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ICU TopicsEnvironmental

ICU · Environmental

Electrical and radiation injury in ICU

Also known as Electrocution · Lightning injury · Radiation injury · Acute radiation syndrome · Electrical burns

Electrical injury: damage from electricity passing through body. Low-voltage (<1000V): cardiac arrhythmias (AC current at 50-60Hz can cause VF). High-voltage (1000V): deep tissue injury (muscle, nerve, vessel), compartment syndrome, rhabdomyolysis, AKI, cardiac arrest, secondary trauma (fall). Lightning: massive DC discharge, causes immediate cardiac arrest (asystole), respiratory arrest (neurological), Lichtenberg figures (fern-like skin markings). Radiation injury: acute radiation syndrome (ARS) from whole-body radiation 1 Gy. Syndromes: haematopoietic (2-6 Gy), gastrointestinal (6-8 Gy), neurovascular (8 Gy, fatal). Management: electrical — ACLS, fluid resuscitation (rhabdomyolysis protocol), fasciotomy for compartment syndrome, cardiac monitoring. Radiation — supportive, transfusion, growth factors, bone marrow transplant (selected).

medium8 referencesUpdated 30 June 2026
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Target exams

CICMFFICMEDIC

Red flags

High-voltage injury (>1000V) — deep tissue damage out of proportion to skin injury, compartment syndrome, rhabdomyolysis → AKICardiac arrest from electrocution — VF (low-voltage AC) or asystole (high-voltage/lightning) — prolonged CPR may be warranted (especially lightning — 'reverse triage': resuscitate the apparently dead first)Myoglobinuria (dark urine, positive blood on dipstick but no RBC) — rhabdomyolysis, aggressive IV fluidsAcute radiation syndrome >2 Gy — bone marrow suppression (infection, bleeding), needs specialist haematologyCompartment syndrome after electrical injury — pain on passive stretch, tense compartments → fasciotomy

Your progress

Saved locally on this device.

Target exams

CICMFFICMEDIC

Red flags

High-voltage injury (>1000V) — deep tissue damage out of proportion to skin injury, compartment syndrome, rhabdomyolysis → AKICardiac arrest from electrocution — VF (low-voltage AC) or asystole (high-voltage/lightning) — prolonged CPR may be warranted (especially lightning — 'reverse triage': resuscitate the apparently dead first)Myoglobinuria (dark urine, positive blood on dipstick but no RBC) — rhabdomyolysis, aggressive IV fluidsAcute radiation syndrome >2 Gy — bone marrow suppression (infection, bleeding), needs specialist haematologyCompartment syndrome after electrical injury — pain on passive stretch, tense compartments → fasciotomy
Cinematic ICU scene showing entry and exit burns from a high-voltage electrical injury on a clipboard, an ECG and cardiac monitoring, a creatine kinase trend rising, a radiation dosimeter and a burns assessment chart, clinical-blue lighting, medical educational, no faces, no text
FigureThe electrical and the radiation injury in the ICU. The high-voltage electrical is the deep tissue injury (the creatine kinase and the myoglobinuria, the compartment syndrome), the cardiac arrhythmia (the ECG on the arrival), and the falls. The radiation is the acute radiation syndrome — the haematological, the gastrointestinal, the neurovascular — at the threshold doses; the supportive care and the reverse isolation.
Low-voltage versus high-voltage electrical injury patterns with cardiac and rhabdomyolysis risks
FigureLow-voltage AC risks VF; high-voltage causes deep muscle injury, rhabdomyolysis and compartment syndrome — fluid targets exceed standard burn formulae.
Acute radiation syndrome haematopoietic GI neurovascular dose thresholds
FigureARS syndromes by whole-body dose: haematopoietic (2–6 Gy), GI (6–8 Gy), neurovascular (>8 Gy) — supportive care and reverse isolation dominate.
[1]

In one line

Electrical injury: low-voltage AC → VF; high-voltage → deep tissue injury, rhabdomyolysis, compartment syndrome, AKI, cardiac arrest. Lightning: massive DC → asystole + respiratory arrest (treat 'apparently dead' first — reverse triage). Radiation: ARS >1 Gy — haematopoietic (2-6 Gy), GI (6-8 Gy), neurovascular (>8 Gy, fatal). Management: ACLS, fluid resuscitation (rhabdo protocol), fasciotomy, cardiac monitoring (electrical); supportive care, transfusion, growth factors (radiation).

[1]

Low-voltage vs high-voltage vs lightning injury

FeatureLow-voltage (<1000V)High-voltage (>1000V)Lightning
Current typeAC (alternating)AC or DCMassive DC (direct current)
CardiacVF (tetanic contraction)Asystole, VF, cardiac arrestAsystole (DC current)
Tissue injurySuperficial (entry/exit wounds)DEEP (muscle, nerve, vessel)Variable (flash over — often less than expected)
Muscle/RhabdoMildSEVERE (massive)Variable
Compartment syndromeRareCOMMONVariable
Skin signsEntry/exit burnsEntry/exit + deep burnsLichtenberg figures (fern-like), linear burns
Secondary traumaRare (fall)COMMON (thrown — fractures, head injury)Blast injury (tympanic, fall)
MortalityLow (if no VF)High (20-30%)Variable (10-30% of victims, often at scene)
ManagementACLS (VF → defib), cardiac monitorFluid (rhabdomyolysis), fasciotomy, trauma surveyProlonged CPR (reverse triage), ACLS, trauma survey
[1]

