Electrical and lightning injury

Electrical and lightning injury is a trauma-toxicology hybrid: the patient is shocked, thrown, burned and crushed at once, and the surface wound almost always understates the damage beneath. The Fellowship candidate must separate three distinct mechanisms — low voltage (household, under 1000 V), high voltage (over 1000 V) and lightning — because each has a different lethal threat, a different monitoring requirement and a different disposition. Every case is resuscitated as blunt trauma first, then investigated for the hidden deep injury.[1]

Definition and classification

An electrical injury is tissue damage from current passing through the body. Three categories are recognised. Low-voltage injury (under 1000 V, typically the 230 to 240 V domestic supply) causes a local contact burn at the entry point and a risk of arrhythmia, but the current rarely crosses deep tissue. High-voltage injury (over 1000 V — power lines, railway overheads, substation equipment) drives current across the whole body, producing deep muscle and nerve destruction, rhabdomyolysis, compartment syndrome and cardiac arrest. Lightning is a separate entity: a massive, near-instantaneous unidirectional discharge of millions of volts and tens of thousands of amperes that behaves as a single direct-current pulse and produces cardiopulmonary arrest and characteristic neurocutaneous signs.[1][3]

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Epidemiology and risk

Electrical injury is uncommon but preventable, clustering in electrical workers (linesmen, electricians, construction), in children at home (flex chewing, socket probes) and in outdoor recreation for lightning (golf, hiking, fishing, sport). Cardiac arrest from ventricular fibrillation is the leading cause of immediate death in low- and high-voltage exposure; in lightning, simultaneous cardiac and respiratory arrest dominate. The case fatality is highest in high-voltage contact with a hand-to-hand or hand-to-foot pathway, where the current traverses the heart and thorax.[1][6]

Pathophysiology — Joule heating, tetany and the lightning pulse

Tissue damage is governed by Joule's law: heat generated is proportional to current squared times resistance times contact time ($H = I^2Rt$). Current, not voltage, is what destroys tissue, and the organs of lowest resistance (nerve, muscle, blood vessel) conduct best while bone — of highest resistance — heats most and cooks the muscle around it. This is why a high-voltage injury shows a tiny entry wound yet extensive deep necrosis tracking along bone.[5]

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Alternating current at mains frequency is the most dangerous waveform: it induces tetanic flexor spasm at around 10 to 20 mA (trapping the hand on the conductor) and throws the heart into ventricular fibrillation at around 100 mA. Direct current produces a single convulsive throw, hurling the victim and causing secondary blunt trauma. Lightning is a unidirectional mega-amp pulse that simultaneously depolarises the entire myocardium, producing asystole; the intrinsic pacemaker often restarts, but the medullary respiratory centre remains stunned, so the victim develops secondary hypoxic ventricular fibrillation unless ventilated.[3][4]

Current thresholds — what each milliampere does

The clinical effect of current is threshold-dependent, and the Fellowship candidate should know the breakpoints that separate a tingle from cardiac arrest. [1]

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Clinical presentation

The presentation ranges from a fully alert patient with a small contact burn to a patient in cardiac arrest. The entry and exit wounds should be sought and mapped — they are often small, charred, painless punctures at flexural creases, and an arc burn may char the flexor surface of a joint as the current jumps across it. High-voltage victims are frequently thrown or fall, so a full blunt-trauma secondary survey is mandatory: intracranial, cervical-spine, intrathoracic and intra-abdominal injury, plus long-bone and pelvic fractures. [1]

Lightning-specific findings include Lichtenberg figures (a transient, fern-like, non-thermal skin pattern that is the pathognomonic cutaneous signature of lightning and fades within hours), keraunoparalysis (a transient flaccid paralysis and vasoconstriction of the limbs that resolves over hours and must not be mistaken for spinal injury), tympanic membrane rupture (examine every lightning victim's ears), and delayed cataracts.[3]

Differential diagnosis — what else causes this picture

The Fellowship candidate must distinguish the electrical mechanism from its mimics, several of which co-exist after a high-voltage fall or an enclosed-space arc. [1]

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Bedside assessment

Assess every electrical-injury patient through the trauma primary survey (ABCDE) with cervical-spine control until cleared, because the throw and the fall generate blunt injury independently of the shock. Map the entry and exit wounds, perform a focused neurovascular examination of all four limbs (compartment syndrome is time-critical), inspect the tympanic membranes in lightning, and examine the eyes (delayed cataract). Pregnancy status is checked in women — even a minor maternal shock carries a fetal risk. [1]

Investigations

Investigations screen for the three hidden threats: arrhythmia, rhabdomyolysis and occult trauma. A 12-lead ECG and continuous cardiac monitoring are mandatory on every patient; creatine kinase (peak around 24 hours, with rhabdomyolysis defined by a CK above about 1000 U/L), urine myoglobin and urinalysis (a positive blood dipstick with no red cells on microscopy is myoglobinuria), urea and electrolytes, troponin and venous gas (acidosis reflects injury severity) are the core bloods. Add amylase or lipase for pancreatic injury, and cross-section imaging (CT) driven by the trauma survey. Bloods are repeated at intervals because CK and potassium rise as muscle necrosis evolves.[2][5]

