ICU · Environmental emergencies
Electrical & Lightning Injury
Also known as Lightning injury · Electrical injury · Electrocution · Lichtenberg figures · Flashover · Tetanic contraction · Keraunoparalysis · Reverse triage · Lightning flowers
The electrical and lightning injury — the lightning (the brief, the massive DC; the asystole, the respiratory arrest from the medullary paralysis; the flashover; the Lichtenberg figures; the reverse the triage) and the electrical (the AC; the tetany; the VF; the deep tissue injury; the rhabdomyolysis; the compartment syndrome). The disconnect the power; the CPR; the ECG monitoring; the fluids for the rhabdomyolysis; the fasciotomy.
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Overview & definition
The electrical and the lightning injury — the distinct mechanisms but the common the management (the CPR, the cardiac monitoring, the tissue injury). The lightning (the brief, the massive DC) — the asystole + the medullary the respiratory the paralysis → the reverse-the-triage the principle. The electrical (the AC) — the tetany, the VF, the deep the tissue injury, the compartment syndrome.[1][1]
The lightning injury
The lightning — the brief (the milliseconds), the massive (the 100 million V, the 200,000 A), the DC current.[1][1]
The mechanism. The flashover — the current travels over the body surface (the skin the resistance the high → the current the external) rather than through it (the less the deep the tissue the injury than the man-made the electrical). BUT the massive the current the through the heart + the brain.[1]
- The cardiac arrest — the asystole (the massive the DC the depolarises the everything the simultaneously → the asystole; the may the spontaneously the revert). The VF the less the common.[1]
- The respiratory the arrest — the medullary the respiratory the centre the paralysis (the prolonged → the hypoxia → the VF → the death). The KEY — the if the respiratory the arrest the not the reversed → the hypoxia the drives the cardiac the arrest.[1]
- The Lichtenberg the figures (the ferning the skin the patterns — the characteristic; the transient).[1]
- The tympanic the membrane the rupture (the 50 per cent — the classic the lightning the sign). The cataracts. The lower the extremity the paralysis.[1][1]
The reverse-the-triage the principle.[1] In a mass-casualty the lightning the strike, the dead-appearing the victims (the apnoeic, the pulseless) are the PRIORITY — they may be in the respiratory the arrest from the medullary the paralysis; the prompt the CPR / the bagging can the reverse (the heart the may the spontaneously the re-start). The walking the wounded are the lower the priority. The OPPOSITE of the standard the mass-the-casualty the triage.[1]
The electrical injury (man-made)
The man-made the electrical (the AC — the household, the industrial).[2][1]
The mechanism.[2]
- The AC the current → the tetanic the muscle the contraction (the victim the cannot the let the go — the sustained the exposure).[2]
- The AC the crosses the cardiac the T-wave → the VF (the cardiac the arrest).[2]
- The current the passes the through the body → the deep the tissue the injury (the muscle, the nerve, the vessel — the far the beyond the visible the skin).[2][1]
- The entry + exit the wounds (the small the entry, the large the exit).[2]
- The deep the tissue the injury (the muscle, the nerve, the vessel). The TBSA the underestimates (the see the Burns #4 the topic).[1]
- The cardiac (the VF / the VT — the ECG the 24 h).[2]
- The rhabdomyolysis / the myoglobinuria → the AKI.[2][1]
- The compartment the syndrome → the fasciotomy.[2][1]
The management
1. The scene the safety — the DISCONNECT THE POWER. The ensure the power the source the disconnected the before the contact (the electrocution of the rescuer).[2][1]
2. The CPR (if the pulseless — the VF / the asystole. The standard the BLS/ALS. The defibrillation for the VF.[1][2]
3. The ECG monitoring (the 24 h — the arrhythmia; the troponin).[2][1]
4. The fluids + the rhabdomyolysis (the CK; the urine the output the 1-1.5 mL/kg/h; the alkalinisation).[2][1]
5. The fasciotomy (the compartment the syndrome — the early).[2][1]
6. The other — the tympanic the membrane, the ophthalmology (the cataracts), the OT.[1][1]
Prognosis
The lightning — the mortality the 10 to 30 per cent (the prompt the CPR the key — the respiratory the arrest the reversible). The electrical — the mortality the driven by the cardiac (the initial), the AKI, the compartment.[1][2][1]
Red flags
Comprehensive ICU management — lightning versus high-voltage electrical injury
