Electrical injury

Brett D. Arnoldo, John L. Hunt, Gary F. Purdue

UT Southwestern Medical Center, Dallas, TX, USA

Introduction

Pathophysiology

Electricity is a ubiquitous, indispensable, and invisible part of modern civilization. We often take it for granted until a natural disaster renders it and us nearly useless. Another instance when an individual is reminded of its presence unfortunately and all too commonly is the severe electrical burn injury. Electrical burns are the most devastating of all thermal injuries on a size by size basis. They affect primarily young, working males, and often lead to legal entanglements. They are the most frequent cause of amputation on the burn service [1]. Cutaneous manifestations of high voltage electrical injuries have been equated to the tip of the iceberg. Index of suspicion must be high, as deep tissue injury is often hidden yet common. Long term morbidity and disability is often the end result of these injuries and this has led to the recommendation for their evaluation and treatment in qualified burn centers.

Electricity causes more than 400 unintentionalinjury fatalities per year in the United States according to the Centers for Disease Control (CDC) data. It is estimated that 10% of all admissions to burn units worldwide are from burns caused by electrical injuries [61]. In 1999 the impact of electrical injuries was estimated to be in excess of $1 billion annually and is the leading cause of work related injury [10, 32, 39].

Some experts have described electrical trauma as a severe form of thermal injury while others more accurately liken it to a crush injury [3]. Electrical burn injury severity is related to voltage, current (amperage), type of current (alternating or direct), path of current flow, duration of contact, resistance at the point of contact, and “individual susceptibility” for lack of a better term. Electrical burns are most simply classified as either low-voltage ( < 1000 volts) or high-voltage (≥ 1000 volts). Low voltage injuries are generally localized to the area immediately surrounding the injury and subsequently are less destructive and easier to manage. Nearly all injuries occurring indoors with the exception of some industrial settings are low voltage. High-voltage injuries are typically deceptive and hide a significant amount of destruction beneath the cutaneous burn. While voltage is generally known or relatively simple to surmise, the amount of current is unknown. Current flow is related to voltage by Ohm’s Law:

Current (I) = Voltage (E)/Resistance (R) Electrical injury experiments in a canine model have shown a three-phase response of amperage due to tissue resistance [25]. The initial slow rise in amperage represents a progressive decrease in skin resistance. The second phase is characterized by an abrupt rapid increase in amperage which coincides

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with the complete breakdown of skin resistance and unimpeded flow of current. The third phase is characterized by the abrupt fall in amperage, representing tissue dessication and carbonization. The charred skin then acts an insulator and current flow ceases [25]. Tissue temperature, the critical factor in the severity of these injuries increases parallel with amperage. Older articles and discussion of electrical injury often emphasize the different resistances of internal tissue (i. e. R: Bone > Fat > Tendon > Skin > Muscle > Blood > Nerve). For all practical purposes however, once the skin resistance is overcome, the internal milieu of the body acts as volume conductor, resistance being averaged. The severity of injury is then inversely proportional to the cross-sectional area of the tissue able to carry current. Clinically this is evident with the most severe injuries typically at the wrist and ankle. An interesting finding in the experimental model was the lack of tissue injury distal to the contact points. Deep tissue tends to retain heat so that peri-os- seous tissue especially between two bones (tibiafibula; radius-ulna) often sustains worse injury. This accounts for the clinical occurrence of a central “core” of necrotic muscle in association with relative sparing of superficial muscle. There is a slower dissipation of heat in deeper tissue around the bone and often then more severe injury [26]. Tissue temperature is of utmost importance and for all practical purposes tissue obeys Joule’s Law:

Power (J-Joule) = I2 (Current) × R (Resistance) Electrical current can flow in one of two types of circuits: direct current (DC) or alternating current (AC). Current type plays a role in tissue injury with alternating current being more hazardous than direct [59]. More than 90% of all electrical burns in the United States are caused by 60 cycle-per-second (60 Hertz) commercial alternating current, which reverses its polarity 120 times per second. This leads to the terminology of ‘contact points’ as opposed to the inaccuracy of entrance and exit wound verbiage. The cyclic flow of electrons also causes muscle tetany that generally prolongs the victim’s contact with the source. If the source of contact is the hand, the strength of the forearm flexors causes the victim to grasp and the “no-let-go” phenomenon is seen. Direct current is seen in some industrial settings, medical appliances, batteries, and battery powered devices. Most DC cir-

cuits are relatively low voltage. A car battery is approximately 12 volts and is as high a DC voltage as most people will ever use. Direct current is more likely to cause a single convulsive contraction and push the victim away from the current source.

