Residency · Residency · Plastic Surgery

Electrical and Chemical Burns

Introduction

Electrical and chemical burns represent distinct burn injury mechanisms with unique pathophysiology, evaluation, and management. Electrical burns account for approximately 4-5% of burn center admissions but carry disproportionately high morbidity and mortality. Chemical burns account for 3-5% of burn center admissions; severity depends on agent type, concentration, duration of contact, and mechanism of action. Both injury types frequently cause deep tissue destruction that is underestimated by surface examination.

Electrical Burns

Physics and Mechanism of Injury

Tissue injury is determined by Joule's law: heat generated = I^2 x R x t (current squared times resistance times time). Low voltage: <1000 volts (household current, 110-220V); primarily causes local contact burns and cardiac arrhythmias. High voltage: >1000 volts; causes extensive deep tissue destruction along current pathway. Arc burns: electrical arc across a flexion crease (e.g., elbow, wrist); temperatures can reach 3000-4000 degrees Celsius; causes deep thermal injury without current passage through body.

Flash burns: brief exposure to radiant heat from an electrical arc; typically superficial; treated as thermal burns. Lightning: massive direct current (up to 300 million volts) with extremely brief exposure (1-5 milliseconds).

Tissue Resistance Hierarchy

Pathophysiology of Deep Injury

Iceberg phenomenon: surface burns dramatically underestimate the extent of deep tissue injury. Progressive thrombosis of nutrient vessels leads to delayed muscle necrosis over 48-72 hours. Muscle compartments adjacent to long bones are most severely affected (current follows bone → heat radiates outward). Rhabdomyolysis: massive release of myoglobin, creatine kinase, potassium, and phosphate from necrotic muscle. Myoglobinuria can cause acute renal failure through tubular obstruction and direct nephrotoxicity.

<image>Cross-sectional anatomical diagram of an upper extremity illustrating the pathophysiology of high-voltage electrical injury. The diagram shows a transverse section through the mid-forearm with the radius and ulna at center surrounded by muscle compartments. Heat generation is depicted radiating outward from the bone surfaces in concentric zones: the innermost zone shows necrotic muscle (dark brown) immediately adjacent to the periosteum, a middle zone of injured but potentially viable muscle (pink with stippling), and an outer zone of relatively spared muscle and subcutaneous tissue. The skin surface shows only small entry and exit wound burns. Thrombosed nutrient arteries are shown within the necrotic zone. Labels identify the radius, ulna, flexor and extensor compartments, interosseous membrane, and the concentric zones of injury from bone outward.</image>

Initial Assessment and Resuscitation

ABCs with cervical spine precautions: electrical injury commonly causes falls and tetanic muscle contractions. Identify entry and exit wounds: entry wound typically on hand/upper extremity; exit wound on foot/contact point with ground. Continuous cardiac monitoring for minimum 24 hours; high-voltage injuries and any arrhythmia require longer monitoring. Cardiac arrhythmias: ventricular fibrillation (AC current), asystole (DC current/lightning), atrial fibrillation, ST changes. ECG on admission; if normal with low-voltage injury and no loss of consciousness, monitoring can be brief (8-12 hours).

Fluid Resuscitation

Standard Parkland formula underestimates fluid requirements (deep tissue injury not reflected by TBSA). Titrate fluids to urine output: 1-2 mL/kg/hr (higher than standard 0.5-1 mL/kg/hr for thermal burns). If urine is dark (myoglobinuria): increase fluids to achieve urine output of 2 mL/kg/hr. Add sodium bicarbonate (50-100 mEq/L of IV fluid) to alkalinize urine (pH >6.5) and prevent myoglobin precipitation. Mannitol (12.5-25g IV bolus) may be used as osmotic diuretic if myoglobinuria persists despite adequate volume.

Surgical Management

Fasciotomy: perform early and aggressively for compartment syndrome (common in extremity injuries). Upper extremity: volar forearm, dorsal forearm, carpal tunnel release, hand intrinsic compartments. Lower extremity: four-compartment leg fasciotomy. Escharotomy: may be needed for circumferential contact burns.