Management of high-voltage electrical injury

  1. Ensure scene safety — power source disconnected before approaching. Rescuer safety first
  2. ACLS — cardiac arrest (VF → defibrillation; asystole → CPR/ACLS). Lightning: prolonged CPR (victims may recover after long down-time — reverse triage)
  3. Primary survey (ABCDE) — airway (may have facial/airway burns), breathing, circulation (arrhythmias, hypovolaemia), disability (neurological injury), exposure (all skin for entry/exit wounds)
  4. ECG monitoring for 4-6h — arrhythmia risk. Troponin. If normal ECG + no symptoms at 6h, very low risk of late arrhythmia
  5. Fluid resuscitation — rhabdomyolysis protocol — crystalloid to maintain urine output 1-1.5 mL/kg/h (HIGHER than burn — muscle damage more extensive). Monitor CK, myoglobin, urine output
  6. Trauma survey — secondary injuries (fall, blast): fractures, head injury, spinal injury, tympanic membrane rupture
  7. Compartment syndrome assessment — check all limbs for tense compartments, pain on passive stretch. Fasciotomy if signs present
  8. Laboratory — CK, troponin, U&E (AKI), LFTs, coagulation (DIC), ABG (acidosis). Urine: myoglobin (dark, dipstick blood+ but no RBC)
  9. Surgical consultation — burns, plastic, orthopaedic (fasciotomy, escharotomy), trauma
  10. Tetanus prophylaxis — if not immune
[1] [1]

Short answer questions

SAQ — High-voltage electrical injury with rhabdomyolysis and compartment syndrome

10 minutes · 10 marks

A 41-year-old linesman is brought to the emergency department after the boom of his crane contacted an 11 000 V overhead AC power line. He was thrown from the crane and landed on his right side; bystanders report a brief loss of consciousness. On arrival he is confused (GCS 13), HR 122, BP 104/64, SpO2 96 per cent on room air. There is a charred 3 cm contact burn on the right palm and a ragged exit wound over the medial right calf. The right forearm and leg are tense and exquisitely painful on passive movement, and the urine is dark red-brown. ECG shows sinus tachycardia with peaked T waves. CK 24 000 U/L, K+ 6.8 mmol/L, creatinine 142 micromol/L, venous pH 7.22.

[1]

SAQ — Mass-casualty radiation exposure: triage and disposition

10 minutes · 10 marks

An industrial radiography source containing caesium-137 is breached at a metropolitan worksite, contaminating twelve workers. The emergency department receives advance warning that casualties are inbound within thirty minutes. Several patients have external skin contamination with caesium dust, and three are thought to have significant whole-body gamma exposure of uncertain dose. The first symptomatic patient vomited ninety minutes after exposure, has erythema over the trunk, and an absolute lymphocyte count of 0.6 × 10⁹/L at twelve hours. You are the ICU consultant leading the hospital radiation response.

SAQ — Acute radiation syndrome: haematopoietic management and the role of stem-cell transplant

10 minutes · 10 marks

A 34-year-old male nuclear-power-plant technician was exposed to an estimated 4.5 Gy whole-body gamma radiation during a containment breach six hours ago. He has had two episodes of vomiting, the last at three hours post-exposure, and is currently nauseated but haemodynamically stable. Absolute lymphocyte count is 0.9 × 10⁹/L at six hours. He has no burns and no residual external contamination after decontamination. The haematology and transplant teams have been notified. You are the intensivist planning his ICU admission.