Resistance of the skin is varied. The moist sweaty palm in summer compared to a dry calloused hand in the winter months will exhibit significant differences in resistance. The path of the current relates to injury. Current path is difficult to interpret clinically and predictions of potential injury may be inaccurate. If current passes across the chest for example this may result in cardiac or respiratory arrest. The mere presence of contact points on both upper extremities however is not proof positive of current flow across the chest. Individual susceptibility is another term like “idiopathic”. There are likely other factors that render one patient more susceptible than another, we simply do not understand them as such.

Progressive muscle necrosis is an often described clinical phenomenon in electrical injuries. Arteriographic studies would suggest that this is in fact the natural progression of the injury. Microvascular thrombosis may occur in marginally injured adjacent muscle accounting for a small portion of muscle necrosis. The bulk of involved muscle appears to sustain irreversible damage at the time of injury. Care must be taken that progression does not occur as a result of inadequately released muscle compartments.

Direct and indirect electrical destruction of cells also plays a role in tissue injury. This is particularly important in the nervous system as injury there is not entirely explained by heating alone. Cell membrane disruption is a potential explanation given that membrane integrity is maintained by the so- dium-potassium-ATPase pump operating at -90mil- livolts direct current. Breakdown of cell membranes via the process of electroporation may also explain injury not apparently caused by heat [37, 38].

Initial assessment and acute care

The first priority is protection of the field team and initial responders. Patients should not be handled until electrical power has been disconnected. Initial

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evaluation follows Advanced Trauma Life Support (ATLS) and the American Burn Association Advanced Burn Life Support (ABLS) protocols. Electrical injuries are associated with trauma in approximately 15% of cases, double the rate of other burns. Most commonly this is due to a fall from a height or the victim being thrown. Tetanic muscle contraction may also generate enough force to cause compression fractures [35]. After the initial assessment is completed several complex management decisions need to be addressed. These are the issues that make the electrical injury somewhat unique. They include:

(1) how to proceed with resuscitation given that there is likely a deep unquantifiable component to the injury, (2) when and how to treat pigmented urine, and what is its implication (3) who needs cardiac monitoring and for how long (4) who needs emergent operative intervention. These unique acute care issues often overlap and will be addressed together in the next section.

Resuscitation should be kept simple. The deep tissue injury makes the use of resuscitation formulas based on body surface area burned inaccurate. The goal of resuscitation should be the maintenance of normal vital signs and a urine output of approximately 30–50 mL/h (or 0.5 ml/kg) with Ringer’s lactate. This rate is adjusted on an hourly basis to achieve goal.

This becomes more difficult in complex circumstances such as glucosuria. Urine output becomes less reliable in the face of this finding. Unreliable urine output may necessitate the monitoring of central venous pressure (CVP) from a subclavian or internal jugular central line. In this instance a goal CVP of 8–10 mmHg is reasonable. Some would also consider monitoring central venous saturations (Scv02) with a goal of 60–65%, or even the placement of a pulmonary artery catheter, although this has not generally been required in our experience.

The presence of pigmented (darker than light pink) urine in this patient population indicates significant muscle damage. This should alert the clinician to be aggressive in efforts to clear the urine and thus prevent renal failure, and also vigilant for compartment syndromes. Myoglobin and hemoglobin pigments present significant risk of acute tubular necrosis (ATN). Dark urine must be cleared promptly to minimize precipitation into the renal tubules.

