Electrocution: A comprehensive review

Mubeena Anjum

Consultant ER, Kauvery Hospital, Salem

Epidemiology

Although not widely discussed, electrocution deaths have been one of the major causes of accidental deaths in India, ranking just behind traffic accidents, drowning, poisoning, and falls.

Physics

Electricity is defined as the flow of electrons across a potential gradient from high to low concentration.

In AC, the direction of electron flow changes rapidly in a cyclic fashion.

  • Eg, standard household current of 110 V flows at 60 c/s

DC – flows constantly in 1 direction across the potential.

  • Eg, batteries, automobile electrical systems, high-tension power lines, lightning.

Which is more dangerous, AC or DC?

Exposure to DC causes a single muscle contraction that throws the victim away from the electrical source, but AC causes tetany that prolongs contact with the source, making it potentially more dangerous.

Hand is the M/C site of contact with a current source and the flexors of the upper extremity are much stronger than the extensors, when the let-go current is exceeded, the arm flexes and pulls the body closer to the source.

Safe range of current

  • Damage caused – the amount of current flowing through the body.
  • Factors that determine damage -voltage, resistance, type of current, current pathway, and duration of contact with an electrical source
  • Tissues that have a higher resistance to electricity like skin, bone, and fat transform electrical energy into heat -> coagulate.
  • Nerves, muscles and blood vessels have low resistance to electricity- conduct electricity readily.
  • Dry skin – intermediate resistance, have extensive superficial tissue damage but lesser deeper structures. Moist skin receives less superficial thermal injury but allows more current to pass to deeper structures, resulting in more extensive injury to internal organs.
  • Because the body’s resistance to EC changes as the tissues break down, the only sure measure of a patient’s electrical exposure is the voltage.

Voltage

>1000 V are classified as high voltage.

low-voltage electrical shocks are < 1000 V

Typical household electricity has 110 to 230 V,

High-tension power lines have voltages of more than 100 000 V.

Lightning strikes are can produce 10 million V or more.

The effects of Electric shock

There are 4 causes of electrocution;

  • Direct effect of current on body tissues, leading to asystole, ventricular fibrillation, or apnea.
  • Blunt mechanical injury from lightning strikes, resulting in muscle contraction or falling.
  • Conversion of electrical energy to thermal energy, resulting in burns; and
  • Electroporation, defined as the creation of pores in cell membranes by means of electrical current.

Unlike thermal burns, which cause tissue damage by protein denaturation and coagulation, electroporation disrupts cell membranes and leads to cell death without clinically significant heating.

1. Cutaneous

Burn injuries ~>4 groups: electrothermal burns, arc burns, flame burns, and lightning injuries.

Electrothermal burns are the classic injury pattern and create a skin entrance and exit wound.

Regardless of the mechanism involved, wounds due to exposure to electricity can be classified as partial thickness, full-thickness, or skin burns involving deeper subcutaneous tissue.

HV injuries commonly produce greater damage to deeper tissues, largely sparing the skin surface. Thus, using estimation of surface burns to guide therapy may lead to critical errors because minor superficial injury may be associated with massive coagulation necrosis of deeper tissue that appearance cannot be used to predict the severity of injury.

The “kissing burn” is sometimes associated with electrical injury.

This burn occurs at flexor creases such as the antecubital fossa when a current arcs across both flexor surfaces.

It is important to recognize this type of injury because it is often associated with extensive underlying tissue damage.

2. Respiratory System

Respiratory arrest immediately following electrical shock may result from inhibition of the central nervous system respiratory drive, prolonged paralysis of respiratory muscles, tetanic contraction of respiratory muscles, or a combined cardiorespiratory arrest 2’ to VF or asystole.

Respiratory arrest may persist after ROSC, presumably because of the inherent automaticity of cardiomyocytes, which cause quicker recovery of cardiac function.

If respiratory arrest is not corrected promptly by ventilation, secondary hypoxic VF may occur. Parenchymal lung damage is rare

3. Cardiovascular System

Arrhythmias, conduction abnormalities, and myocardial damage

Sudden cardiac death due to ventricular fibrillation is M/C in LV AC. Asystole in DC or HV AC.

Potentially fatal arrhythmias M/C in horizontal current flow (hand to hand)

Current passing in a vertical fashion (from head to foot) M/C causes myocardial tissue damage

Arrythmia-sinus tachycardia PVC VT AF

Patients without ECG changes on presentation are unlikely to experience life-threatening arrhythmias

Rationale- patchy areas of myocardial necrosis that serve as arrhythmogenic foci, increased cardiac sodium-potassium pump activity.

The repetitive frequency of AC also increases the likelihood of current flow through the heart during the relative refractory period (the “vulnerable period”) of the cardiac cycle.

This exposure can precipitate ventricular fibrillation (VF), which is analogous to the R-on-T phenomenon.