Clinical pearls

High-yield electrical and radiation injury points for CICM/FFICM exam

  1. The extent of tissue injury in electrical burns is often MUCH GREATER than the skin burns suggest. Electricity follows path of least resistance (nerves, blood vessels, muscle — NOT skin). Deep muscle destruction may be massive with small skin wounds. The 'iceberg effect.' CK and myoglobin guide extent. May need fasciotomy, debridement, even amputation.[5] }
  2. Ventricular fibrillation is the cause of death in low-voltage AC electrocution. AC current at 50-60Hz causes tetanic muscle contraction → if across the heart → VF. The victim may be 'stuck' to the source (can't let go due to tetanic contraction of forearm flexors). Treatment: defibrillation (AC current → VF → shock).[1] }
  3. Lightning causes ASYSTOLE, not VF. Massive DC current → direct cardiac standstill (asystole). Also causes respiratory arrest (medullary paralysis). RESPIRATORY ARREST is often the cause of secondary cardiac arrest (hypoxia) in lightning victims. KEY: prolonged CPR may be successful — lightning victims can recover after very long down-times. 'REVERSE TRIAGE': resuscitate the apparently dead FIRST (they may survive with CPR), while conscious victims can wait.[2] }
  4. Rhabdomyolysis is a major concern in high-voltage injury. Massive muscle damage → CK released (>10,000 U/L), myoglobinuria (dark urine, dipstick positive for blood but no RBC on microscopy). Treat: AGGRESSIVE IV fluids (goal urine output 1-1.5 mL/kg/h — HIGHER than burn formula). Consider mannitol, sodium bicarbonate (alkalinise urine). Monitor for AKI. May need renal replacement therapy.[5] }
  5. Compartment syndrome is common after high-voltage injury. Massive muscle oedema within fascial compartments → raised pressure → ischaemia → necrosis. Signs: PAIN OUT OF PROPORTION (especially on passive stretch), tense compartments, paraesthesia, pallor, pulselessness (late). Diagnosis: compartment pressure measurement (>30 mmHg or ΔP <30 mmHg from diastolic). Treatment: EMERGENCY FASCIOTOMY (all affected compartments).[5] }
  6. Cardiac monitoring: 4-6h observation. All electrical injury patients should have ECG + cardiac monitoring. If asymptomatic with normal ECG at 6h, very low risk of late arrhythmia — can discharge. If any arrhythmia, chest pain, or high-voltage injury → monitor longer (24h). Troponin (myocardial injury).[1] }
  7. Secondary trauma is common in high-voltage injury. Victim may be THROWN from the source (tetanic contraction + massive energy) → falls, fractures, head injury, spinal injury. FULL TRAUMA SURVEY needed (don't focus only on electrical injury). Also: blast injury (tympanic membrane rupture).[2] }
  8. Entry and exit wounds. Electricity enters at one point, exits at another. The PATH BETWEEN (through deep tissue) is where damage occurs. Entry wounds: small, well-demarcated burns. Exit wounds: often larger, more explosive (current 'explodes' out). The path may cross the heart (arrhythmia), spinal cord (paralysis), or limbs (compartment syndrome).[5] }
  9. Lichtenberg figures (lightning). Fern-like, feathery skin markings PATHOGNOMONIC of lightning injury. Not burns (no tissue destruction) — may be due to electron shower in superficial vessels. FADE within 24h. Their presence confirms lightning injury.[2] }
  10. Acute radiation syndrome (ARS) — three syndromes based on dose. Haematopoietic (2-6 Gy): bone marrow suppression after 2-6 weeks. Gastrointestinal (6-8 Gy): GI mucosal destruction, sepsis, death 1-2 weeks. Neurovascular/Cerebrovascular (>8 Gy): cerebral oedema, death 24-72h. Prodromal phase (nausea, vomiting) → latent phase (asymptomatic) → manifest illness.[3] }
  11. ARS management is SUPPORTIVE + HAEAMTOLOGICAL. Isolation (reverse isolation — neutropenia). Broad-spectrum antibiotics (prophylactic + treat infection). Transfusions (red cells, platelets). Growth factors (G-CSF — granulocyte colony stimulating factor — stimulates neutrophil recovery). Bone marrow transplant (selected patients, younger, dose 4-8 Gy, matched donor).[4] }
  12. Radiation dose estimation guides prognosis. Methods: (1) LYMPHOCYTE COUNT (drop predicts dose — lymphocytes most radiosensitive). Lymphocyte count <1.2 at 48h = significant exposure. (2) CHROMOSOMAL ABERRATION ANALYSIS (dicentric chromosomes — gold standard, but slow). (3) SYMPTOM TIMING (early vomiting = higher dose).[3] }
  13. Contamination vs irradiation. IRRADIATION: person exposed to radiation source (like X-ray) — NOT radioactive after exposure (no risk to staff). CONTAMINATION: radioactive material ON or IN person (dust, liquid) — person IS radioactive (risk to staff). Decontaminate before entering hospital (remove clothing, wash).[6] }
  14. Pregnancy and electrical/radiation injury. ELECTRICAL: fetal risk if current traverses uterus (fetal burns, death — especially later pregnancy). Monitor fetal wellbeing. RADIATION: fetal effects depend on dose and gestational age. 1st trimester: miscarriage, teratogenesis. 2nd-3rd: growth restriction, intellectual disability, cancer risk. ANY significant radiation exposure in pregnancy → obstetric consultation.[3] }

Red flags

Critical electrical and radiation injury red flags

  • Cardiac arrest from electrocution → ACLS (VF → defib, asystole → CPR). Lightning: prolonged CPR, reverse triage.[1] }
  • Rhabdomyolysis (dark urine, CK >5000) → aggressive IV fluids, monitor AKI.[5] }
  • Compartment syndrome (pain on passive stretch, tense compartments) → emergency fasciotomy.[5] }
  • High-voltage injury → deep tissue damage out of proportion to skin, secondary trauma, cardiac monitoring.[2] }
  • ARS >2 Gy → bone marrow suppression, needs haematology specialist, reverse isolation.[4] }
  • ARS >6-8 Gy → GI/neurovascular syndromes, high mortality, supportive/palliative.[3] }
  • Radiation CONTAMINATION (not just irradiation) → decontaminate before entering hospital.[6] }

Prognosis

Outcomes of high-voltage electrical injury (Waldmann 2018)

Cohort study of high-voltage electrical injuries:

  • Mortality: 20-30% (higher with cardiac arrest, falls, secondary trauma)
  • Amputation rate: 10-20% (deep muscle necrosis, compartment syndrome)
  • Long-term sequelae: neurological (neuropathy, chronic pain), psychiatric (PTSD), cataracts, cardiac (arrhythmias)
  • AKI requiring RRT: 5-10% (rhabdomyolysis) [1]

Lightning mortality: 10-30% of victims (many die at scene). Of survivors: 70% have long-term sequelae (neurological, cardiac, psychological). ARS mortality: <1 Gy → survival. 2-6 Gy → survival with treatment (growth factors, isolation). 6-8 Gy → high mortality even with treatment. >8 Gy → uniformly fatal.