Immediate management and resuscitation

Resuscitate as blunt trauma first, then address the electrical-specific threats. The scene must be made safe — never touch a victim still in contact with a live source. [1]

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Treat cardiac arrest in an electrical or lightning victim with the standard ALS algorithm — prolonged and aggressive cardiopulmonary resuscitation is justified, especially in lightning, where young otherwise-fit victims are often fully salvageable once oxygenated.[4]

Definitive management — monitoring, fluids and fasciotomy

Three time-critical interventions follow the initial resuscitation: cardiac monitoring, rhabdomyolysis fluid therapy, and compartment-syndrome surgery. The monitoring duration is set by the voltage and the presentation: an asymptomatic low-voltage exposure with a normal ECG is monitored for 4 to 6 hours and discharged with a safety-net if it remains well; any high-voltage contact, any symptomatic patient, any abnormal ECG or any loss of consciousness is admitted for at least 24 hours of telemetry.[1][2]

Rhabdomyolysis is treated with intravenous isotonic crystalloid titrated to a urine output of 1 to 1.5 mL per kilogram per hour in the adult (2 to 3 mL per kilogram per hour in the severe case), guided by serial CK and electrolytes; alkalinisation of the urine and mannitol are not routine per the Eastern Association for the Surgery of Trauma guideline, and bicarbonate is reserved for severe metabolic acidosis or hyperkalaemia.[5]

Compartment syndrome complicates deep high-voltage necrosis and is a clinical diagnosis — pain on passive stretch out of proportion, a tense woody compartment, and paraesthesia — supported by a compartment pressure within 30 mmHg of the diastolic blood pressure. Early fasciotomy is the definitive treatment and has a narrow golden period; delayed decompression is the leading preventable cause of amputation in high-voltage injury.[6][7]

Deep tissue injury — the path of current

Current does not damage tissue uniformly: it follows the path of least resistance, and that path dictates the injury. Tissue resistance ranks nerve less than blood vessel less than muscle less than skin less than fat less than bone. Current therefore races through nerves, vessels and muscle — damaging them by a combination of Joule heating, electroporation (electric-field disruption of cell membranes) and electroconformational denaturation of proteins — while bone, of highest resistance, absorbs the most heat and cooks the muscle surrounding it. The deep track is invisible from the surface, which is the central reason a high-voltage entry wound looks trivial while the limb beneath is dying. [1]

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Management — a stepwise protocol

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Subtypes and special scenarios

Lightning mass-casualty — reverse triage. In a lightning strike on a group, the normal trauma triage order is inverted: the apparently dead, apnoeic victim is resuscitated first. The lightning pulse arrests the heart in asystole, the intrinsic pacemaker often restarts spontaneously, but the respiratory centre remains paralysed — without ventilation the patient descends into secondary hypoxic ventricular fibrillation and dies. The walking wounded can wait.[3]

Paediatric oral-commissure burn. A child chewing a live flex sustains a deep burn at the angle of the mouth. The injury looks localised but risks delayed labial-artery haemorrhage one to three weeks later as the eschar sloughs. Refer to a specialist unit and explicitly warn the parents about delayed bleeding. [1]

Pregnancy. Even a minor maternal low-voltage shock can cause fetal loss; arrange fetal monitoring and obstetric review for any pregnant patient. [1]

TASER and conducted-energy weapons. Largely benign in the adult; a brief period of cardiac monitoring is reasonable in the symptomatic patient, the pregnant patient, or where the dart has struck the chest. [1]

Complications and pitfalls

The complications are immediate (cardiac arrest, ventricular arrhythmia, blunt trauma from the throw), early (rhabdomyolysis with acute kidney injury, compartment syndrome requiring fasciotomy, hyperkalaemia, posterior shoulder dislocation from tetany) and delayed (peripheral neuropathy, autonomic dysfunction, cataracts, complex regional pain and psychological sequelae). The classic pitfalls are assuming a small surface wound means minor injury, discharging a low-voltage patient without the 4 to 6 hour ECG, missing compartment syndrome behind a painful limb, anchoring on the electrical injury and missing an epidural or a splenic injury from the fall, and forgetting delayed labial-artery bleeding in the paediatric mouth burn.[6][7]

Complications in detail

Electrical injury wounds the patient across every system, and the complications are best grouped by the onset and the mechanism. [1]

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Key evidence

[5] [6] [7] [4] [2] [1] [1] [1] [1] [1] [1] [1] [1] [1] [1] [1] [1]

Prognosis and disposition

Mortality is dominated by the initial cardiac arrest; survivors of high-voltage injury face a high rate of limb amputation, chronic neuropathic pain and lifelong psychological morbidity. Disposition follows the voltage and the presentation: asymptomatic low-voltage with a normal ECG after 4 to 6 hours is discharged with a safety-net; high-voltage, symptomatic, abnormal-ECG or any loss-of-consciousness case is admitted under a surgical or burns service with telemetry; the intubated or unstable patient goes to intensive care.[1][2]

