Electrical and radiation injury in ICU

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Meet the patient

A 41-year-old linesman is brought in after the boom of his crane contacted an 11 000 V overhead line and threw him to the ground. He is confused (GCS 13), tachycardic at 122, with a charred contact burn on the right palm and a ragged exit wound over the medial right calf. Both right limbs are tense and exquisitely painful on passive movement, and the urine is dark red-brown. The ECG shows sinus tachycardia with peaked T waves; the potassium is 6.8.^[5]

Two questions frame the whole topic: how much current crossed the body, and along what path? (current — not voltage — sets the injury, and a transthoracic hand-to-hand or hand-to-foot path threatens the heart) and — for the radiation end of the topic — is the patient irradiated or contaminated? (only the second is a hazard to staff).^[2]

Three injuries, one ICU

This topic bundles three distinct physical insults — electrical, lightning, and ionising radiation — and the intensivist must keep them straight because their first actions diverge. Electrical and lightning injury are dose-and-pathway problems solved by ACLS, rhabdomyolysis fluids, fasciotomy and cardiac monitoring. Radiation injury is a dose-dependent multi-syndrome problem solved by supportive care, growth factors, transfusion, and radionuclide-specific decorporation.^[1]

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Current, not voltage, kills — the physics of electrical injury

The severity of an electrical injury is set by current, not voltage — by Ohm law (I = V divided by R) the same 240 V applied to wet skin (about 1000 ohms) drives about 240 mA, while dry skin (about 100 000 ohms) limits it to about 2 mA, the difference between lethal VF and a tingle. Six variables therefore determine outcome: voltage, current, resistance, current type (AC versus DC), the pathway through the body, and the contact duration.^[2]

Heat is governed by Joule law (H equals the current squared times resistance times time): deep, high-resistance tissues — bone and tendon — become the hottest and conduct that heat to adjacent low-resistance muscle, nerve and vessel. This is the structural basis of the iceberg injury, in which trivial surface burns conceal massive deep-tissue necrosis.^[2]

Current magnitude produces a stereotyped clinical ladder. About 1 mA is the threshold of perception; 5 to 9 mA is the maximum harmless current; 10 to 20 mA is the let-go threshold, above which tetanic forearm-flexor contraction fixes the victim's grip onto a live AC source, prolonging contact and converting a survivable shock into a lethal one; about 100 mA of 50 to 60 Hz AC traversing the chest precipitates ventricular fibrillation; currents over 1 to 2 A produce direct myocardial standstill, deep burns and, in survivors, extensive rhabdomyolysis.^[2]

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The classic trap: estimating the danger from the voltage alone. A 240 V mains shock through a wet environment (a bathroom, a flooded basement, a sweating electrician) can be every bit as lethal as a far higher voltage through dry skin. Always read the resistance story — wet, sweating, immersed — before reassuring yourself.^[2]

AC versus DC — why mains current is the most dangerous waveform

The vulnerability of AC at 50 to 60 Hz is not coincidence: this band straddles the effective refractory window of cardiac myocytes, so successive cycles deliver current into the repolarising myocardium and trigger re-entry and VF. The let-go threshold exists because forearm flexor muscles are stronger than extensors, so tetanic flexion locks the hand closed on the conductor.^[2]

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This is why the first action at a low-voltage electrocution scene is to cut the power before touching the victim — pulling a gripped victim from a live source risks further injury to both patient and rescuer.^[2]

High-voltage injury — the iceberg and the management ladder

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The iceberg effect governs the whole surgical plan in electrical burns: high voltages penetrate deep tissues, so injuries not accounted for in formulae based on percentage cutaneous burn — myonecrosis and secondary compartment syndromes driving rhabdomyolysis — dictate debridement and fasciotomy. This is also why urine output, not a cutaneous-burn formula, is the resuscitation endpoint in high-voltage injury: the cutaneous burn underestimates the deep muscle injury, and the job is to flush myoglobin through the tubules before it precipitates.^[11]

Rhabdomyolysis is the renal threat. Myoglobin is the muscle constituent primarily responsible for renal damage, and the diagnosis rests on a creatine kinase more than five times the upper limit of normal (dark urine, dipstick-positive for blood without red cells on microscopy). Early and aggressive IV crystalloid is the agreed mainstay — start as soon as possible, ideally within the first 6 hours of muscle injury, maintaining a urine output of about 1 mL/kg/h after electrical injury (300 mL/h or more in adults with severe rhabdomyolysis, for at least the first day). Do not add sodium bicarbonate routinely — no controlled trial shows fluid-plus-bicarbonate beats fluid alone, so reserve it for systemic acidosis — and monitor for AKI: continuous venovenous haemofiltration is a well-supported adjunct to clear the myoglobin load that haemodialysis cannot.^{[16][9][10][11]}

