nerve injury may be secondary to heterotopic bone formation, which most often occurs at the elbow, resulting in ulnar nerve dysfunction.

Acute and delayed spinal cord injuries have been described distal to the site of electric contact. Such injuries have occurred following contact with electric currents whose voltages varied from 75-75,000 volts. Characteristically, no neurologic deficit was noted immediately after the accident. Symptoms and signs did not develop until days to 2 years following injury, when total quadriplegia or hemiplegia may occur. Signs are variable and may include ascending paralysis, amyotrophic lateral sclerosis, or transverse myelitis. Motor deficits occur more frequently than sensory loss. This syndrome was first termed spinal atrophic paralysis. In patients with electric spinal cord injuries, neurologic recovery is unusual.

Experimental studies demonstrated that electric injury may cause perivascular hemorrhage, demyelinization, reactive gliosis, and neuronal death in the spinal cord in animals. Such neuronal damage was produced in animals with minimal damage to the skin or structures outside the spinal cord. Results of experimental studies parallel the clinical findings of extensive neurologic injury to patients with mild cutaneous injury. Delayed appearance of the spinal cord injury has not been explained experimentally. It may represent direct injury either to the neurons or the vascular supply of the spinal cord.

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Cardiovascular and Pulmonary Complications

High-voltage electric current can produce a wide variety of different cardiac injuries and usually consists of rhythm and conduction disturbances.[25, 26, 27] Cardiac arrest either from asystole or ventricular fibrillation often presents in electrical injuries. The most common electrocardiographic abnormalities following high-voltage electric injuries are sinus tachycardia and nonspecific ST-T segment alterations, which frequently persist for several weeks following injury. Atrial fibrillation also has been reported following contact with high-voltage electric wires. In most of these instances, rhythm reversed spontaneously or after administration of either quinidine or digitalis.

Disturbances in the heart conduction system have rarely been reported in high-voltage electric accidents. In one patient, a partial intraventricular conduction block persisted for 10 days. A nodal rhythm was observed in another patient for a 24-hour period, after which it disappeared. Although these findings imply myocardial or conduction system injury, the necessary extensive surgical procedures performed during treatment of the burn injury were not associated with detectable cardiac complications.

Myocardial infarction, substantiated by cardiac enzyme studies, is an uncommon complication of high-voltage electric injuries. Electric burns of the anterior chest may cause direct thermal injury to the myocardium with perforation that must be closed during cardiopulmonary bypass. Using telemetered monitoring, paramedics should be the first to detect evidence of cardiac injury at the scene of injury. An electrocardiogram is usually repeated on arrival in the emergency department. Institute cardiac monitoring when the patient is hospitalized.

Cardiac enzymes

Cardiac isoenzymes have questionable diagnostic value in electric injuries. A high creatine phosphokinase (CPK) MM fraction is consistent with skeletal muscle damage, yet a significantly elevated CPK-MB fraction may not indicate cardiac damage.[28] Recent studies show that skeletal muscle cells contain up to 20-25% CPK-MB fraction, suggesting that electrical damage to skeletal muscle rather than cardiac muscle may account for an elevated CPK-MB fraction. Ignoring this finding may lead to an incorrect diagnosis of myocardial infarction.

In the presence of cardiac injury, lactic dehydrogenase (LDH) fractionation reveals that LDH-1 rises more than LDH-2, and the LDH-1/LDH-2 ratio exceeds unity. Because LDH-2 exceeds LDH-1 in normal serum, this reversed or "flipped" LDH pattern is present in most acute myocardial infarctions.

Vascular damage

Vascular lesions dominate the clinical presentation of many electric burns.[29] When current passes through large vessels at its entrance or exit points, it may cause a pronounced inflammatory reaction as well as small areas of vascular wall necrosis. The latter may lead to immediate or delayed rupture of the vessel. Current flowing through larger vessels that are located beyond the entrance and exit points of the current may damage the vessel, precipitating the development of mural thrombi, yet vessels usually remain patent. Flow through these larger vessels dissipates heat and limits damage to their walls. In smaller vessels, this heat injury results in vessel thrombosis.