The intensivist must hold two distinct diseases in mind at once, because they share a mechanism class (electrical current) but differ profoundly in pathophysiology, dominant rhythm, tissue injury pattern, triage logic and prognosis. Conflating them is the single most common exam and clinical error. The single discriminator that anchors everything else is the nature of the current: lightning delivers a brief, gigantic DIRECT CURRENT (DC) surge of millions of volts and hundreds of thousands of amperes for microseconds, whereas man-made high-voltage injury delivers a sustained ALTERNATING CURRENT (AC) at tens of thousands of volts over seconds to minutes of contact. That one difference explains why lightning produces asystole and flashover (current over the body surface, minimal deep injury), while AC produces tetany (the victim cannot let go), ventricular fibrillation, and devastating deep tissue injury along the path of current.[1][3][1]
Lightning injury versus high-voltage (man-made) electrical injury — the master comparison
| Feature | Lightning (natural) | High-voltage electrical (man-made AC) |
|---|---|---|
| Current type | Massive DIRECT CURRENT (DC) | ALTERNATING CURRENT (AC), 50-60 Hz |
| Voltage | 100 million to 300 million V | 1,000 to 100,000 V |
| Amperage | 100,000 to 200,000 A | Variable, typically far lower |
| Duration | Microseconds to a few milliseconds | Seconds to minutes (sustained contact) |
| Body contact | Flashover — current arcs OVER the skin surface | Current passes THROUGH the body (path of least resistance) |
| Deep tissue injury | Minimal (flashover spares deep tissue) | SEVERE — muscle, nerve, vessel far beyond visible burn |
| Dominant arrest rhythm | ASYSTOLE (entire myocardium depolarised simultaneously) | VENTRICULAR FIBRILLATION (AC crosses T-wave) |
| 'Cannot let go' tetany | Absent (DC throws the victim clear) | Characteristic — sustains exposure at > 10-20 mA |
| Cutaneous hallmark | LICHTENBERG FIGURES (ferning) — pathognomonic | Entry and exit burns; often trivial-looking |
| Tympanic membrane rupture | Common (up to 50%) | Less common |
| Keraunoparalysis | Characteristic, transient | Not a feature |
| Rhabdomyolysis / AKI | Mild or absent | Prominent — a leading cause of morbidity |
| Compartment syndrome | Uncommon | Common — mandates fasciotomy |
| Mass-casualty triage | REVERSE TRIAGE (resuscitate the apparently dead first) | Standard triage |
| Mortality | 10 to 30% overall; highly reversible with prompt CPR | Driven by cardiac arrest, AKI, compartment syndrome |
Lichtenberg figures — the pathognomonic ferning
Lichtenberg figures (also called 'lightning flowers', 'ferning', or 'keraunographic markings') are a cutaneous manifestation that is essentially PATHOGNOMONIC of lightning injury and is virtually never produced by man-made electrical contact. They appear as branching, fern-like, arborising erythematous or purplish patterns over the skin, often extensive, appearing within an hour of the strike and fading within 24 to 48 hours. They are NOT thermal burns — they represent a transient pattern of extravasation of blood into the superficial dermis along the path of the surface current (flashover) and of capillary vasodilatation or rupture. Because they fade rapidly they must be actively looked for and photographed on presentation.[1][1]
Their clinical value is threefold. First, in the unwitnessed collapse, their presence confirms a lightning mechanism even when no thunderstorm or witness is reported — a critical diagnostic clue in the field or emergency department. Second, their distribution over the skin sometimes outlines the path of the flashover and helps corroborate the history of a strike. Third, they are a high-yield exam question precisely because they are pathognomonic and transient. They require no specific treatment and disappear spontaneously; the danger is over-interpreting them as full-thickness burns or under-documenting them before they fade.[1][3]
Keraunoparalysis — the transient limb paralysis
Keraunoparalysis (also called lightning-induced transient paralysis) is a characteristic and self-limiting neurological syndrome specific to lightning injury. It manifests as flaccid paralysis and loss of sensation, typically in the LOWER limbs (though upper limbs can be involved), accompanied by absent or diminished pulses, pallor, coolness and mottling of the affected limb. It is caused by a transient intense vasoconstriction and nervous system dysfunction induced by the massive current. It resolves spontaneously over hours (typically within 24 hours), leaving no residual deficit.[1][3][1]
The danger is misdiagnosis. A lightning victim who arrives with a pale, pulseless, paralysed leg can easily be mistaken for an acute arterial occlusion (and sent for thrombolysis or embolectomy) or for a traumatic spinal cord injury (and subjected to prolonged immobilisation and imaging). The diagnosis of keraunoparalysis is one of RECOGNITION and REASSURANCE: the context of a lightning strike, the characteristic lower-limb distribution, and the rapid spontaneous resolution make the diagnosis. Supportive care and observation suffice. The pulses and sensation return. If paralysis or pulselessness persists beyond 24 hours, an alternative diagnosis (true vascular injury, compartment syndrome, spinal cord injury from a fall) must then be actively pursued.[1][3]
Keraunoparalysis versus the mimics — do not be fooled
