The Critical Care of Patients with Electrical Injuries: A Comprehensive Review

Dr Neeraj Manikath , claude.ai

Abstract

Electrical injuries represent a unique challenge in critical care, combining thermal injury with the complex systemic effects of current passage through biological tissues. Unlike simple thermal burns, electrical injuries produce both immediate and delayed complications affecting multiple organ systems. This review examines the pathophysiology, clinical manifestations, and evidence-based management strategies essential for optimizing outcomes in this challenging patient population. Understanding the mechanisms of injury and maintaining a high index of suspicion for occult complications are fundamental to preventing morbidity and mortality.

Beyond the Burn: The Pathophysiology of Current Passage through the Body

Electrical Current Dynamics

The severity of electrical injury depends on voltage (high >1000V versus low voltage), current type (alternating versus direct current), resistance of tissues, current pathway, and duration of contact. Contrary to popular belief, the visible cutaneous injury often represents merely "the tip of the iceberg," with extensive internal damage disproportionate to external burns.¹

Pearl: Ohm's law (V=IR) governs tissue injury. Current density, not voltage alone, determines tissue damage. The current follows the path of least resistance—preferentially through nerves, blood vessels, and muscles rather than bone or fat.²

Alternating current (AC) is generally more dangerous than direct current (DC) at similar voltages. AC at 50-60 Hz causes tetanic muscle contractions, preventing victim release from the source and prolonging exposure. The "let-go current" (the maximum current allowing voluntary muscle release) is approximately 10-16 mA for AC and considerably higher for DC.³ AC also has a three-fold higher likelihood of causing ventricular fibrillation compared to DC.

Tissue-Specific Injury Patterns

Current passage generates heat according to Joule's law (H=I²Rt), where heat production is proportional to current squared, resistance, and time. This creates a spectrum of injury:

Direct cellular injury from electroporation—formation of nanopores in cell membranes causing ionic imbalance and cell death
Thermal injury from resistive heating, particularly at contact points and in high-resistance tissues
Mechanical trauma from tetanic muscle contractions or falls secondary to electrocution
Vascular injury with thrombosis, leading to progressive tissue ischemia⁴

Oyster: The "iceberg effect" means that for every visible square centimeter of surface burn, there may be 100 cm³ of damaged muscle beneath. Traditional burn resuscitation formulas (Parkland) significantly underestimate fluid requirements in electrical injuries.⁵

The Progressive Nature of Injury

Unlike thermal burns with immediate tissue demarcation, electrical injury continues evolving for 48-72 hours post-exposure. Microvascular thrombosis, edema, and inflammatory mediator release cause progressive tissue necrosis. This necessitates serial clinical assessment and explains why early debridement is often incomplete.⁶

Cardiac Complications: Myocardial Necrosis, Arrhythmias, and the Need for Prolonged Monitoring

Immediate Cardiac Effects

Cardiac complications represent the leading cause of immediate death in electrical injuries. Current traversing the chest (hand-to-hand or vertical pathways) poses the highest risk. The heart is particularly vulnerable during the vulnerable period of the cardiac cycle (analogous to "R-on-T" phenomenon).⁷

Immediate arrhythmias include:

Ventricular fibrillation (most common in AC exposure)
Asystole (more common with DC or lightning strikes)
Atrial fibrillation
Various conduction blocks

Hack: Any patient with transthoracic current passage, loss of consciousness, abnormal ECG, or cardiac symptoms requires minimum 24-hour telemetry monitoring. Those with documented arrhythmias, abnormal troponin, or hemodynamic instability require ICU admission with continuous monitoring for 48-72 hours.⁸

Myocardial Injury

Direct myocardial necrosis can occur without coronary artery involvement, resulting from current passage through myocardium. Cardiac biomarkers (troponin, CK-MB) may be elevated, but interpretation is complicated by concurrent skeletal muscle injury.⁹

Studies demonstrate that troponin I has superior specificity for myocardial injury compared to troponin T or CK-MB in electrical burn patients.¹⁰ Electrocardiographic changes include ST-segment abnormalities, T-wave inversions, QT prolongation, and bundle branch blocks. These may appear immediately or develop within the first 24 hours.