Small nutrient vessels, like those in muscle, are very susceptible to thrombosis when exposed to high temperature. Pathologic examination of the electrically injured tissue confirms the presence of small arterial and microarterial thrombosis. Because arteriography is capable of identifying only arterial lesions in large and medium vessels, it has limited clinical usefulness in acute electric injuries. This loss of blood supply to muscle may be progressive, occurring over the first 1-3 months after injury. Such changes may account for the progressive muscle fibrosis and flexion contractures that occur frequently after this injury.

Acute pulmonary complications

Acute pulmonary complications are limited to pleural damage resulting in effusions and lobular pneumonitis directly adjacent to the entrance and exit wounds and are usually evident by the end of the first week.[30] A closed tube thoracostomy may be necessary to remove a pleural effusion and typically prevents reaccumulation. Pulmonary infection may result from systemic infection or from inhalation injury.

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Abdominal, Bone, Joint, Eye, and Systemic Complications

Abdominal complications

A wide spectrum of abdominal visceral complications has been reported following high-voltage electrical injury.[31, 32, 33, 34] These injuries result either from direct injuries to intra-abdominal structures from the contact points over the abdomen or are a result of current passing through the abdominal viscera from more distant entrance and exit wounds. In treating high-voltage electric accidents, anticipate the entire spectrum of anatomic and pathologic alterations to the abdominal viscera.

Nausea and vomiting are the most common abdominal symptoms, seen in up to 25% of patients. Numerous different GI complications have been reported following high-voltage electric injury.

Nonspecific adynamic ileus occurs in approximately 25% of patients. Usually a transient finding, adynamic ileus may be a manifestation of a more serious underlying GI injury.

Stress ulceration (Curling ulcer) is probably one of the most serious complications (3%). With this potential for stress ulceration, treatment of patients with high-voltage electric injuries with antacids and histamine H2-receptor antagonists is prudent.

When either the entrance or exit wound is the abdominal wall, localized destruction of the abdominal wall occurs with direct injuries to the underlying intra-abdominal structures, including small and large intestines, bladder, or liver. High-voltage electric burns whose entrance and exit points do not contact the abdominal wall may also result in injury to the intra-abdominal contents (eg, gallbladder, intestine). In the latter case, the initial symptoms of underlying injury to the viscera may be slight and not appreciated until 2-3 weeks after injury.

Pancreatic injury is a rare complication of high-voltage electric current. Hyperamylasemia with prolonged ileus has been encountered in several patients who responded favorably to medical management. A pseudodiabetic state occurred toward the end of the first week after the accident in other patients. Marked hyperglycemia and mild ketosis were treated with small amounts of insulin. After recovery, glucose tolerance curves of these patients returned to normal. After abdominal surgery in patients with high-voltage electric burns, the complication rate was alarming. Repair of bowel anastomoses is associated with a high incidence of leakage, which has been attributed to the surgeon's inability to accurately determine the extent and depth of damage to the intestine. Therefore, lesions of the small intestine should be resected with wide margins.

Treatment of electric injuries of colon

Electric injuries of the colon seem best treated by wide resection and colostomy or exteriorization of the injured segment.[35] When multiple superficial lesions are scattered over the bowel, a "second-look" operation at 2-5 days may be advisable in instances where areas of injury with questionable viability are not resected. Distribution of intravenously injected fluorescein dye may prove helpful in demarcating devascularized intestine. Early staining of the injured bowel with fluorescein is evidence of tissue viability.

At times, active bleeding from the cut ends of the transected bowel may be present, indicating tissue viability. Wound disruption following emergency abdominal surgery in burn patients is frequently noted. On limited occasions when stainless steel wire was not used for fascial closure, wound complications frequently have been encountered. On the basis of this experience, close abdominal wounds in burn patients with stainless steel sutures, usually retention sutures, placed through all muscle and fascial layers of the abdominal wall.

Long-term follow-up care of patients who had recovered from a high-voltage electric injury revealed a high incidence of GI complications. Approximately three fourths of patients had recurrent dysfunction of the GI tract within 12-18 months after injury. No discernible cause for the abdominal complaints was found in most patients, while cholelithiasis was detected in approximately 8%.

