Chapter 97. Electrical Trauma

• Aggressive and prolonged life support maneuvers should be performed as necessary on all electrical injury patients in the first few hours.
• All patients are to be considered to have multisystem injuries, including cervical spine fracture, until such injuries are eliminated diagnostically.
• Intravenous fluid resuscitation should not be underestimated.
• Most patients should be monitored for cardiac dysrhythmias for 24 to 48 hours after injury, particularly if electrocardiographic abnormalities were present or persist.
• The preservation of renal function depends largely on adequate volume resuscitation. If urine is visibly discolored by myoglobin, then renal function may depend on supplemental therapies.
• The neurologic examination should be monitored carefully for seizure activity, which should be treated if it develops.
• Early recognition and decompression of compartment syndromes are critical for maximizing extremity salvage and long-term function.
• Adequate wound care necessitates complete débridement of nonviable tissue followed by wound closure as expeditiously as possible.

Electrical shock is one of the leading causes of work-related injury, comprising 7% of all workplace fatalities. Typical victims of high-voltage electrical injury are young industrial workers or linemen usually between the ages of 20 and 34 years, with 4 to 8 years experience on the job. Immediate death can result from cardiac dysrhythmia, central respiratory arrest, or asphyxia due to tetanic contraction of the muscles of respiration. If victims survive the initial cardiopulmonary or central nervous system (CNS) insult, they then may face potential limb- and life-threatening sequelae from cutaneous injury, internal tissue destruction, and organ system dysfunction. The distribution of the tissues and organs damaged depends on the path of the injury current. Frequently, the injury is complicated by associated blunt trauma when the patient falls from a height or is thrown by the force of the electric current.

When the voltage is less than 1000 V, direct mechanical contact usually is required for electrical contact. For high voltages (>1000 V), arcing usually initiates the electrical contact. Most electrical injuries are due to low-voltage (<1000 V) electrical shock. Whereas low-voltage shocks carry a significant risk of electrocution-induced cardiac arrest, high-voltage shock injury is characterized by extensive tissue damage rather than electrocution. Approximately 3% to 4% of all U.S. hospital burn unit admissions are for electrical injury, mostly a result of high-voltage (>1000 V) shocks.

The duration of contact with the high-voltage power source and the distribution of electric current are important factors in the magnitude of the injury. If the contact is brief (i.e., <0.5 s), cell damage can occur through nonthermal components of electrical injury, called electroporation.1 If the contact is longer, both heating caused by electrical conduction (joule heating) and electroporation play important roles. Prolonged contact can lead to thermal burning of tissues in the current path. The electric current distribution across the tissues between the surface contact points depends on the electrical conductivity of the various tissues and on the variation in electrical field intensity. Usually, current density is greatest at the contact points. Once the current travels away from the contact points into the subcutaneous tissues, the tissues with the least electrical resistance, i.e., muscle, nerve, and blood vessels, will have the largest current densities and will experience the most rapid heating.2

Many cells, such as muscle and nerve cells, use electrical signals to control their function. The application of weak electrical fields from a nonphysiologic source can interfere with cell function and, if the field is strong enough, cause direct cell damage. Electricity at frequencies below 1 MHz may produce tissue injury primarily by permeabilizing cell membranes, electroconformational denaturation of cell membrane proteins, and thermal denaturation of tissue proteins. Factors that determine the anatomic pattern, extent of tissue injury, and relative contribution of heat versus direct electrical damage include the amount of current, the anatomic location, and the contact duration. The type of clothing, use of protective gear, and the power capability of the electrical source also contribute to the wide range of clinical manifestations observed in electrical shock victims.

At the commercial frequency of 60 Hz, the threshold for human perception of a current passed hand to hand is approximately 1.0 mA. As the current reaches 16 mA, the muscles in the arm develop involuntary spasms. Within 10 to 100 milliseconds of the onset of the current (the excitation-contraction response time of human skeletal muscles), muscles located in the current path will contract. If the hand is holding the conductor at that time, the strong forearm flexor muscles will contract, causing the victim to grasp the conductor strongly and thus maintaining contact uncontrollably with the current source. This is called the no-let-go phenomenon. Alternatively, if the victim is close to but not touching the conductor at the time of current passage, the strong muscle contractions generally propel the person away from the contact. Judging from eyewitness reports, the latter phenomenon may be more common. In addition, a very high-energy electrical arc can produce a strong thermoacoustic blast force leading to significant barotrauma.