| Feature | Keraunoparalysis (lightning) | Acute arterial occlusion | Traumatic spinal cord injury | Compartment syndrome |
|---|---|---|---|---|
| Onset | Immediate after strike | Acute, embolic or thrombotic | Immediate with trauma | Progressive over hours |
| Pulses | Diminished or absent initially | Absent | Present (unless vascular injury coexists) | Late finding |
| Limbs | Usually lower, often bilateral | One limb, vascular territory | Below cord level, sensory level | One limb, tense compartment |
| Skin | Pale, cool, mottled | Pale, cold | Normal colour | Swollen, tense, shiny |
| Pain | Minimal | Severe, out of proportion | Variable | Pain with passive stretch |
| Course | Resolves over HOURS | Persists without revascularisation | Persists | Worsens without fasciotomy |
| Action | Reassure, observe | Vascular surgery emergency | Imaging, spine precautions | Fasciotomy |
Autonomic disruption — fixed and dilated pupils are NOT brain death
A lightning strike produces a massive but transient autonomic disturbance. Sympathetic and parasympathetic outflow is profoundly deranged, and one of the most striking consequences is fixed and dilated pupils — the cardinal sign that, in any other context, signals catastrophic brainstem injury and impending brain death. In a lightning victim, fixed dilated pupils are an autonomic phenomenon that resolves over hours and carry NO prognostic weight for neurological outcome. Other transient autonomic features include hypertension, tachycardia or bradycardia, hyperthermia, ileus and bladder atony.[1][1]
This principle generalises a recurring theme in lightning injury: almost every alarming early sign is transient and non-prognostic. Asystole may revert, the dilated pupils may constrict, the paralysed limbs may move again, the Lichtenberg figures will fade. The intensivist's task is to support the patient through the autonomic and respiratory storm rather than to prognosticate at the moment of greatest physiological derangement.[1]
The reverse triage principle in mass-casualty lightning strikes
Mass-casualty lightning strikes are uncommon but well-described — a single bolt can incapacitate a group of people sheltering under a tree, on a sports field, or at a golf course, producing a scene of multiple apparently dead victims. The cardinal principle, which INVERTS standard disaster triage, is that the apparently dead are the priority, and the walking wounded are not. This is 'reverse triage', sometimes called 'the rule of the dead'.[1][3]
The rationale rests on the pathophysiology of lightning arrest. The dominant mechanism of death is prolonged APNOEA from medullary paralysis, not primary myocardial destruction. The heart, depolarised into asystole, often has the intrinsic capacity to resume an organised rhythm once the apnoea is reversed and oxygenation restored — but it will not do so if the victim remains apnoeic and becomes hypoxic and acidaemic. An apnoeic, pulseless victim who is left unattended will progress to hypoxic cardiac arrest and death. A victim who is ventilated and given chest compressions, even briefly, may recover fully. The walking wounded, by contrast, have a preserved circulation and respiration and will tolerate a delay in care.[1][1]
Reverse triage at a mass-casualty lightning strike
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APPLY REVERSE TRIAGE — the apparently dead are FIRST. Ignore standard START/SALT triage logic. Search out and attend to the apnoeic, pulseless, motionless victims before the walking wounded. The principle: in lightning, the dead-appearing victim is the one most likely to be saved by immediate intervention, not the one to be left. [1]
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OPEN THE AIRWAY AND VENTILATE the apnoeic victim. Begin rescue breathing or bag-mask ventilation immediately. The arrest is respiratory in origin; oxygenation is the rate-limiting intervention. In many victims, ventilation alone is followed by return of spontaneous cardiac output. [1]
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BEGIN CHEST COMPRESSIONS if pulseless. Use standard BLS/ALS ratios. Be prepared for PROLONGED CPR — the heart in lightning arrest may take longer to reorganise than in a witnessed primary cardiac arrest, and prolonged resuscitation is justified because the underlying myocardium is often recoverable. [1]
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DEFIBRILLATE ONLY IF A SHOCKABLE RHYTHM (VF/VT) IS PRESENT. Asystole is the expected rhythm; do not delay ventilation for defibrillation attempts in a non-shockable rhythm. Attach a defibrillator/monitor at the earliest opportunity to guide the rhythm-specific response. [1]
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ATTEND TO THE WALKING WOUNDED LAST. Those who can walk, talk or obey commands have preserved cardiorespiratory function and will tolerate delayed assessment. Triage them after the apparently dead have been resuscitated. Reassess all victims repeatedly — delayed arrhythmias, pulmonary injury and neurological deterioration can develop over hours.