Bone lesions

In high-voltage accidents in which the current enters near bony tissue, lesions of the bone are common.[36] High resistance of bone to the passage of electric current results in periosteal necrosis and melting of the calcium phosphate matrix. The resulting destruction is often difficult to diagnose at the time of initial debridement. Stripping of the devitalized periosteum and obtaining early soft tissue coverage limits the magnitude of bony injury.

Despite this aggressive therapy, small sites of bony sequestrum often form sinus tracts 1-8 months after closure. After excision of the sequestra, wound closure is usually accomplished without infection. In accidents where high-voltage current passed through the head, the injury was mainly confined to the scalp and skull. Current was usually dissipated in the skin, galea, and outer table, sparing the brain from direct cerebral injury. This explained the surprising fact that severe cerebral complications were rare in such accidents.

With the progress of microvascular free-tissue transplantation in recent decades, free flaps have come into use in the reconstruction of high-voltage electrical burn injuries. Free-flap coverage is mainly used for upper limb reconstruction, primarily for purposes of forearm reconstruction.

Scalp burns

Scalp burns can be classified according to the depth of burn into the following 4 specific groups: (1) burns without direct bone involvement; (2) burns with direct bone involvement (outer table only or both tables); (3) burns involving dura mater; and (4) burns involving the brain.[37] Depth of the burn injury has considerable influence on treatment. When the injury is confined to full-thickness destruction of the scalp, closure is accomplished with split-thickness skin grafts. If the burn injury is localized to a small region, local flaps can be employed to resurface the defect. When bone death is involved in burn injury, treating these patients becomes considerably more difficult.

Treatment of scalp burns

Problems center around achieving complete skin cover without the development of infection. Two treatments are available for patients with burns of the scalp that involve the underlying bones. One technique is to remove all dead bone, closing the defect by grafting; the other is to close the wound with a skin flap without excision of devitalized bone. There are several different approaches to remove dead bone. The most conservative one is to leave the bone exposed for an undetermined time, usually weeks or months. Eventually, nonviable bone sloughs or is removed as a sequestrum; the defect is then closed either with a skin graft or flap, depending on the availability of local tissue. Holes can be drilled into the skull to permit ingrowth of granulation tissue from a viable diploic cavity to accelerate sequestration. Areas of bone between the holes tend to sequestrate slowly and delay stable skin cover.

Another technique is to remove the outer table completely. Wounds in these patients reportedly heal twice as fast as those treated by the multiple burr hole technique. More recently, surgeons have believed that these approaches to burn injuries of the scalp that involved bone removal were not warranted. They demonstrated that the prolonged course of debridement, sequestrectomy, and subsequent reconstruction can be bypassed effectively with a single, early definitive procedure that included primary excision of the skin eschar followed by rotational flap coverage without removal of devitalized bone. The electrically injured skull acted as an in situ bone graft. In the absence of a local flap, a free flap may prove an important alternative method of wound coverage.

Currently, coverage of devitalized bone by a well-vascularized flap allows regeneration of bone. Several clinical reports have documented the successful centripetal regrowth of bone following coverage with a vascularized flap.

Joint injuries

Because the victim does not continue to grasp the conductor in high-voltage electric injuries, fractures usually result from the patient falling from the electric current.[36] Powerful tetanic skeletal muscle contractions have caused long bone fractures, cervical spinal fractures, and joint dislocations. Anterior and posterior shoulder dislocations from tetanic spasm of the rotator cuff muscles have occurred during electric injuries.

When overlying skin involvement is associated with the fracture, skeletal traction is preferred over internal fixation to reduce the chance of bone infection. Heterotopic ossification of soft tissues is a common consequence of commercial electric injury. This process occurs at joints, other synovial surfaces such as bursa and nerve sheaths, and the end of amputation stumps. This ossification results from tissue injury, constant shear forces between bone and surrounding tissues, and a systemic inflammatory response.

Upper and lower extremity burns

The loss of an arm or leg is one of the most devastating consequences of a burn injury. Reported rates of amputation as a result of high-voltage electric burn injury range from 32-60%. Deep thermal burns complicated by extensive soft tissue necrosis or invasive infection may produce nonsalvageable extremities. Advances in reconstructive surgery have resulted in decreased amputation rates after electrical burn injuries. Traditionally, amputation after burn trauma has been related primarily to high-voltage electric injury. These amputations may be isolated to a major extremity or to digits, hands, or feet.