Pearl: Echocardiography is essential in patients with elevated troponin or ECG changes to assess for:

Regional wall motion abnormalities
Reduced ejection fraction
Valvular dysfunction
Pericardial effusion

Delayed Cardiac Complications

Late arrhythmias (occurring after initial 24-48 hours) are rare in patients without initial ECG abnormalities.¹¹ However, case reports document catecholamine-induced cardiomyopathy (Takotsubo) and late conduction abnormalities. Long-term follow-up studies suggest possible acceleration of atherosclerotic disease in electrical injury survivors, though causality remains uncertain.¹²

Clinical Guideline: Patients with normal initial ECG, no loss of consciousness, and low-voltage exposure (<1000V) without transthoracic current passage may be safely discharged after 6-8 hour observation with normal serial ECGs.¹³

Rhabdomyolysis and Compartment Syndromes: Aggressive Management and Early Fasciotomy

Pathophysiology of Muscle Injury

Massive rhabdomyolysis is pathognomonic of significant electrical injury. Muscle damage occurs through multiple mechanisms: direct cellular injury from current passage, thermal injury from resistive heating, prolonged ischemia from vascular thrombosis, and compression from edema within fascial compartments.¹⁴

Myoglobin released from necrotic muscle precipitates in renal tubules, particularly in acidic urine, causing acute tubular necrosis. The threshold for renal injury occurs when myoglobin exceeds 0.5 mg/dL, manifesting clinically as dark "tea-colored" urine.¹⁵

Aggressive Fluid Resuscitation

Hack: Target urine output of 75-100 mL/hour (not the traditional 0.5 mL/kg/hr) until myoglobinuria clears. This requires significantly more fluid than predicted by surface burn area.¹⁶

Crystalloid remains first-line therapy. The role of sodium bicarbonate for urine alkalinization (target pH >6.5) remains controversial, with recent guidelines suggesting benefit primarily when urine pH is <6.0.¹⁷ Mannitol (0.25 g/kg) provides osmotic diuresis and free radical scavenging but should be used judiciously to avoid acute kidney injury from hyperosmolar states.

Pearl: Serial CK measurements guide resuscitation. CK >5,000 U/L indicates significant rhabdomyolysis; values >15,000 U/L predict high risk of acute kidney injury. Persistently rising CK despite adequate resuscitation suggests ongoing muscle necrosis requiring surgical intervention.¹⁸

Compartment Syndrome Recognition and Management

Compartment syndrome develops in 10-30% of high-voltage electrical injuries affecting extremities.¹⁹ The edema occurs within and beneath the deep fascia, distinguishing it from superficial burn edema.

Classic signs (the "5 P's") are unreliable in electrical injury:

Pain out of proportion (often obscured by analgesics or altered mental status)
Paresthesias (may be confused with direct nerve injury)
Pallor (may reflect vascular thrombosis rather than compartment syndrome)
Pulselessness (late finding, tissue damage already extensive)
Paralysis (late finding)

Oyster: Palpable peripheral pulses do NOT exclude compartment syndrome. Pulses are transmitted through major arteries that traverse compartments; capillary perfusion may be critically compromised despite palpable pulses.²⁰

Direct compartment pressure measurement is diagnostic. Absolute pressures >30 mmHg or delta pressure (diastolic BP minus compartment pressure) <30 mmHg indicate need for fasciotomy.²¹ However, in electrical injury, many surgeons advocate a lower threshold given the progressive nature of injury.

Surgical Decompression

Hack: Early fasciotomy (within 6-8 hours of injury) is preferable to "watchful waiting" in high-voltage injuries with transfascial current pathway. The stakes are high: delayed fasciotomy after 12 hours increases amputation risk threefold.²²

Fasciotomy technique requires release of all compartments at risk. In the forearm, both volar and dorsal compartments must be decompressed. In the leg, all four compartments (anterior, lateral, superficial posterior, and deep posterior) require separate incisions. Carpal tunnel and Guyon's canal release should be strongly considered concurrently.²³

Serial debridement at 48-72 hour intervals is standard, as the full extent of necrosis takes days to demarcate. Second-look surgery allows removal of additional non-viable tissue and reassessment of compartments.²⁴

Neurological Injury: Spinal Cord Damage and Peripheral Neuropathies

Central Nervous System Complications

Neurological injury occurs in 20-50% of electrical injury patients and includes immediate and delayed manifestations.²⁵ Loss of consciousness at the scene is common, typically from either direct brain injury, cardiac arrest with hypoxia, or secondary head trauma from falls.

Spinal cord injury presents in two patterns:

Immediate: Direct current injury causing cord edema, hemorrhage, or necrosis (more common with vertical current pathways)
Delayed: Progressive myelopathy developing days to months post-injury, possibly from vascular insufficiency or demyelination²⁶

Pearl: Any patient with electric shock and neurological symptoms requires urgent MRI of the brain and/or spinal cord. Cervical spine should be imaged in all unconscious patients or those with vertical current passage, as the mechanism may include both electrical and traumatic injury.²⁷

Delayed neurological syndromes include cognitive impairment, personality changes, and movement disorders. The amyotrophic lateral sclerosis (ALS)-like syndrome, though rare, is devastating and may not manifest for months to years.²⁸

Peripheral Nerve Injury

Peripheral neuropathies are the most common delayed neurological complication, occurring in up to 30% of significant electrical injuries.²⁹ Nerves are particularly vulnerable due to their low resistance and high current density.