When a current of 60 mA or greater traverses the mediastinum, there is enough depolarization of myocardial membranes to cause cardiac arrhythmias, particularly if induced during early myocardial repolarization. When the current amplitude reaches 1500 mA through the upper extremity, skeletal muscle and peripheral nerve cells are damaged by electrical forces, independent of heat. Smaller currents, in the range of 200 to 500 mA, can generate enough joule heating to cause tissue damage if the duration of current passage is sufficient. The rise in serum creatine phosphokinase (CPK) levels that results may be a useful prognostic indicator.3

While the spectrum of electrical injury ranges from minor cutaneous trauma to severe multisystem injury, the victims of high-voltage electrical injury are usually the patients who are admitted to a critical care unit (Tables 97-1 and 97-2).

On arrival at a critical care facility, the ABC's of trauma (airway, breathing, and circulation) are assessed, and appropriate therapeutic maneuvers are initiated. Cardiopulmonary resuscitation (CPR) is initiated or continued, as needed, and routine advanced trauma life support (ATLS) procedures and protocols are performed. Life support activities should be continued for a prolonged period because complete functional recovery after lengthy resuscitatory efforts has been well documented.4 Precise time limits for the continuation of life support have not been elucidated.

After the patient is stabilized, a complete history should be obtained, if possible, and a careful physical examination should be performed. Witnesses and family members often give pertinent information regarding the accident, as well as significant medical history. On physical examination, particular attention should be paid not only to the sites of electrical contact but also to other areas of significant patient complaint. It is a misnomer to refer to electrical “entry” and “exit” sites. When the electrical source is an alternating current (e.g., a home 60-Hz electrical socket), any point of physical contact will carry the current in and out of the body at 120 times per second. The location of surface contact points, which usually are full-thickness burns, allows the physician to establish the most likely pathway of the current and the region(s) of potential tissue damage. Obvious cutaneous injury is usually only the tip of a large soft tissue injury (iceberg theory). During resuscitation, electrical trauma victims frequently require large volumes of isotonic intravenous fluids, in excess of calculated needs. These large fluid requirements are due to considerable third-space losses secondary to deep or occult tissue damage. Unlike purely thermal burn injuries, resuscitation formulas such as the Parkland formula are not helpful guides to fluid management. Isotonic fluids should be given liberally, with the initial goal of resuscitation being a urine output of between 0.5 and 1 mL/kg per hour. Any electrolyte abnormalities should be quickly corrected. If hemochromogens (such as myoglobin or free hemoglobin) are found in the urine, the rate of fluid administration is increased to achieve a goal of a urine output of 1.5 to 2.0 mL/kg per hour. Mannitol infusion may aid in maintaining high urine flow. The recommended dosage is 12.5 g administered as an intravenous bolus. If hemochromogens persist in the urine after mannitol bolus therapy, then a mannitol infusion should be started at the rate of 12.5 g/h continuously until the urine clears. Careful observation of electrolytes is required when a patient is treated with continuous mannitol infusion. Other therapies include alkalinization of the urine (to pH >6.5) with bicarbonate to prevent precipitation of urine myoglobin in the renal collecting system. Loop diuretics rarely, if ever, should be used to improve urine output. Reliable large-bore intravenous access is essential, as well as arterial blood pressure monitoring and a urinary catheter. A pulmonary artery catheter is not essential in most patients, but it may be helpful in those with significant left ventricular dysfunction if the volume status cannot be ascertained on clinical grounds.