Sauerbier et al demonstrated that burn and high-voltage injuries are distinct entities that require custom-tailored reconstructive solutions for limb salvage. Even if the surgeon's flap fails during the first 6 weeks, remember that this type of coverage is the only alternative to amputation in select cases. As the versatility and variability of free flaps have significantly increased during recent years, so have indications for free tissue transplantation in burn reconstruction expanded. The progress of free tissue microvascular transplantation in recent decades has led to the increasing use of free flaps for reconstruction in patients with electrical burns. The flaps have reached a high level of surgical sophistication to include fascial flaps, pre-expanded flaps, and composite tissue flaps, as well as multiple flap transplantations in the same patient.

Eye injuries

Electric injuries to the eye occur chiefly when current enters the body through the patient's head.[38] The lenses of both eyes can be equally affected, or one can be more affected than the other. A wide range of voltages, from 220-50,000 volts, results in a cataract in 6% of electric injuries. Time of onset of the symptoms ranges from 3 weeks to 2 years. Lesions of the cornea, fundus, and optic nerve, without alteration of the lens, have also been reported.

Systemic complications

Severe potassium deficiency is an unexplained manifestation of high-voltage electric injury. This problem was identified in patients with normal renal function who were eating well 2-4 weeks after injury. In such patients, respiratory arrest and severe cardiac arrhythmias may lead to the diagnosis. Systemic manifestations of electric current injury are not apparent in high-voltage electric burns that result only from intense heat of the electric arc. Surface burns of varying size and depth result from this injury without hidden destruction of deeper tissues. Occasionally, the arc ignites the patient's clothing, resulting in a flame burn that further damages the skin.

Psychosocial complications

The psychosocial complications following electrical burns have been evaluated through a cross-sectional survey of electrical burn patients using 3 outcome tools: the Burn Specific Health Scale, the Coping with Burns Questionnaire, and the Pain Patient Profile. Patients surveyed more than 5 years from injury showed improvement in their physical health. Optimism was the most commonly used coping strategy for these patients. However, significant levels of emotional distress were encountered in all patients; anxiety was more common in patients with high-voltage electrical injuries. Recognizing that electrical burn patients may have a limited ability to return to work and an overall poor quality of life is important. Emotional distress is the dominant feature that influences long-term outcome in these patients.

Pregnant patients

Electrical or lightning injury carries the additional risk of complications to a pregnant mother or her fetus.[39] Because of the small number of cases reported, the actual risks are unknown. Reports of fetal mortality vary widely, ranging from as high as 73% to as low as 15% after electrical injury and about 50% after a lightning strike. Whether fetal mortality is due to primary electrical injury of the fetus or due to the injury to the pregnant mother is not clear.

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Safety Laws and Accident Prevention

Deaths from electric shock accidents

Almost 1200 people died from electric shock accidents associated with consumer products during a 3-year period (1975-1977). Of these, electrocution by outdoor television and CB radio base station antennas accounted for 355 deaths. Most electrocutions could have been prevented if consumers understood the dangers and followed safety precautions. Most deaths linked with outdoor antennas occurred when the device contacted an overhead power line while the victim was putting up or taking down the antenna.

Consumer alerts

In an attempt to alert consumers to the danger of electrocution, the Consumer Product Safety Commission (CPSC) now requires manufacturers and importers to include warning labels and installation instructions with all outdoor TV and CB base station antennas and masts or other devices intended to support these antennas. This regulation applies to all such products manufactured, imported, packaged, or sold by the manufacturer or importer after September 26, 1978.

Similar incidents occur with ladders, especially metal ladders, when the user fails to observe a nearby power line. Many ladder manufacturers are now labeling their products on a voluntary basis to alert consumers to the possible electrocution hazard. In 1988, the CPSC conducted a human factor analysis of reports of in-depth investigations to assess the electrocution hazard associated with the use of aluminum ladders near power lines. This analysis was based on relating relevant victim characteristics, product characteristics, and environmental factors that may have contributed to the electric injuries. Analysis revealed that while some of the victims were unaware of the electrocution hazard, a number of victims were aware of the electrocution hazard and either lost control of the ladders near power lines or misjudged the clearance distance between the power lines and the ladders.