Clinical patterns include:

Immediate neuropathy: Direct thermal or electrical injury to nerve tissue
Delayed neuropathy: Progressive injury from vascular insufficiency, scar compression, or compartment syndrome
Entrapment neuropathies: Particularly median (carpal tunnel), ulnar (cubital tunnel), and peroneal nerves

Hack: Baseline nerve conduction studies (NCS) and electromyography (EMG) within 3-4 weeks of injury establish a neurological baseline, crucial for disability determination and surgical planning. Immediate NCS/EMG is generally not helpful as denervation changes require 2-3 weeks to manifest.³⁰

Treatment is initially conservative (splinting, physical therapy), as many peripheral neuropathies improve spontaneously over 6-18 months. Persistent deficits may require nerve decompression, grafting, or tendon transfers.³¹

Autonomic Dysfunction

Autonomic nervous system injury manifests as temperature regulation abnormalities, hyperhidrosis, vasomotor instability, and complex regional pain syndrome (CRPS). These complications significantly impact long-term quality of life and often require multidisciplinary pain management.³²

Occult Injuries: The High Index of Suspicion for Hollow Viscus Perforation

Intra-abdominal Complications

Occult visceral injuries are uncommon but potentially lethal if unrecognized. Current traversing the trunk may cause direct thermal injury to hollow viscera, solid organs, or vasculature. Delayed perforation may occur 48-72 hours post-injury as full-thickness intestinal wall necrosis evolves.³³

Oyster: Abdominal wall burns should trigger comprehensive abdominal evaluation regardless of initial symptoms. The abdominal wall may shield underlying visceral injury from immediate detection.

High-risk scenarios include:

Entry/exit wounds on trunk
Abdominal wall burns
Unexplained abdominal pain or distension
Occult gastrointestinal bleeding
Peritoneal signs developing during observation period³⁴

Diagnostic Approach

Physical examination is unreliable initially—signs of peritonitis may be masked by concomitant injuries, sedation, or the patient's clinical condition. Serial abdominal examinations every 4-6 hours for 48-72 hours are essential.

Hack: Low threshold for CT abdomen/pelvis with IV and oral contrast in any patient with trunk involvement. CT findings include:

Free air (perforation)
Pneumatosis intestinalis (intestinal ischemia)
Bowel wall thickening or enhancement abnormalities
Free fluid without solid organ injury (concerning for hollow viscus injury)
Solid organ lacerations or hematomas³⁵

Diagnostic peritoneal lavage (DPL) has largely been replaced by CT but may be considered in hemodynamically unstable patients unsuitable for imaging. Laboratory markers (lactate, white blood cell count) are nonspecific but trending values may indicate evolving pathology.³⁶

Thoracic Complications

Thoracic injuries include pulmonary contusion, pneumothorax, hemothorax, and rarely, esophageal perforation. Respiratory failure may result from:

Direct pulmonary injury
Chest wall burns restricting ventilation (requiring escharotomy)
Aspiration during loss of consciousness
ARDS from systemic inflammation³⁷

Pearl: Chest radiography should be obtained in all significant electrical injuries. Consider CT chest for patients with respiratory symptoms, transthoracic current path, or concerning CXR findings.

Vascular Injuries

Large vessel thrombosis or rupture is rare but catastrophic. The popliteal artery is particularly vulnerable due to its posterior location and fixed anatomic position. Delayed rupture of major vessels has been reported up to 2 weeks post-injury.³⁸

Clinical approach:

Baseline examination documenting all pulses
Ankle-brachial index (ABI) for extremity injuries
Low threshold for CT angiography if diminished pulses or ischemic symptoms
Serial vascular checks for 48-72 hours
Vascular surgery consultation for any concerning findings³⁹

Conclusion and Key Clinical Pearls

Electrical injury management requires a paradigm shift from traditional burn care principles. The critical care physician must maintain vigilant surveillance for delayed complications across multiple organ systems. Key principles include:

Aggressive fluid resuscitation targeting urine output of 75-100 mL/hour in rhabdomyolysis
Cardiac monitoring for minimum 24 hours in transthoracic injuries
Low threshold for fasciotomy in high-voltage extremity injuries
Serial neurological examinations and early imaging for suspected CNS injury
High index of suspicion for hollow viscus injury in truncal burns with serial abdominal assessment

The multidisciplinary approach involving critical care, burn surgery, orthopedics, neurology, and rehabilitation medicine optimizes outcomes in this challenging population. Long-term sequelae are common, emphasizing the need for comprehensive follow-up and patient education regarding potential delayed complications.

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Care of Patients with Electrical Injuries