Electrical Burn Injury

Electrical burn injuries are a unique subset of burn trauma characterized by deep tissue destruction disproportionate to visible cutaneous injury, with potential for multisystem involvement including cardiac arrhythmias, rhabdomyolysis, compartment syndrome, and significant long-term neuropsychological sequelae. [1-3] All electrical burns warrant burn center referral per American Burn Association criteria. [4-5]

• Voltage: Low voltage (<1000 V, typically household 120–240 V) vs. high voltage (≥1000 V, industrial/power lines) — this is the single most important historical detail [3][6]
• Type of current: Alternating current (AC) vs. direct current (DC); AC causes tetanic muscle contraction and prolonged contact, DC causes a single forceful throw
• Duration of contact: Longer contact = greater tissue damage
• Pathway of current: Determine entry and exit wounds; vertical pathway (hand-to-foot) carries higher risk of cardiac and abdominal organ injury [7]
• Loss of consciousness or syncope: Present in ~69% of high-voltage injuries; key predictor of cardiac complications [3]
• Tetany: Inability to release the source (AC current)
• Associated trauma: Falls from height, blast injuries, secondary thermal burns
• Wet skin at time of contact: Decreases skin resistance, increases current flow [8]
• Workplace vs. domestic vs. lightning: Occupational injuries predominate in adults [2]

• Cardiac arrest (VF, VT, asystole, PEA) — occurs in ~20% of high-voltage injuries [3]
• Loss of consciousness or syncope [1][9]
• High-voltage exposure (≥1000 V) — strongest predictor of arrhythmia (AUC 0.804) [6]
• Transthoracic current pathway (hand-to-hand or hand-to-foot) [10]
• Dark/cola-colored urine (myoglobinuria indicating rhabdomyolysis) [11]
• Tense, swollen extremity (compartment syndrome) — the 6 Ps: Pain, Pallor, Paresthesia, Paralysis, Pulselessness, Poikilothermia [12]
• Circumferential burns with vascular compromise
• Respiratory distress — associated with severe electrical injury [2]
• Visible deep tissue necrosis disproportionate to skin burns

• Fluid resuscitation: Crystalloid (LR or NS); goal urine output 1 mL/kg/h for high-voltage injuries (higher than standard burn goal of 0.5 mL/kg/h) [11]
• Sodium bicarbonate: Consider for urine alkalinization (target urine pH >6.5) in rhabdomyolysis, though evidence is limited [13]
• Mannitol: May be used as osmotic diuretic for rhabdomyolysis/compartment syndrome; limited evidence; monitor osmolal gap [13]
• Analgesics: Opioids for severe pain; acetaminophen/NSAIDs for mild injuries [14]
• Tetanus prophylaxis: Update as indicated for any open wound
• Antibiotics: Not routinely indicated unless signs of infection; consider antianaerobic coverage for deep necrotic wounds [15]
• Avoid: Succinylcholine in the subacute phase (hyperkalemia risk from rhabdomyolysis)

• Aggressive hydration is the cornerstone — patients may require up to 10 L/day in severe rhabdomyolysis [13]
• High-calorie, high-protein diet for wound healing in admitted patients with significant burns
• Monitor and correct electrolyte abnormalities (hypokalemia in 18%, hypocalcemia in 3.3%) [9]
• Adequate nutritional supply and early treatment of anemia expedite wound healing [15]

• Cardiac: Palpitations, chest pain, syncope, dyspnea
• Neurological: Paresthesias (15%), weakness, confusion, memory problems, headache, seizures [9][16]
• Musculoskeletal: Myalgias, muscle weakness, joint pain (fractures/dislocations from tetanic contraction or falls)
• Renal/GU: Dark urine, decreased urine output
• Psychiatric: Anxiety, insomnia, flashbacks, nightmares — screen early [17-18]
• Ophthalmologic: Visual changes (cataracts can develop weeks to months post-injury)
• ENT: Hearing loss, tinnitus (especially lightning)

• Witnesses: Determine duration of contact, whether patient was thrown or had tetanic grip, any CPR performed
• Occupational details: Type of electrical source, voltage, safety equipment used
• Pre-existing cardiac history: Increases risk and monitoring requirements [19]
• Medication history: Beta-blockers or antiarrhythmics may mask or alter cardiac response
• Social context: Workplace safety compliance, potential for non-accidental injury in children (especially oral burns in toddlers)

• High-voltage exposure (≥1000 V): Strongest predictor of arrhythmia and severe injury [3][6]
• Male sex: ~85–98% of electrical injuries [3][9]
• Occupational exposure: Electricians, linemen, construction workers [20]
• Age: Bimodal — toddlers (oral burns from biting cords) and working-age adults [2]
• Wet skin/water contact: Reduces skin resistance from ~100,000 Ω to ~1,000 Ω
• Vertical current pathway (upper-to-lower body): Predictor of myocardial damage [7]
• Greater TBSA burned: Only positively related factor to cardiac complications in one large series [21]
• Summer months: Peak incidence [2]

