Electrical Injury: Reconstructive Problems

Introduction

Severe cases [of electrical injury] coming for reconstruction present a formidable problem of flexion contracture and loss of many tendons and nerves, new pedicled skin and grafted-in tendons and nerves usually being necessary. One encounters inside the limb the same type of destruction and cicatrix as is found after any severe infection. STERLING BUNNELL, 1948

This chapter will focus on the multitude of surgical and reconstructive problems that result from electrical injury. The injury severity is complex due to various factors determining manifestation and the distribution of the resulting tissue damage. In common with other types of trauma, especially burn injuries, the consequences of electrical injury may affect a wide range of physiological functions. Its distinct features warrant a differentiated approach to this unique kind of trauma. The resulting tissue loss and the damage to essential structures of the involved body areas often require extensive plastic-reconstructive procedures.

Although the incidence of low-voltage burns has declined steadily over recent decades, most probably due to progress made in the field of home and occupational safety education and equipment, electrical injuries still account for 3–5% of all admissions to major burn centers. Electrical fatalities are relatively uncommon, and most of them occur accidentally. Earlier reported limb amputation rates of up to 71% decreased over recent decades with the increasing ability to reconstruct anatomic parts and restore function, but limb salvage remains a surgical challenge.

Physiological Basis of Tissue Destruction

The traditional pathophysiological understanding of electric injury was based on the assumption that the passage of electric current produces heat and triggers tissue damage. Thus tissue-specific susceptibility (and vulnerability) is considered to increase progressively from nerve to blood vessels, muscle, skin, tendon, and fat to bone. As osseous tissue shows the highest electrical resistance, it will generate the most heat. Electric current will preferentially take the path of least resistance through the body so that the current will pass particularly along the neurovascular bundles. This theory further postulated that the lesions produced by the current would result in delayed vascular occlusion and progressive tissue necrosis.

In high-voltage injuries, the internal milieu acts as a single uniform resistance. Instead of conduction through specific preferential tissues, the body conducts the current with a composite resistance of all tissue components. The crucial factor in determining the resistance and hence the magnitude of tissue damage is the cross-sectional diameter of the affected body part. Devastating injuries to the extremities occur with a significantly higher frequency than tissue damage to the thorax and abdomen ( Fig. 57.1 ). Because muscle tissue occupies the largest cross-sectional area in the limb it also carries the predominant electric current. Because joint areas are regions where the cross-sectional tissue composition changes from low-resistance muscle to high-resistance bone, tendon, and skin, a proportionally higher current and heat are produced in these areas according to Ohm's Law.

Arcing describes the energy transmitted by a hot electrically conducting gas. However, this requires a voltage of more than 20,000 V to bridge even a short distance of 1 cm. Effects on tissue vary from minimal skin wounds to charring and tissue vaporization.

The different trauma mechanisms of the burns induced by the arcing phenomenon are often referred to as “flush burns,” heat burns that are induced by the massive heat generation. “Electrothermal burns” are caused by current passage through the body and the concomitant heat production.

Electrical damage to a large artery represents a grave prognostic sign for limb survival. The reported risk of amputation is high, at between 37% and 65%.

Further nonthermal mechanisms of cellular injury have been defined. This includes a voltage-induced loss of cell membrane semipermeability. When the integrity of the cell membrane is lost, the impedance is markedly reduced, leading to a simultaneous increase in the area exposed to current flow. In addition to breakdown in cellular integrity, electrical fields also induce denaturation of membrane proteins by altering their structural conformation and rendering them nonfunctional. Both mechanisms are responsible for rhabdomyolysis and secondary myoglobin release, which depends directly on the imposed electric current and is not a thermal effect.

The human body consists of about 60% water. The intra- and extracellular water content and their highly resistive plasma membrane separate these two compartments from each other. Change in the current transporters from electrons to ions at the skin surface appears as metallic condensations of dark-grayish skin lesions that resemble eschar.

Another central factor of the cellular effect of electrical current is its frequency, which can arbitrarily be divided into low (<10 kHz) and high (>10 kHz, e.g., radio frequency, microwave, and ionizing frequencies).

Diagnosis and Acute Treatment

Diagnosis and acute treatment of electrical injury are described in Chapter 38 .

Assessment of Tissue Damage

Accurate assessment of the extent of tissue damage is difficult. The percentage of burned body surface area grossly underestimates the injury to underlying tissue. Electrical burns may appear as mere pinpoint marks. In contrast, fatal electrocution may even take place without visible skin burns in the case of a large contact area ( Table 57.1 ).

In contrast to thermal burns, deposition of metallic iron and copper is found on the epidermis after electrical injuries as electrolysis occurs in the extracellular fluid of the skin.

Clinical determination of tissue viability is based on inspection and the demonstration of muscle contractility. As yet, there are no other diagnostic tools available to accurately assess the extent of tissue damage in the early phase following electrical injuries. The value of magnetic resonance imaging (MRI) for the detection of nonperfused nonedematous muscle is debated. Angiography, although not providing information on tissue viability, demonstrates the absence of tissue perfusion and may lead to an early indication for limb amputation.

Rhabdomyolysis and Myoglobinuria

Destroyed muscle cells release myoglobin, resulting in myoglobinemia. Hemolysis also often occurs with electrical injury. Serum levels of creatinine and creatinine phosphokinase (CPK) are used as indicators of rhabdomyolysis. After muscle injury CPK levels will peak by 24 h and return to baseline within 48–72 h. This diminishes the diagnostic value of serum and urine chemistry testing.

Renal Failure

Myoglobinuria has traditionally been considered a major risk factor for the development of acute renal failure. Recently patients with electrical injuries have been shown to have a surprisingly low risk for renal failure. In 162 patients, only 14% had myoglobinuria and none developed renal failure. Suggested criteria to evaluate the risk of acute renal failure after electrical injury include prehospital cardiac arrest, full-thickness burns, compartment syndrome, and high-voltage injury. The presence of at least two of these criteria should instigate immediate treatment because the timeframe to prevent progression to acute renal failure is limited to a few hours post injury.