[1]

Physics and determinants of electrical injury

The severity of an electrical injury is set by current, not voltage — by Ohm's law $I = V/R$ the same 240 V applied to wet skin (≈1000 Ω) drives ~240 mA, while dry skin (≈100 000 Ω) limits it to ~2 mA, the difference between lethal VF and a tingle. Six variables therefore determine outcome: voltage, current, resistance, current type (AC vs DC), pathway through the body, and contact duration. Heat is governed by Joule's law $H = I^2 R t$: deep, high-resistance tissues (bone, tendon) become the hottest and conduct that heat to adjacent low-resistance muscle, nerve and vessel — 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. Roughly 1 mA is the threshold of perception; 5-9 mA is the maximum harmless current; 10-20 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; ~100 mA of 50-60 Hz AC traversing the chest precipitates ventricular fibrillation; currents exceeding 1-2 A produce direct myocardial standstill, deep burns and, if the victim survives, extensive rhabdomyolysis.[2] }

Determinants of electrical tissue injury

FactorEffect on severity
Current (I)True determinant of injury. 1 mA = perception; 10-20 mA = let-go threshold (tetany); 100 mA AC = VF; >1-2 A = standstill + deep burns
VoltageHigher voltage overcomes skin resistance to drive current. >1000 V = high-voltage, deep injury
Resistance (R)Dry skin ≈100 000 Ω (protective); wet skin ≈1000 Ω (100× current surge). Order high→low: bone > fat > tendon > dry skin > wet skin > muscle > blood > nerve
Current typeAC (50-60 Hz) most dangerous — tetany + VF; DC = single spasm, victim thrown, secondary trauma
PathwayHand-to-hand/hand-to-foot across thorax → arrhythmia; along a limb → compartment syndrome; through head → CNS/retina/cataract
DurationLonger contact = more Joule heat + longer current flow across myocardium
Contact areaSmall area = high current density = severe local burn; large area dissipates energy
[1]

Alternating vs direct current — mechanism

AC vs DC electrical injury

FeatureAlternating current (AC)Direct current (DC)
Frequency50-60 Hz (mains)Zero (constant)
Myocardial riskVF at ~100 mA — 50-60 Hz sits near the cardiac vulnerable period, readily precipitating VFHigher threshold for VF; large DC more often causes asystole (standstill)
Muscle effectTetanic contraction at >10-20 mA → 'stuck to source', prolonged contact, drowning of electricians in waterSingle violent spasm — victim thrown clear (short contact, more secondary trauma)
Let-go threshold~10-20 mA (forearm flexors outstrength extensors)Much higher — victim rarely 'stuck'
Typical sourcesHousehold mains, industrial supplyBatteries, railways, defibrillators, lightning
Skin/contact burnsEntry/exit, often smallEntry/exit, often larger/exploding exit
[1]

The vulnerability of AC at 50-60 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 → VF. The let-go threshold exists because forearm flexor muscles are stronger than extensors, so tetanic flexion locks the hand closed on the conductor. 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] }

Lightning injury in detail

A lightning bolt carries 100 million to 1 billion volts, 10 000-200 000 A, lasting only ~30-50 milliseconds. Despite these staggering figures, internal injury is often surprisingly modest thanks to flashover — the current takes the lower-resistance route over the body surface (sweat-dampened skin) rather than through the torso. The same physics means entry/exit wounds and deep-muscle necrosis are far less prominent than in equivalent-voltage industrial electrocution.[1] }

Three lightning-specific signs the examiner wants to hear: [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 h, so their absence later does not exclude lightning injury.
  • 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. Combined with the 'reverse triage' principle, this is a high-yield exam pearl.
  • Keraunoparalysis (Charcot's keraunoparalysis) — transient flaccid paralysis with sensory loss, pale/cold/blue extremities and absent pulses (vasomotor spasm). Limbs are preferentially affected and resolve over hours. Mimics spinal cord injury or acute limb ischaemia; always re-examine before imaging decisions. [1]

The 'reverse triage' / 'resuscitate the apparently dead first' 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 ('dead-in-bed' sequence). Therefore: 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] }