• Lightning strike: DC current, unique Lichtenberg figures (ferning pattern), different cardiac effects
• Thermal/flame burn: From arc flash or ignited clothing — may coexist
• Chemical burn: Especially in industrial settings
• Crush injury/rhabdomyolysis from other causes: Trauma, prolonged immobilization, drugs
• Non-accidental injury: Especially in pediatric patients with inconsistent history
• Acute coronary syndrome: If ECG changes or troponin elevation present
• Spinal cord injury: If neurological deficits present — may be from direct electrical injury or fall

• Pre-existing cardiac disease: Arrhythmias, pacemakers/ICDs, coronary artery disease — lowers threshold for monitoring [19]
• Renal disease: Increases risk of AKI from rhabdomyolysis
• Epilepsy: May confound post-injury seizures
• Psychiatric history: Pre-existing conditions excluded from some outcome studies; baseline depression predicts worse long-term adjustment [22]
• Previous electrical injuries: Cumulative neurological effects possible

• Entry and exit wounds: Charred, depressed, centrally necrotic lesions; exit wounds often larger and more destructive
• "Iceberg" phenomenon: Cutaneous burns dramatically underestimate deep tissue injury, especially in high-voltage injuries [23]
• Vital signs: Tachycardia, hypotension (hypovolemia from third-spacing), arrhythmias
• Vascular exam: Distal pulses (Doppler if needed), capillary refill — assess for compartment syndrome [24]
• Compartment assessment: Tense swollen extremities, pain with passive stretch
• Neurological exam: Motor/sensory deficits, cranial nerves, mental status
• Oral exam: In children — commissure burns from biting electrical cords (risk of delayed labial artery hemorrhage at 7–14 days)
• Musculoskeletal: Posterior shoulder dislocations, vertebral compression fractures from tetanic contraction
• Secondary survey: Full trauma assessment — falls, blast injuries

• CK (creatine kinase): Key marker for rhabdomyolysis; CK >850 U/L is an independent risk factor for arrhythmia; serial monitoring recommended [6]
• Troponin: Elevated in ~5.7% of cases; CK >850 and troponin >250 ng/mL predict arrhythmia [6][9]
• BMP/CMP: Potassium (hyperkalemia from rhabdomyolysis), calcium, creatinine, BUN for renal function
• Lactate: >2.1 mmol/L is an independent predictor of arrhythmia [6]
• Urinalysis: Myoglobinuria (dipstick positive for blood without RBCs on microscopy)
• CBC: Baseline
• Coagulation studies: DIC can occur with severe injuries [25]
• ABG/VBG: Assess acid-base status in severe injuries
• CK-MB: Less useful than troponin for cardiac risk stratification [10]

An algorithmic approach to lab testing can reduce unnecessary workup without increasing mortality or readmission rates. [26]

• CT head: If loss of consciousness, altered mental status, or fall from height
• CT C-spine/trauma CT: Per trauma protocol if associated fall or blast
• X-rays: Shoulder (posterior dislocation), spine (compression fractures from tetanic contraction)
• CT angiography: If vascular injury suspected
• Echocardiography: If troponin elevated, wall motion abnormalities suspected, or hemodynamic instability [21]
• MRI: For delayed neurological deficits or spinal cord injury evaluation
• Imaging of the burn wound itself is generally not useful acutely — clinical assessment guides management

• Compartment pressure measurement: When clinical exam is equivocal; >30 mmHg indicates need for fasciotomy [12]
• Doppler ultrasound: Assess distal perfusion in circumferential or extremity burns [24]
• McMahon score: Risk stratification tool for rhabdomyolysis-associated AKI [27]
• Nerve conduction studies/EMG: For delayed peripheral neuropathy evaluation [16]
• Neuropsychological testing: For cognitive complaints in follow-up [17][20]

• Obtain 12-lead ECG on all patients with electrical injury [1][9]
• Common findings: Sinus tachycardia (4.4%), sinus bradycardia (10.4%), ST-T wave changes (3%), conduction abnormalities (8.1%) [9-10]
• Dangerous patterns: VF, VT, PEA — typically occur immediately at time of injury, not delayed [9-10]
• Normal initial ECG: Strong negative predictor of severe electrical injury; a normal ECG within 1 hour post-injury correlates with low risk of severe complications [2]
• Delayed arrhythmias: Malignant delayed arrhythmias were not observed in multiple large series; however, monitoring is still recommended for high-risk patients [9-10]
• Monitoring indications: High voltage, LOC/syncope, abnormal initial ECG, transthoracic pathway, cardiac history — monitor for at least 24 hours [1][19]