Further study of the in-depth investigations revealed that the human visual system has limited ability to estimate the clearance necessary to avoid contacting power lines; therefore, carrying the ladder in its extended position and misjudging the significant instability of the ladder resulted in victims inadvertently contacting the high wires or losing control of the ladder. Unusually severe consequences from such accidents led NIOSH (National Institute for Occupational Safety and Health) to recommend greater safety precautions. NIOSH required employers and workers to comply with Occupational Safety and Health Association (OSHA) regulations prohibiting the use of portable metal ladders for electrical work or in locations where they may contact electrical conductors (Code of Federal Regulation, 1988).

NIOSH also suggested that arrangements be made with the power company to de-energize the lines or to cover the lines with insulating line hoses or blankets. Furthermore, employers were encouraged to provide workers with training in emergency medical procedures, such as cardiopulmonary resuscitation, because fatalities may be prevented by prompt medical care. CPSC recommended changing the American National Standards Institute's (ANSI) warning sticker that now appears on ladders to a more descriptive sticker, including the type of hazard, the result of ignoring the warning, and how to avoid the hazard. CPSC also suggested that approaches aimed at reducing this type of electrocution hazard that do not rely solely upon people taking some action may be more effective.

Preventing electric burns

One solution is to place a fiberglass link in all new ladders, thereby providing isolation so that electricity does not have a path to the ground. This type of ladder is already in use by some power-line companies. An alternative solution is to cover the top half sliding section of extension ladders with an insulating, nonconducting material such as heavy Teflon. This suggestion has been used successfully in the installation of roof top antennae.

In 1989, the Commonwealth of Virginia created the Overhead High Voltage Line Safety Act to promote the safety and protection of anyone working around overhead power lines. This law applies to individuals and businesses whose work requires close proximity to overhead power lines, excluding cable television and telephone companies. It specifies limits for working safely near overhead power lines and requires a safe work area when those limits cannot be maintained to perform the necessary work. This law states that no mechanized equipment can be operated within 10 feet of a power line within the range of 600-50,000 volts, and a person cannot come within 6 feet. When working within these limits, the worker must notify the power company, which will then turn off or relocate the line or make specific recommendations regarding equipment.

Special protective apparel should be worn by employees who have to work near high-voltage lines, including helmets, rubber gloves and sleeves, and goggles. According to OSHA, employees working near high-voltage lines should wear class B helmets (as defined by ANSI) that are designed to withstand 20,000 volts of alternating current at a frequency of 60 Hz for a total of 3 minutes. In addition, these helmets should resist burn-through at 30,000 volts.

High-voltage wires are prone to occasional discharges or arcs of electricity that can damage the corneal epithelium. This protective eyewear prevents such an injury. In Washington, irrigation pipes (IP) used by farmers are the most common source of fatal human contact with high-voltage electric lines. Groups such as public utility companies and cooperative extension services have recognized the dangers of IP electrocution and have advised caution when IPs are handled near electric lines. All agencies and groups (including state and county health departments, utility companies, agriculture extension services, school districts, civic associations, and agricultural workers groups) in rural areas irrigated with metal pipes are encouraged to remind agricultural workers of the life-threatening hazard of IP electrocution.

Scientific basis for selecting gloves

Rubber insulating gloves are necessary for manipulation of high-voltage wires and for protection against burn injury.[40] Class 2 gloves, as defined by the American Society for Testing and Materials, provide protection at 20,000 volts. Class 4 gloves provide protection at 40,000 volts and should be worn by those working near and with high-voltage wires. Tinted protective eyewear also should be worn. Despite expensive regulatory and safety program efforts, electrical hazards still represent an important occupational health and safety issue for workers in the electric utility industry.