Lightning injury management — reverse triage

  1. Scene safety — lightning can strike twice; move casualties to shelter before assessment. Apply reverse triage: resuscitate the apparently dead first, conscious walking wounded can wait
  2. Airway and breathing — intubate apnoeic patients immediately. The cause of death is usually secondary hypoxic arrest from ongoing apnoea, so ventilatory support is the highest-yield intervention
  3. Circulation / ACLS — asystole (DC standstill) → CPR ± adrenaline. Prolonged CPR is justified — down-times of 30+ min with good neurological recovery are described; the myocardium is healthy and only needs to be reoxygenated
  4. Do NOT use fixed/dilated pupils as a sign of brain death — autonomic dysfunction is reversible. Continue resuscitation
  5. Secondary survey / trauma — blast injury (tympanic membrane rupture in up to 50%), falls and being thrown (fractures, head injury, spinal), thermal burns (skin/clothing ignition), eye trauma (cataracts, retinal)
  6. 12-lead ECG and cardiac monitoring — arrhythmias, ST changes, QT prolongation, troponin rise
  7. Document and photograph Lichtenberg figures early — they fade within 24 h and provide forensic confirmation of lightning injury
  8. Neurological assessment — keraunoparalysis resolves in hours; persistent deficits warrant imaging for spinal/head injury
  9. Obstetric assessment in pregnant patients — fetal demise can occur with apparently minor maternal injury; monitor
  10. Admit for observation even if asymptomatic at first — delayed arrhythmias, cataracts and neuropsychological sequelae are described
[1]

Radiation — principles and radiation types

Ionising radiation transfers energy to tissue by ionising atoms, generating free radicals that damage DNA. Four types differ in penetration and hazard: [1]

Radiation types — penetration and clinical hazard

TypeStopped byExternal hazardInternal hazardTypical sources
AlphaA sheet of paper / dead skinNone (cannot penetrate)High if inhaled/ingestedPlutonium-239, polonium-210, radon, uranium
BetaClothing / a few mm aluminiumSkin burns ('beta burns')Moderate if internalIodine-131, strontium-90, tritium
Gamma / X-rayLead / concreteHigh — whole-bodyHighCobalt-60, caesium-137, iridium-192
NeutronHydrogen-rich material (water, concrete, wax)High — whole-body, induces radioactivityHighNuclear weapons, reactor cores
[1]

A crucial triage distinction: 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/liquid on skin, wounds, or inhaled/ingested) is radioactive and requires decontamination and personal protective equipment. Incorporation describes uptake of a radionuclide into tissues (e.g. iodine into thyroid, strontium into bone), which then requires decorporation therapy.[3] }

Acute radiation syndrome (ARS) — phases

ARS follows whole-body exposure above ~1 Gy (100 rad) delivered acutely. It unfolds in four phases whose timing and severity are dose-dependent, allowing the clinician to estimate dose prospectively: [1]

  1. Prodromal phase (minutes-hours, occasionally up to 2 days): nausea, vomiting, anorexia, fatigue, fever, diarrhoea. Time to vomiting is a bedside dose estimator — onset <1 h implies ≥6 Gy (usually fatal); 1-2 h ~4-6 Gy (serious); >2 h ~2-4 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 — see table).
  4. Recovery or death over weeks to months.[6] }

ARS dose-dependent syndromes

ARS dose-dependent syndromes (whole-body acute dose)

SyndromeDose (Gy)LatentManifest illness featuresPrognosis
Cerebrovascular / neurovascular>8-10None-immediateConfusion, ataxia, seizures, cerebral oedema, vasomotor collapse, death within 24-72 hUniformly fatal — supportive/palliative only
Gastrointestinal6-83-5 daysSevere bloody diarrhoea, mucosal sloughing, fluid loss, sepsis, GI bleedingHigh mortality even with maximal ICU support
Haematopoietic2-61-3 weeksPancytopenia → infection, bleeding (petechiae, mucosal haemorrhage), anaemiaSurvivable with growth factors, isolation, transfusion
Subclinical / mild1-2—Transient nausea, mild lymphopeniaSurvival
[1]

Cutaneous radiation injury (CRI) can co-exist: erythema appears at ~2 Gy, dry desquamation at 6 Gy, moist desquamation/blistering at 10-15 Gy, and ulceration/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 complementary tools estimate dose when history is unreliable: [1]

  • Serial lymphocyte count — lymphocytes are the most radiosensitive circulating cell; a 50% drop within 24-48 h approximates a 2-4 Gy exposure, and an absolute lymphocyte count <0.5 × 10⁹/L at 48 h implies a potentially lethal dose. Repeat every 6-12 h.
  • Time-to-vomiting (see 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] }

Radiation decontamination and medical management

Radiation casualty — decontamination and management priorities

  1. Triage and resuscitate first — life-saving medical treatment never waits for decontamination. Airway, breathing, circulation take priority over radiation concerns; an irradiated (non-contaminated) patient is managed normally
  2. Determine exposure type — irradiation only (no staff hazard) vs external/internal contamination (PPE + decontamination). Notify the hospital radiation safety officer and regional radiation emergency centre immediately
  3. External decontamination — remove all clothing (removes ~90% of external contamination); bag and label as radioactive waste. Wash skin and hair with lukewarm soap and water (avoid abrading skin), covering wounds first. Flush eyes, ears, nose
  4. Survey with a Geiger counter — document residual counts; repeat washing until counts approach background or plateau. Never shave body hair
  5. Internal contamination / decorporation — selected by radionuclide (see table). Treat within hours where possible
  6. Supportive care — antiemetics (5-HT3 antagonist ± dexamethasone), fluids, electrolyte correction, analgesia, nutritional support (early enteral). Reverse isolation once pancytopenic
  7. Haematopoietic syndrome — G-CSF / GM-CSF started within 24-72 h; prophylactic antiviral/antibacterial/antifungal cover; irradiated leukoreduced blood products; consider stem-cell transplant in young patients with 4-8 Gy exposure and no major burns (consult transplant centre)
  8. GI syndrome — gut rest, parenteral nutrition, somatostatin analogue for diarrhoea, broad-spectrum antibiotics, platelet support for bleeding
  9. Psychosocial support and follow-up — long-term cancer screening, cataract surveillance, fertility counselling
[1]