Severity stratification

• Low-risk: Low voltage (<1000 V), no LOC, normal ECG, no significant burns, asymptomatic → may be candidates for ED discharge [1][9][28]
• Moderate-risk: Low voltage with LOC, abnormal ECG, or significant burns → cardiac monitoring, lab workup, observation
• High-risk: High voltage (≥1000 V), cardiac arrest, rhabdomyolysis, compartment syndrome, large TBSA → ICU admission, burn center transfer [3][6]

Key clinical pearls

• Surface burns dramatically underestimate the extent of deep tissue injury ("iceberg effect") [23]
• Cardiac arrhythmias develop in ~21% of patients overall; high voltage is the strongest predictor [6]
• Rhabdomyolysis occurs in ~12–20% of cases; compartment syndrome in ~16% of high-voltage injuries [17]
• Amputation rate: ~24% for high-voltage vs. ~6% for low-voltage injuries [3]

Initial stabilization

• ABCs per ATLS; treat as a trauma patient with potential multisystem injury
• Secure airway early if facial/neck burns or inhalation injury [29]
• Aggressive IV crystalloid resuscitation: Standard Parkland formula underestimates needs in electrical injury; target urine output 1 mL/kg/h (vs. 0.5 mL/kg/h for thermal burns) [11][30]
• If myoglobinuria present: increase fluids to achieve UOP 200–300 mL/h; consider sodium bicarbonate for urine alkalinization [13][31]

Surgical management

• Fasciotomy: Emergent for compartment syndrome — more commonly needed than escharotomy in electrical burns. Fasciotomy may also provide long-term protection against chronic peripheral nerve dysfunction. [23-24][32]
• Escharotomy: For circumferential burns with vascular compromise; performed in ~40% of electrical burn patients in one series [33]
• Serial debridement: Delayed 24–48 hours to allow tissue demarcation unless compartment syndrome present [23]
• Amputation: Required in ~13.5–24% of high-voltage injuries [3][33]

The following figure illustrates the role of fasciotomy in protecting against long-term peripheral nerve dysfunction in electrical burn patients:

Cardiac management

• Continuous telemetry for high-risk patients ≥24 hours [1]
• Treat arrhythmias per ACLS protocols [34]

Renal protection

• Aggressive hydration is the cornerstone [13][35]
• CVVH for refractory myoglobin-induced AKI [11][36]

Discharge from ED (low-risk criteria — all must be met): [1][9-10][28]

• Low-voltage injury (<1000 V)
• No loss of consciousness
• Normal 12-lead ECG
• No significant burns or trauma
• Asymptomatic
• Normal labs (if obtained)

Admit for monitoring (≥24 hours)

• High-voltage injury
• Abnormal ECG
• LOC or syncope
• Significant burns
• Elevated CK, troponin, or lactate [6]
• Transthoracic current pathway
• Pre-existing cardiac disease [19]

Burn center transfer (per ABA criteria): [4-5]

• All electrical burns warrant burn center referral
• Especially: high-voltage injuries, significant TBSA, injuries to hands/feet/face/genitalia, compartment syndrome, rhabdomyolysis

ICU admission

• Cardiac arrest survivors
• Active rhabdomyolysis with AKI
• Compartment syndrome requiring fasciotomy
• Hemodynamic instability
• Large TBSA burns requiring aggressive resuscitation

Follow-up timing

• Burn clinic within 24–48 hours of discharge for wound reassessment
• Ophthalmology referral within 1–2 weeks (cataracts can develop weeks to years post-injury)
• Neuropsychological screening at follow-up — neurological symptoms (81.6%) and psychological symptoms (71%) are the most common long-term sequelae [20]

Long-term sequelae to monitor: [16-17][37-38]

• Neurological: Paresthesias, neuropathy, chronic pain, seizures, memory problems — may develop up to 5 years post-injury [16]
• Psychiatric: PTSD (33%), anxiety (62%), depression (25%), insomnia (68%) — occur regardless of voltage; baseline depression predicts worse long-term adjustment [17][22]
• Functional: 19% of work-related injuries unable to return to any employment; 61% return to preinjury work [17]
• Aesthetic sequelae: 43.9% at 2-year follow-up [2]

Return precautions (patient counseling)

• Return immediately for: chest pain, palpitations, syncope, dark urine, increasing limb swelling/pain/numbness, fever, wound changes
• Oral commissure burns in children: risk of delayed labial artery hemorrhage at 7–14 days post-injury — parents must be counseled
• Expected recovery: minor low-voltage injuries typically resolve within days; high-voltage injuries may require months of rehabilitation with potential for permanent disability

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