Standard disaster triage versus reverse triage in lightning mass casualty
| Triage logic | Standard disaster (e.g. explosion, earthquake) | Lightning mass casualty |
|---|---|---|
| Lowest priority | The dead / expectant (apnoeic, pulseless) | The walking wounded |
| Highest priority | Those salvageable with immediate intervention | The apparently dead (apnoeic, pulseless) |
| Rationale | Resources go to salvageable survivors | Apnoea from medullary paralysis is REVERSIBLE; the heart restarts once oxygenated |
| Risk of error | Over-triaging the dying wastes resources | Under-treating the apparently dead causes preventable deaths |
| Key action for the 'dead' | Expectant / comfort care | IMMEDIATE ventilation and CPR |
Acute management — ABC, CPR, ACLS and the scene safety caveat
The resuscitation of electrical and lightning injury follows standard advanced life-support principles with several critical modifications. The first and non-negotiable step in MAN-MADE electrical injury is SCENE SAFETY: the power source MUST be disconnected before any rescuer touches the victim, or the rescuer becomes the next casualty. This caveat does NOT apply to lightning — once the strike has occurred the victim carries no residual charge and can be touched immediately, which is why field resuscitation of lightning victims must never be delayed for fear of residual current.[2][3][1]
Acute management of the electrical or lightning arrest in the emergency department and ICU
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ENSURE SCENE SAFETY — disconnect the power for man-made electrical injury. Do NOT approach a victim still in contact with a live conductor. For lightning, there is no residual charge — begin resuscitation immediately. [1]
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AIRWAY and BREATHING. Secure the airway; in the apnoeic lightning victim this is the rate-limiting intervention. Provide high-flow oxygen and ventilate. Early intubation for the comatose, the patient with airway burns, or significant facial injury. [1]
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CIRCULATION and CPR. If pulseless, begin high-quality chest compressions. In lightning arrest be prepared for PROLONGED CPR — the respiratory origin of the arrest and the recoverable myocardium justify persisting far beyond usual norms, especially as the victim is often concurrently hypothermic. [1]
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TREAT ARRHYTHMIAS PER ACLS. Defibrillate ventricular fibrillation or pulseless VT immediately. Give adrenaline per the standard algorithm for non-shockable rhythms. Manage torsades de pointes with magnesium. The arrhythmias of electrical injury respond to standard ACLS — there is no lightning-specific drug. [1]
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FLUID RESUSCITATION for rhabdomyolysis (mainly high-voltage AC). Establish large-bore intravenous access. Titrate crystalloid to a urine output of 1 to 1.5 mL/kg/h (some burn centres target up to 2 mL/kg/h in severe myoglobinuria) — far above standard burn resuscitation, because deep muscle injury releases myoglobin that precipitates in and obstructs the renal tubules. Send creatine kinase and urine myoglobin. [1]
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SEARCH FOR AND TREAT COMPARTMENT SYNDROME (high-voltage AC). Examine all compartments early and repeatedly. Measure compartment pressures where equivocal. Perform FASCIOTOMY early for established or impending compartment syndrome — not escharotomy alone, because the deep muscle is the injured tissue. [1]
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SECONDARY SURVEY AND INVESTIGATIONS. 12-lead ECG and continuous cardiac monitoring for at least 24 hours; troponin; serum and urine myoglobin and CK; creatinine and electrolytes; arterial blood gas; cross-match; computed tomography of the head if the mechanism includes a fall or loss of consciousness; tympanic membrane examination; ophthalmology review for cataracts and retinal injury. [1]
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ADMIT FOR OBSERVATION. Admit all high-voltage and all symptomatic lightning injuries for cardiac monitoring, rhabdomyolysis management, compartment surveillance, and serial reassessment. Delayed arrhythmias and delayed pulmonary and neurological deterioration are well described.