Victims of electrical trauma should be viewed as potentially having multiple traumatic injuries. A large percentage of high-voltage electrical trauma patients have either fallen from a height or been thrown by the force of the electric current. Cervical spine as well as other orthopedic injuries should be suspected and sought, and therapy should be initiated as appropriate. A falling hematocrit or hemodynamic instability must be investigated thoroughly. Changes found by the mental status examination must be explained. An unstable level of consciousness cannot be attributed to changes secondary to electricity until any systemic hypoperfusion or surgically correctable head trauma has been eliminated. The initial physical examination also should include a careful evaluation and documentation of both the central and peripheral nervous systems. A paralyzed ventilated patient may need electroencephalographic (EEG) monitoring to assess seizure control. The manifestation of neurologic deficits may be delayed, so these evaluations should be repeated daily.

Appropriate tetanus prophylaxis is provided, as delineated by the American College of Surgeons Committee on Trauma guidelines. Antistreptococcal and anticlostridial antibiotics should be administered prophylactically in patients with significant soft tissue injuries. Appropriate evaluation and management of corneal injury and tympanic membrane rupture should be instituted.

Cardiac

Lethal ventricular dysrhythmias are a major cause of immediate death from electrical injury. If an initial dysrhythmia is corrected and the patient is stabilized hemodynamically, recurrence of a potentially fatal dysrhythmia is unusual unless a cardiac pathology exists. As stated earlier, it is important to remember that electrical injury victims who require CPR because of a dysrhythmia should be given prolonged ACLS because reports of complete functional survival after significant periods of CPR do exist.4

Close to 50% of patients exhibit electrocardiographic (ECG) changes or rhythm disturbances after injury. The most common ECG alterations are nonspecific ST-T-wave changes and sinus tachycardia, which usually revert with time. Most dysrhythmias are transient, and therapeutic intervention is rarely needed. The difficulty lies in identifying the existence of new myocardial damage and determining its physiologic significance. Some patients may suffer long-term damage to the conductive system.4a

The usual clinical diagnostic criteria for myocardial infarction include ECG changes and elevation of cardiac isoenzyme levels in a setting compatible with myocardial ischemia. These pieces of evidence are not reliable, however, in the circumstance of electrical injury. ECG abnormalities after electrical trauma are common, temporary, and usually physiologically insignificant. The levels of the CPK MB isoenzymes may be elevated owing to large-scale muscle damage and may give a false impression of myocardial damage.5 Clinical symptomatology of cardiac ischemia, which is subjective at the best of times, usually is not helpful in the face of multisystem electrical trauma. The technetium-99m pyrophosphate scan also has been used to try to identify myocardial damage. However, transmural myocardial damage is rare, and this test does not assess nontransmural injury accurately. Since diagnostic tests are not helpful and significant myocardial injury historically is known to be unlikely, aggressive volume resuscitation and surgical intervention should proceed as required. The exception to this principle is the patient who has been hemodynamically unstable as a result of congestive heart failure, malignant dysrhythmia, or clinically obvious myocardial ischemia.

The evaluation of these patients includes daily ECGs for 3 days following injury, as well as serial cardiac isoenzyme determinations. The results of these tests are interpreted in light of the clinical situation. It has been suggested that not all patients need to have continuous cardiac monitoring after injury unless they have a history of (1) loss of consciousness, (2) recurrent dysrhythmia in the field or emergency room, (3) abnormal ECG on admission, or (4) other injuries that necessitate cardiac monitoring.6

Renal

Renal dysfunction occurs in approximately 10% of patients who suffer high-voltage electrical trauma. The most frequent cause of renal dysfunction, and the most easily treated, is hypovolemia. A common mistake is to grossly underestimate the volume requirements in electrically injured patients. The extent of soft tissue damage and the resulting third-space losses are not always immediately apparent, so fluid resuscitation may be inadequate. Intravascular volume depletion can lead to a decrease in the renal blood flow, which leads to decreasing glomerular filtration rate, renal cortical ischemia, and acute tubular necrosis. Aggressive volume replacement is therapeutic by restoring the circulating plasma volume. The goal for urinary output is 0.5 to 1 mL/kg per hour.