Conduction Abnormalities: Sinus Brady and high degree blocks

Rationale- SA and AV nodes ion channels are the easiest to disrupt and that ischemia and infarction in the right coronary artery distribution (running closest to the chest surface and supplying both nodes)

Myocardial Injury: Directly by electrothermal conversion and electroporation or 2’ by contusion or coronary spasm leading to ischemia and arrhythmias

 4. ANS

Autonomic dysfunction following electrical injuries can cause serious cardiovascular complications related to the release of catecholamines.

This may lead to cardiac arrest, transient hypertension, tachycardia, vasovagal syncope, thermodysregulation, and vasoconstriction.

Patients with a history of vasovagal reactions may be at increased risk of sudden death from cardiac arrhythmia after an electrical injury.

Autonomic dysfunction has been implicated in keraunoparalysis, a phenomenon seen with lightning injury in which the extremities are temporarily paralyzed.

5. Vascular

Electrical injuries cause the greatest damage to the media layer of blood vessels and can lead to delayed aneurysm formation or rupture.

Damage to the intima may result in thrombosis and occlusion immediately or over several days.

Most severe in the small muscle branches where the blood flow is slower; this can create tissue necrosis.

Any vascular injury can also lead to edema and compartment syndrome.

6. CNS

HV & LV EI- affect both the CNS and PNS. CNS lesions are more common with lightning injury, while PNS lesions are seen more often with electrical injuries.

A retrospective review of 90 patients that focused on the neurologic consequences of electrical burns found that 50% of patients with LVI and 67% of patients with HVI had immediate neurologic symptoms.

The M/C CNS symptom was LOC.

Other neurologic symptoms were acute peripheral neuropathy and transient paralysis or paresthesia. However,

Spinal cord damage is the M/C delayed consequence of electrical injury may resemble LMN disease, ALS, or transverse myelitis.

The incidence of spinal cord injury following HV electrical trauma ranges from 2% to 27%.

This type of injury may occur when an electric current travels from arm to arm or from arm to leg, with the site of onset associated with current entry or exit.

Partial or even complete recovery may occur, but delayed neurologic symptoms have an overall poor prognosis.

7. Musculoskeletal

Direct electrothermal energy leading to coagulation necrosis is the main cause of muscle injury and usually occurs only after HVEI.

The damaged muscle may become edematous and necrotic, resulting in rhabdomyolysis or compartment syndrome.

As bone has the highest degree of resistance, severe electrothermal bone damage such as periosteal burns and osteonecrosis is seen.

Falls secondary to electrical injury and forceful tetanic muscle contractions create fractures and joint dislocations. The full range of motion of all joints should be tested to assess for fractures and dislocations.

8. Renal

The kidneys are susceptible to ischemia after severe electrical injury. Muscle injury resulting in myoglobin release may also cause renal tubular damage and subsequent renal failure.

Pre-hospital Management

Modifications to Basic Life Support

  • Turn power off
  • ACLS protocol
  • Trauma protocol
  • Burn protocol

The rescuer must first be certain that rescue efforts will not put him or her in danger of electric shock.

When the scene is safe (the danger of shock has been removed), determine the victim’s cardiorespiratory status. Vigorous resuscitative measures are indicated even for those who appear dead on initial evaluation. Because many victims are young, without preexisting cardiopulmonary disease, they have a good chance for survival if immediate support of cardiopulmonary function is provided.

Maintain spinal stabilization during extrication and treatment if there is a likelihood of head or neck trauma.13, 14 Both lightning and electrical trauma

Remove smoldering clothing, shoes, and belts to prevent further thermal damage

Patients who are unresponsive after an electrical injury may be in either respiratory or cardiac arrest. Thus, airway control, prompt CPR, and attempts at defibrillation (if indicated) are critically important. Early intubation should be performed for patients with evidence of extensive burns even if the patient has begun to breathe spontaneously

For victims with hypovolemic shock or significant tissue destruction, rapid intravenous fluid administration is indicated to counteract shock and correct ongoing fluid losses due to third spacing. Fluid administration should be adequate to maintain diuresis to facilitate excretion of myoglobin, potassium, and other byproducts of tissue destruction.

As significant as the external injuries may appear after electrothermal shock, the underlying tissue damage is far more extensive.

Early consultation with or transfer to a physician and a facility (eg, burn center) familiar with treatment of these injuries is recommended.

In Hospital Management

Tetanus immunization status should be determined and patients vaccinated as needed. Cutaneous burns -antibiotic dressings, such as mafenide acetate or sulfadiazine silver .

Mafenide acetate is preferred for localized full-thickness burns because it has better penetration, whereas SSD is preferred for extensive burns because it is less likely to cause electrolyte abnormalities.

When electrothermal burns affect an upper extremity, the limb should be splinted with the wrist at 35° to 45° of extension, the MCP joint at 80° to 90° of flexion, and nearly full extension of the PIP and DIP joints (Z position) to minimize the space available for edema formation.

The extremity should be kept elevated above the level of the heart to reduce edema. Frequent neurovascular checks of all extremities are crucial because compartment syndrome may become evident at any time.

Fluid resuscitation should be directed at maintaining a U/O of 1.0 to 1.5 cc/kg/hr until the urine is clear of myoglobin.

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