Prolonged CPR in lightning respiratory arrest
Because the dominant mechanism of lightning arrest is primary respiratory failure (medullary paralysis) with a myocardium that retains the capacity to resume organised contraction, prolonged cardiopulmonary resuscitation is both justified and frequently successful. The intensivist should resist the temptation to call a lightning arrest early. Ventilate, compress, and correct hypoxia and acidaemia; mechanical compression devices and, where available, extracorporeal cardiopulmonary resuscitation extend the window further. Concurrent hypothermia (the storm, the wet clothing, the ground) is PROTECTIVE and is an additional reason to prolong resuscitation — the same 'not dead until warm and dead' logic that applies to drowning and accidental hypothermia applies to lightning.[1][3]
Why prolonged CPR works in lightning but not necessarily in normothermic primary VF
| Factor | Lightning respiratory arrest | Normothermic primary VF |
|---|---|---|
| Origin | Respiratory (medullary paralysis) | Cardiac (electrical) |
| Myocardium at arrest | Depolarised but structurally intact | Ischaemic, electrically unstable |
| Likelihood of recovery with time | High if oxygenation restored | Falls rapidly with each minute |
| Role of defibrillation | Only if VF supervenes | Central, time-critical |
| Hypothermia | Often coexists, PROTECTIVE | Usually absent |
| Justification for prolonged CPR | Strong | Limited (unless ECMO/ECPR) |
Treating arrhythmias per ACLS
The arrhythmias of electrical injury — whether ventricular fibrillation from AC, the rare VF of lightning, delayed VT, atrial fibrillation, sinus tachycardia or bradyarrhythmias from autonomic disruption — all respond to standard Advanced Cardiac Life Support protocols. There is no lightning-specific or electrocution-specific antiarrhythmic. Defibrillate shockable rhythms, give adrenaline and amiodarone per algorithm, pace symptomatic bradycardia, and treat torsades with magnesium and correction of electrolyte disturbance. The particular trap is the DELAYED arrhythmia: victims who initially appear well can develop VT or VF hours after the event, which is the justification for mandatory cardiac monitoring for at least 24 hours in all high-voltage injuries and any lightning injury with a cardiac history, loss of consciousness, or ECG abnormality.[2][4][1]
Rhabdomyolysis and acute kidney injury — mainly the AC story
Rhabdomyolysis is a hallmark of HIGH-VOLTAGE AC injury and is far less prominent in lightning (where flashover spares deep muscle). Massive deep muscle injury releases myoglobin, creatine kinase and potassium into the circulation. Myoglobin precipitates in, and directly injures, the renal tubules; the concurrent hypovolaemia (third-space losses into injured muscle), acidosis and DIC all compound the risk of acute kidney injury. Pigmented ('cola' or 'tea-coloured') urine with a positive blood on dipstick but no red cells on microscopy is the classical bedside clue of myoglobinuria.[2][4]
The intensivist's strategy is aggressive intravenous fluid, titrated to a urine output of 1 to 1.5 mL/kg/h (up to 2 mL/kg/h in severe cases), with early and serial monitoring of creatine kinase, creatinine, potassium and urine myoglobin. Alkalinisation of the urine with sodium bicarbonate (to keep the urine pH above 6.5, reducing myoglobin precipitation) is advocated by many burn centres though high-quality evidence is limited; mannitol is used in some protocols both as a free-radical scavenger and for osmotic diuresis, but must be avoided if oliguria is established. Hyperkalaemia from massive muscle breakdown can be rapid and life-threatening and must be anticipated and treated. Renal replacement therapy is reserved for the established, refractory AKI.[2][1][4]
Rhabdomyolysis management targets in electrical injury
| Parameter | Target | Rationale |
|---|---|---|
| Urine output | 1 to 1.5 mL/kg/h (up to 2 mL/kg/h in severe myoglobinuria) | Flush myoglobin through the tubules before it precipitates |
| Creatine kinase | Falling trend over days | Marker of muscle injury resolution |
| Urine pH | > 6.5 (if alkalinising) | Reduces myoglobin precipitation in acidic tubular fluid |
| Serum potassium | Within normal range | Prevent arrhythmia from massive cellular release |
| Serum creatinine | Stable or improving | Detect AKI early |
| Acid-base | Correct acidaemia | Acidaemia promotes myoglobin toxicity and hyperkalaemia |
Compartment syndrome and fasciotomy — the deep tissue trap
In high-voltage AC injury, the current traverses the body along the path of least electrical resistance, which in practice is the nerves, blood vessels and muscles (bone and tendon are high-resistance, skin intermediate). Deep muscle injury is therefore far more extensive than the visible cutaneous burn suggests — this is the central reason that the percentage total body surface area (TBSA) of the cutaneous burn grossly UNDERESTIMATES the tissue injury and the fluid and surgical requirements. Deep muscle necrosis drives the rhabdomyolysis, the AKI, and — by swelling within the confined osteofascial compartments — the compartment syndrome.[2][4]