Special populations

Children are at risk of the deep oral-commissure burn and its delayed labial-artery bleed; pregnant women require fetal monitoring after any shock; the elderly and comorbid tolerate the fluid load of rhabdomyolysis therapy poorly and need careful titration; electrical and outdoor-construction workers need occupational-health and safety follow-up to prevent recurrence. [1]

Evidence and regional guidelines

The contemporary framework follows ATLS for the trauma component, the Eastern Association for the Surgery of Trauma rhabdomyolysis guideline for fluid therapy, and the regional burns-centre pathway for wound care and transfer.[5] Recent emergency-department reviews consolidate the assessment and the monitoring intervals, and multicentre data identify the predictors of amputation that mandate early surgical referral.[1][6]

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Exam pearls

• Joule's law: heat $\propto I^2Rt$. Current, not voltage, kills; contact time is fatal because tetany locks the hand on the source.
• Small wound, big injury. A high-voltage entry wound is tiny — the deep track along bone is what amputates limbs.
• Lightning = reverse triage. In a group strike, resuscitate the apnoeic "dead" first — the heart auto-restarts, the respiratory centre does not.
• Lichtenberg figures = lightning. Transient ferning plus tympanic rupture is pathognomonic.
• 4 to 6 h, then go. Asymptomatic low-voltage with a normal ECG is safe to discharge after a 4 to 6 hour telemetry window.
• Oral-commissure burn bleeds late. Warn parents about labial-artery haemorrhage one to three weeks out.
• AC vs DC. AC causes tetany ("no let-go") and VF at around 100 mA; DC causes a single throw and tends to asystole. Lightning is the extreme DC pulse.
• 100 mA kills. That is the ventricular fibrillation threshold for mains-frequency AC — well within the reach of a domestic socket.
• Resistance ranks nerve < vessel < muscle < skin < fat < bone. Bone cooks the muscle around it; that is the deep track the entry wound hides.
• Blood on the dipstick, no red cells. Myoglobinuria — the bedside signature of rhabdomyolysis. Start fluids on the finding.
• Hyperkalaemia peaks fast. Massive muscle breakdown releases potassium by the gram — check it early and repeat before the QRS widens.
• Urine output 1 to 1.5 mL/kg/h. The EAST target for rhabdomyolysis; no routine mannitol or bicarbonate.
• Compartment pressure within 30 mmHg of diastolic. Clinical diagnosis — pain on passive stretch, tense compartment — fasciotomise within the 6 to 12 hour golden period.
• Posterior shoulder dislocation. Tetany dislocates the shoulder posteriorly — examine both shoulders on the secondary survey.
• Keraunoparalysis resolves in hours. Do not confuse it with spinal injury — but keep precautions if the mechanism supports trauma.
• Pregnant patient — always fetal monitoring. Amniotic fluid conducts to the fetus; even a trivial shock can cause fetal loss.
• Tympanic rupture = think lightning. Examine both ears on every lightning victim — a ruptured drum in an unwitnessed collapse is the clue.
• Cataracts are delayed. Bilateral, weeks to months out, especially with lightning and head-path current — warn and follow up ophthalmology.
• Make the scene safe first. Never touch a victim still in contact with a live source — the rescuer becomes the next patient.
• Ventilate the apnoeic lightning victim. The heart auto-restarts; the respiratory centre does not. Ventilation alone may reverse the secondary arrest — never give up early.
• Map entry AND exit. The exit may be larger or absent (broad earth contact); do not let a small wound reassure you about the deep track.
• Troponin and CK both, serially. They peak around 24 hours; a single normal value on arrival is meaningless because the muscle is still breaking down.
• Reverse triage only in lightning mass-casualty. Resuscitate the apnoeic first; the walking wounded can wait. This does NOT apply to other trauma scenes. [1]

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Red flags

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References

1. [1]Smith I. Assessment and Management of Electrical Injuries in Adults in the Emergency Department Cureus, 2026.PMID 42147553
2. [2]Yazici R, et al. Prevalence and risk factors of developing cardiac arrhythmia in patients presenting to the emergency department with electrical injuries PLoS One, 2025.PMID 41364707
3. [3]Samia AM, et al. Cutaneous Manifestations of Lightning Injury: A Review of the Literature Skinmed, 2023.PMID 37634096
4. [4]Jensen PJ, Thomsen PE, Bagger JP, Naylor PD, Baandrup U. Electrical injury causing ventricular arrhythmias Br Heart J, 1987.PMID 3566986
5. [5]Sawhney JS, et al. Management of rhabdomyolysis: A practice management guideline from the Eastern Association for the Surgery of Trauma Am J Surg, 2022.PMID 34836603
6. [6]Pedrazzi N, et al. Predictors for limb amputation and reconstructive management in electrical injuries Burns, 2023.PMID 36031494
7. [7]Putri AC, et al. The Evaluation of a Golden Period of Fasciotomy for High Voltage Electrical Burn Injury Patients With Compartment Syndrome Ann Burns Fire Disasters, 2023.PMID 38680908