Compartment syndrome is common after high-voltage injury because massive muscle oedema raises pressure within the osteofascial compartment. The signs are the classic five Ps in evolution — pain out of proportion (especially on passive stretch), tense compartments, paraesthesia, pallor, pulselessness (late). Pressure monitoring helps in uncooperative, unconscious or sedated patients; the critical absolute intracompartmental level is unclear, so a delta pressure (diastolic minus compartment pressure) under 30 mmHg with clinical signs mandates an emergency fasciotomy of all compartments.^[12]

Cardiac monitoring — who can go home

All electrical-injury patients get an ECG and clinical assessment of the current path and possible internal injury. Delayed arrhythmia is the main concern in an apparently stable patient and may require ICU-level monitoring. Discharge from the emergency department is reasonable only in selected patients — low-voltage injury, no syncope and a normal ECG — a policy the retrospective evidence and common Australian practice support; any arrhythmia, loss of consciousness, or a high-voltage mechanism warrants monitoring for at least 24 hours. Troponin flags myocardial injury; late structural cardiomyopathy is uncommon but described, so high-voltage survivors need cardiac follow-up.^[1][13]

Lightning — reverse triage and the apparently dead

A lightning bolt carries 100 million to 1 billion volts and 10 000 to 200 000 A for only 30 to 50 milliseconds — yet the internal injury is often surprisingly modest thanks to flashover, in which the current takes the lower-resistance route over the wet skin surface rather than through the torso. Entry or exit wounds and deep-muscle necrosis are far less prominent than in equivalent-voltage industrial electrocution.^[1]

Three lightning-specific signs the examiner wants:^[1]

• Lichtenberg figures — fern-like, feathery, branching skin markings that are pathognomonic for lightning. They are not thermal burns (no tissue necrosis) — thought to be an electron shower in superficial capillaries (a keraunographic mark). They fade within 24 hours, so their absence later does not exclude lightning.
• Fixed, dilated pupils — in lightning, dilated unreactive pupils reflect transient autonomic (ciliary) dysfunction, NOT brain death. A lightning victim with fixed pupils and apnoea must never be declared dead on that basis; outcomes after prolonged CPR are excellent.
• Keraunoparalysis (Charcot's keraunoparalysis) — a transient flaccid paralysis with sensory loss, pale, cold or blue extremities and absent pulses from vasomotor spasm, resolving over hours. It mimics spinal cord injury or acute limb ischaemia; always re-examine before imaging or vascular decisions.^[1]

The reverse-triage principle is unique to mass-casualty lightning incidents. Lightning causes simultaneous asystole (massive DC standstill) and respiratory arrest (medullary paralysis). The cardiac rhythm often auto-restarts within minutes, but if the victim remains apnoeic they suffer a secondary hypoxic arrest (the "dead-in-bed" sequence). So in a group of lightning casualties, the conscious walking wounded can wait while the apnoeic, pulseless victims are intubated and CPR'd first — they may recover fully after very long down-times.^[1]

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The lightning mantraShowHide

Reverse triage — resuscitate the apparently dead first, because lightning causes asystole plus apnoea, the heart often restarts on its own, and the secondary hypoxic arrest is the killer. Fixed pupils are not brain death.^[1]

Radiation — principles and the triage distinction

Ionising radiation transfers energy to tissue by ionising atoms, generating free radicals that damage DNA. Four types differ in penetration and hazard, and the bedside distinction that governs staff risk is irradiation versus contamination.^[3]

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The cardinal rule: an irradiated patient (exposed to a beam, e.g. gamma) emits no radiation and poses no risk to staff — manage them like any other critically ill patient. A contaminated patient (radioactive dust or liquid on skin, wounds, or inhaled or ingested) is radioactive and requires decontamination and PPE. Incorporation describes uptake of a radionuclide into tissues (iodine into the thyroid, strontium into bone), which then requires decorporation therapy. Life-saving medical treatment never waits for decontamination.^[3]

Acute radiation syndrome — phases and dose-dependent syndromes

ARS follows whole-body exposure above about 1 Gy delivered acutely, and it unfolds in four phases whose timing and severity are dose-dependent — which lets you estimate the dose prospectively.^[6]

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The phases, with their dose-estimation value:^[6]

1. Prodromal phase (minutes to hours, occasionally up to 2 days): nausea, vomiting, anorexia, fatigue, fever, diarrhoea. Time-to-vomiting is a bedside dose estimator — onset under 1 h implies 6 Gy or more (usually fatal); 1 to 2 h about 4 to 6 Gy (serious); over 2 h about 2 to 4 Gy (moderate).
2. Latent phase (days to weeks): the patient looks and feels well — a dangerous interval that can mislead clinicians into under-resourcing. Higher doses shorten the latent phase.
3. Manifest illness phase: the dose-dependent syndrome emerges (haematopoietic, GI, neurovascular).
4. Recovery or death over weeks to months.^[6]