The precipitation of intravascular hemochromogens in the renal tubules is another cause of renal dysfunction. Hemochromogens can be visualized in the urine in approximately 25% of patients with electrical injuries. The responsible pigments are myoglobin, secondary to rhabdomyolysis, and free hemoglobin, from lysed red blood cells. The detrimental effect of pigments deposited in the tubules is thought to increase with hypovolemia, which further underscores the need for adequate fluid resuscitation.

The best prophylactic and therapeutic regimen to prevent renal toxicity secondary to hemochromogen deposition is to maintain adequate intravascular volume and high urine output. This is accomplished with lactated Ringer's solution and mannitol infused hourly in 12.5-g increments. The resulting solute diuresis must be monitored carefully to prevent intravascular volume depletion and electrolyte abnormalities. In the presence of urine pigments, the goal is to create a flow of urine of at least 1 to 2 mL/kg per hour.

Myoglobin is much more soluble and less likely to be retained by the kidney when the urine is alkaline. Some contend that the provision of adequate resuscitation and a solute diuresis will automatically create a urine pH that is clinically therapeutic. However, others recommend maintaining a urinary pH of greater than 6.5 by adding sodium bicarbonate to the intravenous fluids. This treatment is continued until urinary myoglobin has cleared, which may take from 48 to 60 hours. There is evidence that bicarbonate also participates in the solute diuresis; hence its value may be twofold.8 If the urine does not clear of hemochromogens within 24 hours and the serum levels of CPK isoenzymes continue to rise, then a source of undetected muscle ischemia or myonecrosis should be sought actively. Careful, repeated physical examination, specifically looking for areas of swelling and tenderness, should be performed. Technetium-99m nuclear scanning may be helpful in localizing areas of ischemic muscle, although its lack of specificity may lead to false-positive results.8a Xenon 131 scanning and arteriography have both been shown to be generally unhelpful in localizing areas of muscle ischemia or myonecrosis. Magnetic resonance imaging (MRI) provides a reliable method of evaluating edematous muscle. When occult muscle ischemia is discovered, surgical decompression or débridement may or may not lead to functional recovery of that muscle group but may alleviate the systemic problems related to toxic effects of injured or dying muscle.

Pulmonary

There are relatively few pulmonary complications that are characteristic of electrical injury. Acute ventilatory failure secondary to electrical injury is usually related to CNS injury or to chest wall impairment. Depressed respiratory drive due to CNS damage may lead to respiratory failure, necessitating mechanical ventilation. The chest wall and the muscles of respiration may be injured directly, compromising neuromuscular efficiency and leading to the need for ventilatory support.

Long-term pulmonary sequelae such as pneumonia or effusion are treated as in any other injury. There are isolated reports of current-induced bronchopleural fistula, but in most cases the need for ventilatory support is not due to current injury to the pulmonary parenchyma.

When the transient path of the current passes through the pharynx, significant upper airway swelling may develop. All patients at risk should undergo serial examinations of the upper airway by fiberoptic endoscopy and should be intubated prophylactically if hypopharyngeal edema is found.

Gastrointestinal

Abdominal complications following electrical trauma are relatively infrequent. Most often gastric atony and adynamic ileus are seen. These complications usually resolve with nasogastric suction, intravenous fluid administration, nutrition, and time. More serious complications, such as gastrointestinal bleeding, acalculous cholecystitis, and rupture of colon, gall bladder, and other organs, have been reported. It is difficult to know whether all these processes are due to electricity or to the stresses of severe shock and systemic illness. If a contact point on the abdomen has caused a full-thickness burn, the wound should be excised surgically. If this wound includes the posterior fascia of the abdominal wall, then formal exploratory celiotomy should follow. Intraabdominal pathology may be present even without abdominal wall injuries, however. Systemic signs of sepsis or changes on serial physical examination of the abdomen should alert the clinician to intraabdominal pathology. White blood cell counts, liver function tests, amylase and lipase determinations, and examination of the abdomen by ultrasound, computed tomography (CT), MRI, and peritoneal lavage may be required in making the correct diagnosis and directing therapy. Virtually any abdominal catastrophe can be caused by electrical current, and thus the physician must be alert and respond appropriately to subtle clinical changes in abdominal signs and symptoms.9 If intraabdominal injury is not suspected, then enteral feedings should be instituted within 6 hours of admission, if possible.