Serial debridement: preferred over aggressive early amputation; tissue viability evolves over 48-72 hours. Technetium-99m pyrophosphate scan or MRI can help delineate viable from nonviable muscle. Delayed reconstruction with flaps after wound stabilization; free tissue transfer often required.

Specific Complications

Cataracts: develop in 5-20% of high-voltage injuries; may present months to years later; bilateral. Neurologic injury: peripheral neuropathy (most common long-term neurologic sequela), spinal cord injury (delayed transverse myelitis), cognitive and psychological sequelae. Vascular injury: progressive thrombosis and delayed hemorrhage from vessel wall necrosis; aneurysm formation. Oral commissure burns: common in children biting electrical cords; risk of labial artery hemorrhage when eschar separates (7-14 days); managed with commissure splints and delayed reconstruction.

Chemical Burns

Mechanism of Injury

Chemical agents cause tissue injury through different mechanisms than thermal burns. Acids: cause coagulation necrosis — protein denaturation creates an eschar that limits penetration depth. Alkalis: cause liquefactive necrosis — saponification of fats and solubilization of proteins allows progressive deepening; generally more severe than acid burns. Organic compounds (phenol, petroleum): dissolve cell membranes and cause systemic toxicity. Severity determined by: agent identity, concentration, volume, duration of contact, and mechanism of action.

Initial Management

Immediate copious water irrigation is the single most important intervention (30-60 minutes minimum). Remove all clothing, jewelry, and contaminated materials; protect healthcare workers with PPE. Do NOT attempt neutralization: exothermic neutralization reactions generate heat and worsen injury. Continue irrigation until wound pH normalizes (use pH paper to test wound surface; target pH 7.0-7.5). For powdered chemicals: brush off dry powder before irrigation to prevent activation.

Specific Chemical Agents

Hydrofluoric Acid (HF)

Used in glass etching, semiconductor manufacturing, rust removers. Fluoride ion penetrates deeply and binds calcium and magnesium → profound hypocalcemia, hypomagnesemia. Concentrated HF (>50%): immediate tissue destruction and pain. Dilute HF (<20%): symptoms may be delayed 12-24 hours; deep tissue destruction can occur silently.

Treatment: copious irrigation, then topical calcium gluconate gel (2.5% gel applied liberally and continuously). Severe cases: subcutaneous calcium gluconate injection (5% solution, 0.5 mL/cm^2 of affected area). Digits: intra-arterial calcium gluconate infusion (10 mL of 10% calcium gluconate in 40 mL NS via radial artery over 4 hours) to prevent digital necrosis. Monitor serum calcium, magnesium, and ECG (QT prolongation indicates systemic fluoride absorption). Cardiac arrest from fatal hypocalcemia can occur with >2.5% TBSA exposure to concentrated HF.

Cement (Calcium Hydroxide)

Strong alkite (pH 12-14); prolonged contact under clothing or in boots causes deep alkali burns. Often presents late because initial exposure is painless. Full-thickness burns common despite seemingly minor exposure history. Treatment: prolonged irrigation; early wound assessment.

Phenol (Carbolic Acid)

Causes coagulation necrosis and systemic toxicity (cardiac arrhythmias, CNS depression, hepatotoxicity). Poorly water-soluble; water irrigation alone is insufficient. Treatment: initial dilution with copious water, then swab with polyethylene glycol (PEG 300-400) or glycerol, which dissolves phenol. If PEG unavailable, use isopropyl alcohol. Monitor for systemic absorption (dark urine from phenol metabolites).

White Phosphorus

Military incendiary and fireworks component; ignites spontaneously in air. Burns continue as long as phosphorus remains in contact with air. Treatment: immediate copious water irrigation (keeps phosphorus submerged and prevents reignition); keep wound wet. Debride all phosphorus particles under water; use Wood's lamp (phosphorus fluoresces) to identify retained particles.

Copper sulfate (1%) wash turns phosphorus black for identification; use sparingly (systemic copper toxicity). Cover debrided wounds with saline-soaked dressings to prevent re-exposure to air.