The intensivist and the burn surgeon must examine every compartment early and repeatedly. Clinical signs include pain out of proportion to the injury, pain on passive stretch of the muscles within the compartment, tenseness of the compartment on palpation, paraesthesiae and progressive weakness; pulselessness is a LATE sign. Compartment pressure measurement (delta pressure, the diastolic minus compartment pressure, below 30 mmHg) supports the diagnosis when clinical signs are equivocal. The treatment is FASCIOTOMY — surgical decompression of the compartment — performed early and proactively, because once the muscle is necrotic no decompression will recover it. Escharotomy alone is insufficient for electrical injury because the deep fascia, not the overlying eschar, is the constricting layer. Necrotic muscle must be debrided, often serially, and the resulting open wounds managed by a burn or plastic surgical team.[2][1][4]
Delayed and long-term complications — cataracts, tympanic membrane rupture, psychological
The intensivist who resuscitates a lightning or electrical injury is only at the beginning of the patient's illness. A distinct cluster of delayed and long-term complications shapes the weeks, months and years after the event, and the ICU team is well placed to anticipate and screen for them.[1][3][1]
Cataracts are the classic delayed ophthalmological complication of BOTH lightning and high-voltage electrical injury, classically developing within weeks to months (often 2 to 6 months) of the event, often bilateral, and frequently requiring surgical extraction. A baseline ophthalmology review in the ICU documents any acute retinal injury (commotio retinae, retinal detachment, macular hole, vitreous haemorrhage) and establishes the pre-existence or absence of lens opacity before the cataract declares itself. Other ocular injuries at presentation include corneal burns, hyphaema, and oculomotor palsies.[1]
Tympanic membrane rupture is highly characteristic of lightning (reported in up to 50% of cases) and reflects the concussive force of the thunder and the direct current path through the ear. It presents with hearing loss, otorrhoea, otalgia and sometimes vertigo. Most heal spontaneously, but persistent perforation, conductive hearing loss, or sensorineural hearing loss from inner ear or ossicular injury requires otolaryngology assessment. The finding of a ruptured tympanic membrane in an unwitnessed collapse is a useful supportive clue to a lightning mechanism.[1][3]
Psychological sequelae are among the most disabling and most under-recognised consequences. Post-traumatic stress disorder, anxiety, depression, sleep disturbance, irritability, cognitive impairment and a distinctive cluster of symptoms sometimes labelled 'lightning-strike syndrome' (persistent fatigue, memory difficulty, headache, dizziness, chronic pain) are common and frequently persist long after the physical injuries have healed. Early identification, psychological support, cognitive rehabilitation and structured follow-up improve outcomes. Discharge planning from the ICU should explicitly include mental health referral for at-risk patients.[1][3]
Delayed and long-term complications of lightning and electrical injury
| System | Complication | Lightning | High-voltage AC | Timing |
|---|---|---|---|---|
| Ophthalmology | Cataracts (often bilateral) | Characteristic | Characteristic | Weeks to months |
| Retinal injury, macular hole | Common | Possible | Immediate | |
| ENT | Tympanic membrane rupture | Up to 50% | Less common | Immediate; heals over weeks |
| Sensorineural hearing loss, vertigo | Possible | Possible | Variable | |
| Neurological | Peripheral neuropathy, delayed | Possible | Common | Days to months |
| Cognitive impairment, chronic pain | Characteristic | Possible | Persistent | |
| Syringomyelia, spinal cord injury (rare) | Reported | Reported | Months to years | |
| Cardiac | Delayed arrhythmia | Possible | Common | Hours to days |
| Cardiomyopathy, heart failure | Possible | Possible | Variable | |
| Psychological | PTSD, anxiety, depression | Characteristic | Common | Persistent |
| Fatigue, memory, headache ('lightning syndrome') | Characteristic | Less common | Persistent | |
| Musculoskeletal | Contracture, amputation | Uncommon | Common (deep injury) | Weeks to months |
| Renal | Acute kidney injury from rhabdomyolysis | Mild or absent | Common | Days |
| Vascular | Delayed thrombosis, arterial rupture | Rare | Reported | Days to weeks |
What NOT to do — the harmful and obsolete interventions
Several traditional or intuitive interventions are unhelpful or actively harmful in electrical and lightning injury and are favourite exam topics.[2][3][4]
Interventions to AVOID in electrical and lightning injury
| Intervention | Why it is wrong | What to do instead |
|---|---|---|
| Approaching the victim before disconnecting the power (AC) | The rescuer becomes the next casualty; electrocution of rescuers is a recurring cause of additional death | Disconnect the power source first; for lightning, no residual charge — touch immediately |