Neurologic

It is possible for any aspect of the human nervous system to be affected by high-voltage trauma. Neurologic deficits may appear in either the central or peripheral nervous system. Evidence of injury may be immediate or delayed. Finally, the duration of neurologic deficit ranges from transient to permanent.9a

Neurologic changes often are poorly described and documented when they do occur, and hence evaluation of retrospective data is difficult. Immediate neurologic deficits occur in more than 40% of patients. The most common symptom is loss of consciousness. This occurs in up to 65% of symptomatic patients and usually resolves without permanent sequelae. However, long-term complaints include headache, dizziness, vertigo, and seizure activity, as well as psychosocial behavioral disorders such as impotence and personality changes.

Spinal cord injuries can have acute or delayed presentations. Acute neurologic deficiencies can demonstrate a frighteningly complete motor and sensory loss. Yet acute deficits have a tendency to resolve over hours or days. Delayed spinal cord symptomatology is much more ominous and less likely to resolve. The pathophysiology of these delayed findings is not well understood.10

Peripheral nerve injuries account for 5% to 23% of all posttraumatic neurologic sequelae. The most common injury is to the median nerve, followed by the ulnar, radial, and peroneal nerves. In the acutely damaged edematous arm and hand, immediate operative decompression of the carpal tunnel, cubital tunnel, and Guyon's canal is urgent if peripheral neuropathy develops. Following appropriate release, signs of acute peripheral nerve compression should dissipate if thermal injury to the nerve has not occurred.

Extremity and Wound

Care of the extremity and the wound caused by electrical trauma will be discussed concurrently. The rationale behind this approach is that the attempted salvage of the extremity, particularly the arm and hand, best demonstrates the principles of maximal tissue preservation with optimal residual function.

After life-threatening emergencies are addressed, attention should be turned to assessing the soft tissue injury. The injury always should be suspected of being more extensive than it initially appears because visible cutaneous injury is only a portion of the total tissue destruction. Compartment syndromes are a common manifestation of the electrically traumatized extremity. Within minutes after injury, tissue edema begins to increase owing to increased vascular permeability and release of intracellular contents into the extracellular space. Pain with passive movement is an early finding. Tense compartments may be recognized by palpation, but compartment pressure should be documented.

Compartment fluid pressures in excess of 30 mm Hg are abnormal and indicate the need for decompressive fasciotomy. Measurement of pressure in smaller compartments such as that of the intrinsic muscles of the hand is notoriously unreliable. Exploration of the fascial compartments of the acutely swollen hand should be performed empirically whenever high-voltage trauma involves the hand and there is a high index of suspicion of compartment syndrome. Fasciotomy of any fascially bound muscle group may salvage an otherwise moribund muscle. Complete release may be facilitated by incising the epimysium of each muscle. All nonviable skin is débrided. Deciding which tissue is irretrievably injured and requires débridement is often a difficult problem. We define healthy muscle as that which is of normal color and contracts with electrocautery stimulation. All noncharred nerves and tendons are preserved, as is marginal muscle when intermixed with healthy muscle.

It is at this point in management that controversy exists. The most widely practiced surgical approach is to reinspect the wound and débride obviously necrotic tissue every 48 hours.11 Between débridements, one must be careful to avoid tissue drying or desiccation. Typically, allograft is applied to decompressed exposed, viable muscle, and a topical antimicrobial is applied to marginal tissue. Closure is usually delayed until the wound is in bacteriologic balance and is free of all dead or marginal tissue. Whether a finding of additional nonviable tissue at each of the serial débridements represents progressive necrosis or progressive recognition of fatally damaged tissue remains an unresolved question.