Once the electrical current has been disconnected, the emergency medical technicians and paramedics responding to an electrical injury situation should wear emergency medical examination gloves with a glove hole leakage rate of 1% rather than examination gloves used in the hospital, which have a glove hole leakage rate of 4% (as required by the Food and Drug Administration [FDA]).[41]

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Smoke Evacuation During Electrosurgery Procedures

Electrosurgical techniques have been used in hospitals for more than a century. Electrosurgery in the operating room may be associated with smoke that contains the same airborne contaminants as laser smoke. This plume contains toxic gases and vapors, such as benzene, hydrogen cyanide, formaldehyde, and dead and living cellular material, including blood and viruses. The contaminants have an unpleasant odor, may cause visibility problems at the surgical site, and may produce upper respiratory tract and eye irritation. The contaminants have mutagenic and carcinogenic potential.

The National Institute of Safety and Health recommends the use of smoke evacuation systems. A smoke evacuator and an ultra-low particulate air filter should be used when large amounts of smoke or plume can be generated in the operative procedure. This filter can remove 99.9999% of the bacteria, dust, pollen, mold, and particles with a size of 120 nanometers or larger from the air.[42]

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Contributor Information and Disclosures
Author

Richard F Edlich, MD, PhD, FACS, FACEP FASPS, Distinguished Professor Emeritus of Plastic Surgery, Biomedical Engineering and Emergency Medicine, University of Virginia Health Care System

Richard F Edlich, MD, PhD, FACS, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Burn Association, American College of Emergency Physicians, American College of Surgeons, American Society of Plastic Surgeons, American Spinal Injury Association, Plastic Surgery Research Council, Society of University Surgeons, Surgical Infection Society, American Surgical Association, American Trauma Society

Disclosure: Nothing to disclose.

Coauthor(s)

David B Drake, MD, FACS Professor, Department of Plastic Surgery, Medical Director, DeCamp Burn and Wound Center, Program Director. UVA Hand Fellowship, University of Virginia School of Medicine

David B Drake, MD, FACS is a member of the following medical societies: American Association for Hand Surgery, American Burn Association, American College of Surgeons, American Society of Plastic Surgeons, American Society for Reconstructive Microsurgery, Association for Surgical Education, Southeastern Society of Plastic and Reconstructive Surgeons, Southern Medical Association

Disclosure: Nothing to disclose.

William B Long, III, MD, FACS President, Trauma Specialists, LLP; President, Pacific Surgical, PC; Trauma Medical Director, Legacy Emanuel Trauma Center, Legacy Emanuel Hospital

William B Long, III, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, American Thoracic Society, American Trauma Society, Society of Thoracic Surgeons, Pacific Coast Surgical Association, Western Trauma Association, North Pacific Surgical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Wayne Karl Stadelmann, MD Stadelmann Plastic Surgery, PC

Wayne Karl Stadelmann, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society of Plastic Surgeons, New Hampshire Medical Society, Northeastern Society of Plastic Surgeons, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Deepak Narayan, MD, FRCS Associate Professor of Surgery (Plastic), Yale University School of Medicine; Chief of Plastic Surgery, West Haven Veterans Affairs Medical Center

Deepak Narayan, MD, FRCS is a member of the following medical societies: American Association for the Advancement of Science, American College of Surgeons, American Medical Association, American Society of Maxillofacial Surgeons, American Society of Plastic Surgeons, Plastic Surgery Research Council, Royal College of Surgeons of England, Royal College of Surgeons of Edinburgh, Indian Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Dennis P Orgill, MD, PhD Professor of Surgery, Harvard Medical School; Associate Chief of Plastic Surgery, Brigham and Women's Hospital

Dennis P Orgill, MD, PhD is a member of the following medical societies: American Society for Reconstructive Microsurgery, Plastic Surgery Research Council, American Medical Association, Massachusetts Medical Society

Disclosure: Received consulting fee from Integra LifeSciences, Inc for consulting; Received consulting fee from Integra LifeSciences, Inc. for program and training services agreement; Received grant/research funds from Integra LifeSciences, Inc. for clinical research; Received grant/research funds from KCI for basic science research; Received grant/research funds from KCI for clinical research; Received consulting fee from DSM for consulting; Received consulting fee from Musculoskeletal Transplant Foundatio.

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