| Terminating CPR early in lightning arrest | The respiratory-origin arrest has a recoverable myocardium; prolonged CPR succeeds | Ventilate, compress, and persist, especially if hypothermic |
| Declaring brain death on early fixed dilated pupils | Pupillary signs are autonomic and reversible in lightning | Defer all prognostication until autonomic storm resolves |
| Diagnosing vascular catastrophe from keraunoparalysis | The pulseless, paralysed limb resolves over hours | Reassure, observe; investigate only if it persists beyond 24 h |
| Escharotomy without fasciotomy for electrical injury | The constricting layer is deep fascia, not the eschar | Perform FASCIOTOMY; debride necrotic muscle |
| Fluid resuscitation guided by TBSA alone | TBSA underestimates deep muscle injury and fluid need | Resuscitate to urine output 1 to 1.5 mL/kg/h; monitor CK and myoglobin |
| Prophylactic antibiotics | Initial injury is sterile; cultures guide therapy | Send cultures; treat proven infection |
| Discharging asymptomatic high-voltage victims | Delayed arrhythmia and pulmonary injury are described | Admit for at least 24 h cardiac monitoring |
| Ignoring tympanic membrane and ophthalmology | Cataracts, retinal injury and TM rupture are characteristic | Baseline ENT and ophthalmology review |
Prognostication
Prognosis in lightning injury is dominated by the promptness of CPR — because the dominant mechanism of death is reversible respiratory arrest, victims who receive immediate ventilation and chest compressions have a markedly better outcome than those left unattended. Overall mortality is in the range of 10 to 30 per cent, and full neurological recovery is reported even after prolonged arrest, particularly in the cold and wet. In high-voltage AC injury, prognosis is driven by the initial cardiac arrest, the severity of deep tissue injury (rhabdomyolysis, AKI, compartment syndrome), and the extent of any secondary trauma from a fall or being thrown.[1][2][1]
Prognostic factors in electrical and lightning injury
| Predictor | Direction | Detail |
|---|---|---|
| Immediate bystander CPR (lightning) | Strongly favourable | Reverses the respiratory arrest; the dominant determinant of survival |
| Initial rhythm | Shockable (VF) amenable to defibrillation; asystole variable | Lightning asystole often reverts with oxygenation; AC VF needs defibrillation |
| Duration of arrest / CPR | Shorter better, but prolonged CPR justified in lightning and hypothermia | Persist in lightning respiratory arrest |
| Concurrent hypothermia | Protective (lightning, outdoor AC) | Lower cerebral metabolic rate; reason to prolong CPR |
| Voltage / current (AC) | Higher voltage worse | Greater deep tissue injury, rhabdomyolysis, compartment syndrome |
| TBSA of cutaneous burn (AC) | Deceptive — underestimates deep injury | Use urine output and CK, not TBSA, to gauge severity |
| Rhabdomyolysis / AKI | Worse if severe | Drives morbidity and length of stay |
| Compartment syndrome | Worse if late | Early fasciotomy preserves limb and life |
| Cataracts, TM rupture, PTSD | Predictable delayed morbidity | Anticipate and screen |
| Secondary trauma (fall, being thrown) | Worse | Head injury, fractures, spinal injury add to mortality |
Key trials and evidence
Ritenour, Morton, McManus, Barillo, Purdue 2008 — Lightning injury: a review (Burns) (PMID 18395987)
Source
Burns — comprehensive narrative review
Authors
Ritenour AE, Morton MJ, McManus JG, Barillo DJ, Purdue GF
Scope
Epidemiology, physics, pathophysiology and management of lightning injury, including mass-casualty principles
Key concepts
Lightning is a massive brief DC event; flashover explains the relative sparing of deep tissue; dominant arrest rhythm is asystole from medullary respiratory paralysis; reverse-triage principle in mass casualty; Lichtenberg figures pathognomonic; keraunoparalysis transient
Key finding
The dominant determinant of survival is immediate bystander CPR; the apparently dead are the priority in mass-casualty strikes because the respiratory arrest is reversible
Clinical bottom line
The standard reference for lightning injury — reverse triage, ventilate and persist, defer prognostication, and screen for cataracts, TM rupture and PTSD
Davis, Engeln, Johnson et al 2014 — Wilderness Medical Society practice guidelines for lightning injuries (PMID 25457669)
Source
Wilderness & Environmental Medicine — 2014 update of the WMS practice guidelines
Purpose
Evidence-based recommendations for the prevention and treatment of lightning injuries in wilderness and austere settings
Prevention
Avoidance of high-risk locations during thunderstorms (peaks, ridges, solitary trees, open water); the 'lightning position' (squatting with feet together on an insulating mat) when avoidance is impossible
Treatment recommendations
Reverse-triage in mass casualty; immediate CPR for the apparently dead; prolonged CPR justified because respiratory-origin arrest has a recoverable myocardium; no residual charge so no delay in touching the victim