Based on the hypothesis that marginally viable tissue is potentially salvageable if covered acutely with well-vascularized tissue, another more aggressive therapeutic regimen exists for selected patients. After decompression of tense compartments, obviously nonviable muscle and skin is débrided. Exposed, devascularized tendons and nerves, as well as marginal muscle, are covered acutely with well-vascularized tissue. Consideration is given to replacement of injured major arteries and veins with healthy vein grafts before they rupture or thrombose. Owing to the limited availability of suitable local tissue, distant flaps or microvascular free tissue transfers are generally used for coverage.12

The decision to salvage an injured extremity must involve careful weighing of the potential morbidity and mortality. A cold, insensate, stiff extremity will be less useful to the patient than a functional prosthesis. This decision of whether to attempt salvage or to amputate should be made as soon as possible, thereby minimizing the risks as well as the physical and psychological efforts invested in salvaging an extremity that eventually will be amputated.

Injuries due to lightning are often fatal, and the pathophysiology is relatively complex.12a Lightning injury is a powerful manifestation of arc-mediated electrical contact. Arcing occurs when the voltage gradient in air exceeds 2 million V/m. The arc consists of a hot ionized gas of subatomic particles that is highly conductive. Peak lightning currents reach into the range of 30,000 to 50,000 A for a duration of 5 to 10 microseconds. Lightning arc temperatures reach up to 30,000 K, which generates thermoacoustic blast waves commonly called thunder. Peak blast pressures reach 4 or 5 atm in the immediate vicinity of a lightning strike and up to 1 or 2 atm 1 m away. Clearly, substantial barotrauma can result. Lightning produces a high transient electrical field and resulting magnetic field. Because of its high-frequency characteristics, the electrical field only penetrates the outer surface of the body, but the huge magnetic field can penetrate throughout. Victims of direct lightning strikes experience a multimodal injury. Superficial burns on the skin represent the current path along the skin surface. The intense brief shock pulse seems to arrest all electrophysiologic processes. The victim appears lifeless. Prolonged CPR may be necessary. Muscle and nerve necrosis is rare in survivors. Deeper injury results when the victim is in contact with a large conducting object such as a truck or fence that has been struck by lightning, which then will discharge over several milliseconds through the victim.

Hundreds of fatalities occur in the United States alone each year as a result of lightning injury.13 Delay in resuscitation is the most common cause of death. Bystanders usually are afraid to touch the victim while precious minutes pass. However, unless the victim is on an insulating platform, there is no residual electric charge on the body after several milliseconds. When needed, CPR should be given without hesitation. Victims should be cared for in an ICU until life-threatening CNS and cardiac injuries are ruled out. Late neurologic and ophthalmologic sequelae often develop. Treatment of lightning injury should follow the guidelines given for major electrical trauma. In addition to the electrical effects, one may expect tissue injury from the electrothermal-acoustic shock waves that also occur.

Survivors of lightning injury are not likely to be the victims of a direct hit. Rather, they are likely to have been in the vicinity of the hit and to have experienced surface burns and arc effects.

The late sequelae of electrical injury generally result from the acute loss or damage of tissue. The extent of tissue damage may not be recognized acutely. Neuromuscular problems usually are due to muscle fibrosis and peripheral neuropathies coupled with loss of tissue from débridements and joint stiffness. Sensorimotor neuropathies, paresthesias, dysesthesias, and reflex sympathetic dystrophy may manifest long after the wounds have healed. Severely injured victims may require functional muscle and nerve reconstruction, as well as correction of scar contractures. Cold intolerance may persist for up to 2 to 3 years, and growth disturbances producing skeletal deformities in children are frequent long-term sequelae.

There are also late sequelae of electrical trauma in which the etiology is unknown. Cataracts occur in 1% to 2% of victims even though the current path did not necessarily involve the head and neck. A full spectrum of central neurologic disorders has been described as late sequelae of electric shock. Persistent peripheral neurologic, psychological, and neurocognitive problems often require detailed evaluation and therapeutic intervention. Although unusual, paraplegia and quadriplegia may manifest up to 5 years after the injury.

Rehabilitation into society and gainful employment are the ultimate objectives of the care of these patients. Subtle mental status and personality changes may have a severe effect on the patient's motivation and participation in the rehabilitation program that is crucial to optimal function.14 Workforce reentry should be guided by consultation with the employer, the patient, coworkers, and an experienced occupation medicine and rehabilitation team.14a