Fig. 1. Pigmented urine

Gross pigmenturia is diagnosed visually (Fig. 1) and confirmed positive on dipstick test for blood and negative on microscopy for red blood cells. Confirmatory urine myoglobin is unnecessary and may lead to over treatment and over resuscitation. The most important component of treatment is adequate fluid resuscitation with Ringer’s in an effort to more or less double the urine output. Typically the urine output goal is approximately 100 mL/hr until the urine visually appears clear. Treating to a negative myoglobin level in the urine can lead to volume overload. Several methods to enhance this process have been recommended, including osmotic diuresis with mannitol and alkalinization of the urine with bicarbonate. These adjuncts while seemingly affective are not supported by level I evidence [23, 52, 62]. The authors however have had success treating grossly pigmented urine with 2 ampules of sodium bicarbonate and 25 grams of mannitol, both given as an IV push, as an adjunct to increased IV fluid infusion. Patients who do not clear their urine are candidates for repeat doses. These patients however require careful evaluation for ongoing ischemia and muscle necrosis. They will very likely need surgical intervention requiring either fasciotomy or amputation. Additional evidence of muscle necrosis is confirmed by checking serial serum creatine kinase isoenzymes. This is generally not required however and are often too sensitive to to be used as a guide for therapy. Diagnosis can most commonly be made by physical exam.

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Both lowand high-voltage electrical can interfere with the conducting system of the heart. Ventricular fibrillation is the most common cause of death at the scene, however any cardiac dysrhythmia may be encountered in the setting of electrical injury. Dysrhythmias are treated as per Advanced Cardiac Life Support (ACLS) algorithms, similar to those of medical etiology. All electrical injured patients require a twelve lead electrocardiogram (ECG). This should occur as soon as is practical in the emergency department. Cardiac monitoring is recommended for: (1) ECG abnormality, (2) cardiac dysrhythmia during transport or in the emergency department, (3) documented cardiac arrest, (4) loss of consciousness, and (5) patients with other standard indications for monitoring. The duration of monitoring is generally between 24 and 48 hours, however this is based on scant data. [2]. Most patients with low voltage injuries and no indications for monitoring can generally be discharged from the emergency department. The authors have applied this same criteria to high-voltage injuries based on their own published data, however this is not universally accepted in all institutions [4, 54]. Direct myocardial injury may also occur. This injury presents more like a myocardial contusion rather than myocardial infarction. Creatine kinase (CK) and MB-cre- atine kinase in these patients are poor indicators of myocardial damage especially in the presence of muscle injury [8, 24, 42]. Utility of troponin levels in these patients has yet to be determined.

Patients with high voltage electrical injuries may harbor deep tissue injury (Fig. 2) and may require immediate operative exploration for compartment syndrome, and/or debridement. Damaged muscle, swelling within the investing fascia of the extremity, may increase pressures to the point where muscle blood flow is impaired. Loss of pulses is one of the last findings of compartment syndrome unlike early loss of pulses occurring in circumferential burns requiring escharotomy. Conventional wisdom states that compartment syndromes may develop over the first 48 hours. While this is true the author’s experience has been that the decision to operate can generally be made with confidence at initial evaluation in the emergency department. These are not subtle injuries. Those patients who were operated on in the subsequent 24–48 hours

Fig. 2. High voltage injury with deep tissue necrosis

after admission generally had findings at admission or else had larger total body surface area (TBSA) burns and required generous resuscitation volumes. A good teaching point here is that these patients either have normal extremities on physical exam or they have significant findings, and if they have significant findings they generally need to be explored. Having said that, ABA guidelines recommend extremity exploration for: (1) progressive neurologic dysfunction, (2) vascular compromise, (3) increased compartment pressure, (4) systemic clinical deterioration from suspected ongoing myonecrosis [2]. If compartment pressures are measured as an adjunct to diagnosis, a pressure greater than 30 mmHg is considered significant. Patients not meeting indications for exploration may be debrided on the third to fifth postinjury day [41]. Elevated CK levels have been correlated to the extent of muscle damage and the requirement for surgical intervention [34]. Four compartment fasciotomies of the lower leg and anterior/posterior fasciotomies of the upper extremity done in the operating room under general anesthesia is standard of care. Upper extremity decompression will generally require carpal tunnel release and may in some cases require release of intrinsic muscles of the hand. The carpal tunnel release which is challenging in elective settings is made simpler by the significant underlying edema. By inserting the open jaw of the straight scissors under the proximal end of the transverse carpal ligament (while remaining ulnar to the Palmaris longus ten-

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