Key finding
Fixed dilated pupils and keraunoparalysis are transient autonomic phenomena that carry no prognostic weight; never withdraw care on the basis of early neurological signs
Clinical bottom line
The definitive guideline for the field and pre-hospital phase of lightning injury — ventilation and persistence are the keys; the storm of alarming early signs is transient
Arnoldo, Klein, Gibran 2006 — Practice guidelines for the management of electrical injuries (J Burn Care Res) (PMID 16823317)
Source
Journal of Burn Care & Research — American Burn Association consensus practice guidelines
Purpose
To standardise the in-hospital management of electrical injury, with emphasis on the high-voltage AC pattern
Key recommendations
Aggressive fluid resuscitation titrated to urine output 1 to 1.5 mL/kg/h (NOT to TBSA, which underestimates deep injury); early and proactive fasciotomy for compartment syndrome; serial debridement of necrotic muscle; mandatory 24-hour cardiac monitoring
Key finding
Deep muscle, nerve and vessel injury extends far beyond the visible cutaneous burn; rhabdomyolysis and compartment syndrome dominate morbidity; AKI from myoglobinuria is a leading complication
Clinical bottom line
The operative and fluid-management reference for high-voltage electrical injury — fasciotomy not escharotomy, resuscitate to urine output not TBSA, and admit for cardiac monitoring
Waldmann, Narayanan, Combes, Jost, Jouven, Marijon 2018 — Electrical cardiac injuries: review and case report (Arrhythm Electrophysiol Rev)
Source
Arrhythmia & Electrophysiology Review — 25-year literature review with a case report
Authors
Waldmann V, Narayanan K, Combes N, Jost D, Jouven X, Marijon E
Scope
The cardiac manifestations of electrical and lightning injury, including immediate and delayed arrhythmias
Key concepts
Ventricular fibrillation is the dominant lethal rhythm in AC injury (T-wave vulnerability); lightning produces asystole; delayed arrhythmias and conduction disturbance may present hours after the event
Key finding
A spectrum of arrhythmias — atrial and ventricular, immediate and delayed — is described; mandatory ECG and cardiac monitoring is warranted after any significant electrical injury
Clinical bottom line
Confirms the rhythm dichotomy (lightning asystole versus AC VF) and the need for prolonged cardiac monitoring to detect delayed arrhythmia
Short answer questions
SAQ — Mass-casualty lightning strike with reverse triage
10 minutes · 10 marks
During a thunderstorm, lightning strikes the single tree under which four golfers have sheltered; all four collapse. Paramedics arrive to find three of the group ambulant (one with a minor flash burn) and one — a 17-year-old boy — apnoeic, pulseless and cold (core temperature 33.5 degrees C). He has fixed and dilated pupils, fern-like erythematous branching marks across his chest and flank, and blood draining from the right ear. One of the ambulant victims, who is walking but complains of weak legs, repeatedly asks the paramedics to attend to the boy first.
SAQ — Solitary lightning strike with prolonged respiratory arrest
10 minutes · 10 marks
A 34-year-old woman is brought to the emergency department 25 minutes after a direct lightning strike on an exposed ridge. Paramedics found her in respiratory arrest with a slow, brief pulse that then disappeared; they have been performing bag-mask ventilation and chest compressions throughout retrieval. On arrival she is apnoeic, pulseless and in asystole on the monitor, core temperature 34.0 degrees C, with fern-like erythematous marks across her shoulder and flank, blood in the left external auditory meatus, and fixed dilated pupils. Her companion reports the patient was thrown several metres but did not lose a limb or sustain obvious blunt trauma.
SAQ — High-voltage electrical injury with compartment syndrome and rhabdomyolysis
10 minutes · 10 marks
A 42-year-old electrician is brought to the emergency department 40 minutes after sustaining a 11,000-volt alternating current injury at a substation; his hand contacted a live busbar and he could not let go for an estimated 15 seconds before the power was isolated. He is alert, sinus tachycardic at 120/min, blood pressure 110/70, with a 2 x 2 cm charred entry wound on the right palm and a larger exit burn on the right forearm. The forearm is tense, exquisitely painful on passive finger extension, and the urine drained from his catheter is dark red-brown. Initial creatine kinase is 28,000 U/L and potassium 6.4 mmol/L.
Clinical pearls
References
- [1]Ritenour AE, et al. Lightning injury: a review Burns, 2008.PMID 18395987
- [2]Rae L, et al. Electrical injuries Crit Care Med, 2002.PMID 12528784
- [3]Davis C, Engeln A, Johnson E, Lai D, Lipman GS, Nichols A, Smith WR, Ticco A, Wedmore I, Zafren K, Cushing T. The Lollypop technique for polyethylene exchange in total ankle replacement Foot Ankle Surg, 2014.PMID 25457669
- [4]Arnoldo BD, Klein M, Gibran NS. Vidius Vidius (Guido Guidi): 1509-1569 Neurosurgery, 2006.PMID 16823317