<image>Emergency management algorithm for chemical burn injuries. The flowchart begins with scene safety and provider PPE at the top, then branches to removal of contaminated clothing and jewelry. The next step is immediate copious water irrigation for 30-60 minutes minimum with a decision point checking wound pH with litmus paper. If pH is abnormal, irrigation continues. If pH is normal, the algorithm branches based on chemical agent type: acid burns directed to wound assessment and standard burn care; alkali burns directed to extended irrigation and early surgical assessment (deeper injury expected); hydrofluoric acid directed to calcium gluconate protocol with serum calcium monitoring; phenol directed to PEG wash after water dilution; and white phosphorus directed to continuous water submersion with particle debridement under Wood lamp. All branches converge on a final assessment box for tetanus prophylaxis, systemic toxicity monitoring, and burn center transfer criteria.</image>

Surgical Management of Chemical Burns

Chemical burns often require early excision due to progressive tissue destruction (especially alkali). Tangential excision until viable tissue reached; may need serial debridement. Wound coverage with STSG or FTSG depending on location and depth. Full-thickness hand burns from HF may require flap coverage or amputation. Delayed reconstruction as needed for contractures and functional deficits.

Complications Common to Both

Acute kidney injury: rhabdomyolysis (electrical), systemic toxicity (chemical). Compartment syndrome: requires urgent fasciotomy. Amputation: higher rate than thermal burns; electrical burns have 40-70% amputation rate for high-voltage injuries. Psychological sequelae: PTSD, depression, body image disturbance; higher rates than in thermal burns.

Heterotopic ossification: particularly in electrical burns involving the elbow. Long-term rehabilitation needs are typically greater than for equivalent TBSA thermal burns.

<image>Comparison illustration of acid versus alkali chemical burn mechanisms at the cellular level. The left panel shows acid coagulation necrosis: acid molecules contacting the epidermal surface cause immediate protein denaturation and formation of a firm, leathery coagulum eschar layer at the surface that acts as a barrier to further acid penetration, depicted as a dense dark layer at the surface with intact deeper tissue layers beneath. The right panel shows alkali liquefactive necrosis: alkali molecules penetrate through the epidermis and dermis, dissolving cell membranes through saponification of lipids and denaturing structural proteins, shown as progressive tissue dissolution extending deep into the subcutaneous fat with no protective barrier layer formed and arrows indicating continued progressive penetration. Labels identify the epidermis, dermis, subcutaneous tissue, and the depth of injury in each panel.</image>

Key Clinical Pearls

In electrical burns, surface wounds dramatically underestimate the extent of deep tissue injury (iceberg phenomenon); always assume muscle necrosis along the current pathway and perform fasciotomies liberally. Fluid resuscitation for electrical burns must target urine output of 1-2 mL/kg/hr (double the standard thermal burn target) to prevent myoglobin-induced renal failure; alkalinize the urine with bicarbonate. For chemical burns, immediate copious water irrigation for at least 30 minutes is the most important initial intervention; never attempt neutralization, as the exothermic reaction will worsen the injury. Hydrofluoric acid is uniquely dangerous because the fluoride ion causes fatal systemic hypocalcemia; any HF exposure warrants serum calcium monitoring and immediate calcium gluconate therapy. Children with oral commissure electrical burns from biting cords must be followed for 2-3 weeks for delayed labial artery hemorrhage when eschar separates; parents must be counseled on this risk.

References

• Lee RC, Zhang D, Hannig J. Biophysical injury mechanisms in electrical shock trauma. Annu Rev Biomed Eng. 2000;2:477-509.
• Arnoldo BD, Purdue GF, Kowalske K, et al. Electrical injuries: a 20-year review. J Burn Care Rehabil. 2004;25(6):479-484.
• Palao R, Monge I, Ruiz M, Barret JP. Chemical burns: pathophysiology and treatment. Burns. 2010;36(3):295-304.
• Hatzifotis M, Williams A, Muller M, Pegg S. Hydrofluoric acid burns. Burns. 2004;30(2):156-159.

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