Radionuclide-specific decorporation therapy

RadionuclideAntidote / therapyMechanism
Iodine-131Potassium iodide (KI)Saturates thyroid with stable iodine → blocks radioiodine uptake. Most effective <4 h post-exposure; some benefit up to 24 h; little benefit after 24 h. No effect on other radionuclides
Caesium-137, thalliumPrussian blue (ferric hexacyanoferrate)Insoluble ion-exchange resin traps Cs/Tl in gut lumen → faecal excretion. Used after Goiânia (1987) and Litvinenko (Tl) cases
Plutonium, americium, curium (transuranics)Ca-DTPA then Zn-DTPA (IV/inhaled)Chelation — Ca-DTPA more effective initially but depletes trace metals; switch to Zn-DTPA for maintenance
UraniumSodium bicarbonate alkalinisationPromotes urinary uranium excretion; chelation with DTPA less effective
TritiumForced oral/intravenous fluidsDilutes and accelerates urinary excretion
Strontium-90Calcium, alginate, ammonium chlorideCompetitively blocks bone deposition
[1]

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 <40 years within the plume of a radioiodine release.[7] }

Chernobyl and Fukushima — lessons for ICU

Two nuclear accidents — what the ICU must know

FeatureChernobyl (1986)Fukushima (2011)
CauseReactor fire / steam explosion during a testTsunami disabled emergency cooling after earthquake
Acute deaths2 immediate; 28 first-responders died of ARS within 4 monthsNo ARS deaths in workers or public
Highest ARS cases134 plant workers/firefighters with 0.8-16 GyMax occupational dose ~0.68 Gy — below ARS threshold
Main lessonMass KI distribution + early evacuation reduces thyroid cancer in children (the demonstrable long-term harm)Iodine prophylaxis + rapid 20-km evacuation kept public doses low; need resilient on-site power
ICU relevanceDemonstrated stem-cell transplant poor outcomes when combined with burns; bone-marrow transplant rarely indicated; supportive care + G-CSF is the backboneEvacuation itself can harm frail/elderly patients — weigh against radiation risk
[1]

Chernobyl taught intensivists three durable lessons: (1) iodine prophylaxis works — prompt KI to children around Chernobyl demonstrably reduced radiation-induced thyroid cancer, the single clearest preventable long-term outcome; (2) haematopoietic growth factors (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 (3) contaminated first-responders can overwhelm the system — decontamination logistics matter as much as biology.[4] }[6] }