Cutaneous radiation injury (CRI) can co-exist: erythema appears at about 2 Gy, dry desquamation at 6 Gy, moist desquamation or blistering at 10 to 15 Gy, and ulceration or necrosis above 20 Gy. Unlike a thermal burn, radiation skin injury recurs and progresses over weeks as a wave of erythema — biopsy avoidance and specialist wound care are key.^[1]

Radiation biodosimetry — three tools at the bedside

Three complementary tools estimate dose when the history is unreliable, and the viva asks for all three.^[3]

• Serial lymphocyte count — lymphocytes are the most radiosensitive circulating cell; a 50% drop within 24 to 48 h approximates a 2 to 4 Gy exposure, and an absolute lymphocyte count under 0.5 times 10-to-the-9 per litre at 48 h implies a potentially lethal dose. Repeat every 6 to 12 h.
• Time-to-vomiting (above) — the fastest bedside estimator.
• Dicentric chromosome assay — the gold standard biodosimetry; dicentric chromosomes in cultured peripheral lymphocytes are scored, but the assay takes days and is available only in specialist reference laboratories. Useful for confirmation and dose reconstruction.^[8]

Decontamination and medical management

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Potassium iodide warrants a specific exam point: KI does not protect against external radiation, caesium, strontium or any radionuclide other than radioiodine, and it works only if given before or shortly after intake while the thyroid is still taking up iodine. The American Thyroid Association endorses KI distribution to those under 40 years within the plume of a radioiodine release — greatest benefit in children and pregnant or lactating women; in adults over 40 the risk of KI-induced thyroid dysfunction generally outweighs benefit at low-dose exposures.^[7]

Chernobyl and Fukushima — the lessons for ICU

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Chernobyl taught intensivists three durable lessons: iodine prophylaxis works (prompt KI to children demonstrably reduced radiation-induced thyroid cancer, the single clearest preventable long-term outcome); G-CSF, reverse isolation and transfusion support are the mainstay of the haematopoietic syndrome, while allogeneic stem-cell transplant was largely disappointing in the 1986 cohort, especially when ARS was complicated by burns; and contaminated first-responders can overwhelm the system, so decontamination logistics matter as much as biology.^[4]

The named traps and preventable-harm list

Seven errors recur across electrical and radiation injury, and each one is exam material.^[1]

• Reading the voltage, not the current. Estimate the current from the resistance story (wet, sweating, immersed) — a low voltage through wet skin can kill.^[2]
• Reaching for the victim before cutting the power. Pulling a gripped victim from a live AC source injures both; cut the power first.^[2]
• Judging depth by the surface burn. The iceberg effect means formulae based on percentage cutaneous burn miss the deep injury — urine output, CK, myoglobin and compartment pressures guide surgery.^[11]
• Under-resuscitating with a Parkland formula. High-voltage injury needs urine output above the standard burn target — about 1 mL/kg/h in adults.^[11]
• Writing off the lightning arrest victim. Reverse triage applies because victims in cardiopulmonary arrest may gain the greatest benefit from resuscitation efforts, though evidence for longer-than-usual resuscitation times is lacking.^[14]
• Giving potassium iodide for caesium. KI blocks only radioiodine, only if given early — for caesium-137 the decorporation agent is Prussian blue, with calcium and zinc DTPA for transuranics.^[15][3]
• Treating decontamination as resuscitation. Estimating the absorbed radioactive material guides management; medical countermeasures are adjuncts to — never substitutes for — supportive care and resuscitation.^[3]

Red flags

Outcomes

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Etymology for viva gold: keraunoparalysis and the Lichtenberg figure carry the topic's history. Keraunos is Greek for "thunderbolt"; Charcot named the transient paralysis after lightning. The Lichtenberg figure is named for Georg Christoph Lichtenberg, the 18th-century physicist whose dust-pattern experiments prefigured the fern-like marks lightning leaves on skin. Both are named because the physics they describe has not changed.^[1]

Ward-round test

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The three mantras — electrical, lightning, radiationShowHide

Electrical: current not voltage kills — cut the power, fluidise for rhabdomyolysis at twice the burn target, and fasciotomise the tense limb. Lightning: reverse triage — resuscitate the apparently dead first, and fixed pupils are not brain death. Radiation: an irradiated patient is not radioactive and a contaminated patient is — but never delay ABC for decontamination, and give KI only for radioiodine, only early.^[2]

Key trials and evidence

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References17ShowHide

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13. [13]Cunningham PA. The need for cardiac monitoring after electrical injury Med J Aust, 1991.PMID 2046576
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15. [15]Rump A, Stricklin D, Lamkowski A, et al. Benefit-Cost Analysis of Radiocesium Decorporation by a Prussian Blue Treatment and Stockpiling Drug Res (Arzneimittelforschung), 2018.PMID 29036734
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17. [17]Gupta AA, Self M, Mueller M, et al. Dispelling myths and misconceptions about the treatment of acute hyperkalemia Am J Emerg Med, 2022.PMID 34890894