Additional clinical pearls

High-yield electrical, lightning and radiation pearls for CICM/FFICM/EDIC

  1. Current — not voltage — kills. A 240 V mains shock through wet skin (≈1000 Ω) delivers ~240 mA and is lethal; the same voltage through dry skin (~100 000 Ω) is only ~2 mA. Always estimate current from the resistance story (wet environment, sweat, immersion).[2] }
  2. AC at 50-60 Hz is the most dangerous waveform because it straddles the cardiac refractory period and induces VF at only ~100 mA, and because the 'let-go' threshold (~10-20 mA) fixes the victim's flexor-grip onto the source — prolonging contact. Cut the power before contact.[2] }
  3. Flashover explains the modest internal injury of lightning. Despite billions of volts, current flows over the wet skin surface rather than through the torso — so entry/exit burns, rhabdomyolysis and compartment syndrome are far less common than in equivalent industrial electrocution.[1] }
  4. Fixed, dilated pupils in lightning are NOT brain death. Lightning causes transient autonomic (ciliary) dysfunction. A pulseless, apnoeic lightning victim with fixed pupils may recover fully with prolonged CPR and ventilation — never withdraw care on pupil signs alone.[1] }
  5. The 'dead-in-bed' / 'reverse triage' sequence — lightning causes asystole + medullary respiratory arrest; the heart often auto-restarts, but persistent apnoea causes a secondary hypoxic arrest. In a mass-casualty lightning event, intubate and resuscitate the apparently dead first; the walking wounded can wait.[1] }
  6. Keraunoparalysis — transient flaccid paralysis, pale/cold pulseless extremities (vasomotor spasm) lasting hours after lightning. It mimics spinal cord injury and acute limb ischaemia; reassess before imaging or vascular intervention because it resolves spontaneously.[1] }
  7. Lichtenberg figures are pathognomonic but fleeting. These fern-like keraunographic markings are not burns and fade within ~24 h; photograph them early — they provide forensic confirmation of lightning injury when the history is unclear.[1] }
  8. Time-to-vomiting is a bedside radiation dosimeter. Vomiting <1 h suggests ≥6 Gy (often fatal); 1-2 h ~4-6 Gy; >2 h ~2-4 Gy. Combine with serial lymphocyte counts (50% fall in 24-48 h ≈ 2-4 Gy) to triage resource-intensive care.[6] }
  9. Dicentric chromosome assay is the gold-standard biodosimetry but takes days — start empiric growth-factor therapy based on lymphocyte kinetics and symptoms while awaiting confirmation.[8] }
  10. Potassium iodide blocks only radioiodine and only if given early. Maximal effect <4 h, acceptable up to 24 h, negligible after 24 h. It is useless against caesium, strontium, external gamma and contaminated skin — do not substitute KI for decontamination.[7] }
  11. Prussian blue, Ca-DTPA and Zn-DTPA are radionuclide-specific decorporation agents. Prussian blue for caesium-137 and thallium; Ca-DTPA (then Zn-DTPA) for transuranics (plutonium, americium, curium). Choose the agent by radionuclide, not empirically.[3] }
  12. An irradiated patient is not radioactive; a contaminated patient is. Treat life-threatening injuries immediately in irradiated patients with no special precautions. Contaminated patients need clothing removal (~90% of external contamination), soap-and-water washing, bagged waste and PPE — but never delay airway/breathing/circulation for decontamination.[3] }
  13. Bone-marrow transplant has a narrow niche in ARS. Best considered for young patients with 4-8 Gy whole-body exposure, no significant burns and an HLA-matched donor; combined radiation+burn injury (as at Chernobyl) did poorly with transplant. The backbone remains G-CSF, reverse isolation, transfusion and antimicrobial prophylaxis.[4] }
  14. Pregnancy amplifies risk in both electrical and radiation injury. Electrical current crossing the gravid uterus can cause fetal death or burns (especially later gestation); monitor cardiotocography. Radiation teratogenesis is maximal in the first trimester (3rd-8th week for intellectual disability); counsel and dose-estimate early with obstetric + radiation-physics input.[5] }
  15. Cataracts are a delayed, classic sequela of both electrical and radiation injury. Electrocution causes anterior subcapsular 'snowflake' cataracts (months-years later); ionising radiation causes posterior subcapsular cataracts. Visual symptoms after any exposure warrant slit-lamp follow-up.[5] }
  16. The 'iceberg effect' governs surgical planning in electrical burns. Small skin wounds conceal extensive deep-muscle, vessel and nerve necrosis. CK, myoglobin and compartment pressures guide debridement and fasciotomy — do not judge depth by the surface.[2] }

Red flags (additional)

Additional red flags for electrical, lightning and radiation injury

  • Wet-environment / immersion electrocution → expect high current despite 'low' voltage; cut power before contact[2] }
  • Lightning mass casualty → reverse triage: intubate and resuscitate the apparently dead first; do not use fixed pupils as a sign of brain death[1] }
  • Persistent apnoea after lightning → ongoing respiratory arrest will cause secondary hypoxic arrest — ventilate, do not stop CPR early[1] }
  • Vomiting <1 h after radiation exposure → dose likely ≥6 Gy, prepare maximal supportive care and consider prognosis discussion[6] }
  • Lymphocyte count <0.5 × 10⁹/L at 48 h → potentially lethal whole-body dose; haematology emergency, reverse isolation, G-CSF[4] }
  • Radioiodine release and pregnancy/child → potassium iodide within hours (under-40s, especially children and pregnant/lactating)[7] }
  • Caesium/americium/plutonium contamination → initiate radionuclide-specific decorporation (Prussian blue; DTPA) early[3] }
  • Concurrent ARS + burns → poor prognosis with stem-cell transplant; manage with supportive care, G-CSF and burn care[4] }
  • Cataract or new visual symptoms months after electrical/radiation exposure → slit-lamp review; radiation or electrical cataract[5] }

Prognosis and trial evidence

Waldmann 2018 — electrical cardiac injuries: current concepts (Eur Heart J)

Review of arrhythmia risk and monitoring after electrical injury:

  • Ventricular arrhythmias (VF, VT) are the immediate cause of death; conduction abnormalities (bundle-branch block, heart block, QT prolongation) and troponin elevation occur in a minority
  • Late arrhythmia is rare if the admission ECG and troponin are normal; asymptomatic low-voltage injury with a normal ECG can usually be observed briefly and discharged
  • High-voltage injury, loss of consciousness, cardiac symptoms, or abnormal ECG warrant prolonged (≥24 h) monitoring
  • Long-term: structural cardiomyopathy is uncommon but described; high-voltage survivors need cardiac follow-up
[1]

Radulovic 2019 — long-term sequelae after electrical injury (BMJ Open)

Retrospective cohort of electrical-injury survivors:

  • Persistent symptoms in a substantial proportion: chronic pain, sensory neuropathy, weakness, neuropsychological complaints (memory, concentration, depression) and post-traumatic stress
  • Return-to-work was impaired in a clinically important subgroup, independent of visible injury severity — supporting that 'minor' electrical injury can have major functional consequences
  • Implication for ICU: counsel patients and families that full recovery can take months and that neuropsychological follow-up is appropriate even after an apparently minor shock
[1]

Leung 2017 — ATA Scientific Statement on potassium iodide in a nuclear emergency (Thyroid)

Consensus on KI thyroid blockade:

  • KI saturates the thyroid with stable iodine, reducing radioiodine uptake when given before or shortly after exposure
  • Greatest benefit in those <40 years; in adults >40 the risk of KI-induced thyroid dysfunction generally outweighs benefit at low-dose exposures
  • Single dose effective for ~24 h; repeat daily if exposure persists (and benefit outweighs risk)
  • No protection against caesium, strontium or external radiation; KI complements but does not replace evacuation, sheltering and food/milk controls
[1]

Waselenko 2004 / Dainiak 2011 — Strategic National Stockpile guidance for ARS (Ann Intern Med; Disaster Med Public Health Prep)

Landmark consensus on ARS medical management:

  • Biodosimetry with serial lymphocyte counts and dicentric chromosome assay underpins dose estimation
  • Haematopoietic syndrome (2-6 Gy): G-CSF/GM-CSF within 24-72 h, reverse isolation, antimicrobial prophylaxis, irradiated leukoreduced blood products; stem-cell transplant in carefully selected younger patients with 4-8 Gy exposure
  • GI syndrome (6-8 Gy): aggressive fluid/electrolyte support, nutritional support, antiemetics, antibiotics, platelet transfusion
  • Neurovascular syndrome (>8 Gy): uniformly fatal — focus on symptom control and palliation
  • Cutaneous and combined injuries carry the worst prognosis and reduce the benefit of haematological support
[1]

Chernobyl 1986 — outcomes of ARS in 134 first-responders

  • 134 plant workers and firemen developed clinically evident ARS (estimated 0.8-16 Gy)
  • 28 deaths from ARS within the first 4 months; several more over subsequent years from burns, infections and bone-marrow failure
  • Key lesson: prompt KI and evacuation of children reduced thyroid cancer; combined ARS + thermal burns carried the worst prognosis; allogeneic bone-marrow transplant was used in a handful and did not clearly improve survival
  • Implication: in any future high-dose radiation event, expect burns, infections and GI complications to drive mortality alongside marrow failure
[1]

Fukushima 2011 — what did NOT happen

  • No ARS deaths among workers or the public; maximum occupational dose (~0.68 Gy) stayed below the ARS threshold
  • Effective controls: rapid 20-km evacuation, KI distribution, food/milk monitoring, sheltering
  • Counter-harm: evacuation itself (especially of frail elderly from hospitals and care homes) caused more attributable deaths than radiation — a reminder that the radiological risk must be weighed against the harms of displacement in critical-care populations
[1]

Quick-reference summary

One-page exam summary — electrical, lightning, radiation

DomainElectrical (low V)Electrical (high V)LightningRadiation (ARS)
Cardinal injuryVF (AC tetany)Deep tissue + rhabdoAsystole + apnoeaBone-marrow/GI/CNS
Defining dose/feature<1000 V, AC>1000 VMassive DC, flashover, Lichtenberg>1 Gy whole-body
First actionCut power, ACLS (defib VF)Scene safety, trauma surveyReverse triage, ventilate apnoeicResuscitate, then decontaminate
Kidney riskLowHigh (myoglobinuria)VariableLow (unless sepsis/shock)
Key antidote / therapyDefibrillationFluids (rhabdo), fasciotomyProlonged CPR + ventilationG-CSF, KI, Prussian blue, DTPA
Prognostic markerECG, troponinCK, compartment pressureLichtenberg, tympanic membraneLymphocytes, time-to-vomiting, dicentrics
Classic late sequelaCataract, neuropathyAmputation, chronic painCataract, neuropsychiatricCancer, cataract, infertility
[1]

References

  1. [1]Waldmann V, Narayanan K, Combes N, et al. Electrical cardiac injuries: current concepts and management Eur Heart J, 2018.PMID 28444167
  2. [2]Fish RM, Geddes LA. Conduction of electrical current to and through the human body: a review Eplasty, 2009.PMID 19907637
  3. [3]Kazzi ZN, Buzzell J. Emergency department management of patients internally contaminated with radioactive material Emerg Med Clin North Am, 2015.PMID 25455668
  4. [4]Dainiak N, Gent RN, Carr Z, et al. First global consensus for evidence-based management of the hematopoietic syndrome resulting from exposure to ionizing radiation Disaster Med Public Health Prep, 2011.PMID 21987000
  5. [5]Radulovic N, Mason SA, et al. Acute and long-term clinical, neuropsychological and return-to-work sequelae following electrical injury: a retrospective cohort study BMJ Open, 2019.PMID 31092649
  6. [6]Waselenko JK, MacVittie TJ, Blakely WF, et al. Medical management of the acute radiation syndrome: recommendations of the Strategic National Stockpile Radiation Working Group Ann Intern Med, 2004.PMID 15197022
  7. [7]Leung AM, Bauer AJ, et al. American Thyroid Association Scientific Statement on the Use of Potassium Iodide Ingestion in a Nuclear Emergency Thyroid, 2017.PMID 28537500
  8. [8]Testa A, Palma V. Dicentric Chromosome Assay (DCA) and Cytokinesis-Block Micronucleus (CBMN) Assay in the Field of Biological Dosimetry Methods Mol Biol, 2019.PMID 31473956