Electrical Injuries and Lightning

• Direct thermal injury from Joule heating: When electrical current passes through tissues with high electrical resistance, energy is converted to heat at a rate proportional to the square of current intensity. Tissues with high water content (nerve, blood, muscle) conduct current more readily and generate less heat, while tissues with low water content (bone, fat, skin) have high resistance and generate tremendous heat locally. This explains why deep muscle damage can occur beneath intact overlying skin—the current follows the path of least resistance through conductive tissues while generating lethal heat in resistant tissues. Skin temperature at the contact point can exceed 500°C, creating full-thickness burns, while deeper tissues experience coagulation necrosis from sustained temperatures of 65°C.

• Disruption of cellular electrical gradients and membrane integrity: Electrical current creates an electrical field across cell membranes that destabilizes the normal resting membrane potential. The sudden depolarization overwhelms the capacitive properties of the lipid bilayer, leading to pore formation in the plasma membrane and loss of selective permeability. This allows uncontrolled calcium influx into cells, triggering excessive muscle contraction (tetanic contraction) and activating calcium-dependent proteases that cause cellular autodigestion. In cardiac myocytes, this can lead to immediate depolarization of the entire myocardium, resulting in ventricular fibrillation (VF) or asystole depending on the timing relative to the cardiac cycle (most likely during the vulnerable period of the T wave). The "let-go current" threshold (typically 50-100 mA for humans) represents the point at which sustained muscle contraction prevents voluntary release from the current source.

• Respiratory center paralysis and skeletal muscle tetany: Electrical current passing through the thorax causes tetanic contraction of respiratory muscles (diaphragm and intercostal muscles), resulting in respiratory arrest even when cardiac function remains intact. The current creates a sustained depolarization of motor neurons innervating respiratory muscles, preventing the normal cycling of contraction and relaxation. This is particularly significant in lightning injuries where the massive current exceeds thresholds needed for respiratory paralysis, explaining why some lightning strike survivors who appear apneic can recover spontaneously if ventilation is provided during the immediate post-strike period. Skeletal muscle tetany produces the characteristic injury pattern of flexor-dominated contractions (flexors are stronger than extensors), potentially causing traumatic injuries such as fractures of long bones, vertebral compression fractures, and posterior shoulder dislocations.

• Coagulation necrosis and tissue destruction along current pathways: Current follows the path of least electrical resistance through the body, typically tracking along blood vessels and nerve pathways (which conduct current readily due to high electrolyte content) before branching through surrounding tissues. As current density increases, tissue undergoes coagulation necrosis with protein denaturation beginning at temperatures above 42°C but accelerating dramatically above 65°C. Unlike thermal burns that affect primarily superficial layers, electrical burns create deep zones of necrosis along the entire current pathway with surrounding zones of tissue edema and inflammation. The initial zone of coagulation is surrounded by zones of stasis (where tissue viability is uncertain) and hyperemia (relatively preserved tissue). This creates the clinical pattern of deep muscle necrosis (rhabdomyolysis) with intact or minimally burned skin, potentially delaying recognition of the severity of injury.

• Vascular thrombosis and delayed tissue loss: Electrical current directly injures the endothelium of blood vessels along the current pathway, triggering platelet aggregation and activation of the coagulation cascade. Vessels may appear initially patent but develop progressive thrombosis over hours to days, leading to demarcation of tissue necrosis that becomes apparent only after initial evaluation. This mechanism explains why initial examination can underestimate the extent of tissue damage and why some electrical burn victims develop unexpected massive tissue loss requiring amputation despite initially appearing salvageable. The thrombosis extends into healthy-appearing tissue at the margins of injury, making determination of the true boundary of necrosis difficult initially.

• Compartment syndrome from muscle edema and rhabdomyolysis: The combination of direct thermal injury, cellular edema from disrupted ionic gradients, and inflammatory mediator release creates massive swelling within fascial compartments. Muscle cells damaged by electrical current release myoglobin and cellular contents into the interstitium, increasing interstitial fluid osmolarity and drawing additional fluid into the compartment. The rigid fascial compartments of the extremities cannot accommodate this volume expansion, creating progressively higher compartment pressures that compromise microvascular perfusion and lead to secondary ischemic necrosis. Myoglobin release into the circulation overwhelms the renal threshold for reabsorption, leading to dark ("cola-colored") urine and acute tubular necrosis if adequate fluid resuscitation is not provided.

• Direct contact with energized electrical sources (household and occupational): Low-voltage electrical sources (typically <1000 volts) in homes and workplaces account for the majority of non-fatal electrical injuries. Common sources include damaged appliances, faulty wiring, wet conditions promoting current flow (bathtubs, swimming pools), and occupational exposure in construction, utility work, and manufacturing. Low voltage is more likely to cause ventricular fibrillation due to current patterns, while high voltage (>1000 volts) more typically causes asystole or respiratory paralysis. Contact can be intentional (self-harm) or unintentional, with the risk increased in the very young (household exploratory contact) and occupationally exposed individuals without adequate training or safety equipment.

• Lightning strike (naturally occurring high-voltage injury): Lightning represents a natural phenomenon delivering 100 million to 1 billion volts with currents of 20,000-200,000 amperes in extremely brief duration (0.0001-0.002 seconds). The massive current overwhelms typical thresholds for cellular injury, frequently causing immediate cardiac arrest (asystole more common than VF), respiratory arrest, and loss of consciousness. Lightning injuries follow seasonal patterns with peaks in summer months, afternoon hours (when thunderstorm activity peaks), and geographic locations with higher thunderstorm frequency (southeastern United States, tropical regions). Risk factors include outdoor occupations, outdoor recreation, standing near tall objects or bodies of water, and use of metal objects during thunderstorms.

• Environmental and behavioral risk factors: Wet skin dramatically reduces surface resistance from approximately 1,000-600,000 ohms (dry skin) to 100 ohms or less, greatly increasing current flow for a given voltage. Immersion injuries (bathtub, pool contact with electrical source) have particularly high mortality due to the large contact area and low environmental resistance. Occupational exposure occurs in utility workers, electricians, construction workers, and agricultural workers exposed to downed power lines. Behavioral factors include failure to use proper safety equipment, working on live circuits, and outdoor activities during thunderstorms. The involvement of children in household electrical injuries often reflects access to outlets and appliances rather than risk-seeking behavior.

• Specific current pathway risk factors: The "hand-to-hand" pathway (typically through both hands, across the chest, and through the heart) is associated with the highest risk for fatal dysrhythmia due to direct passage of current through the cardiac conduction system. The "head-to-foot" pathway (common in lightning strikes where current enters through the head and exits through the feet or ground contact) has a lower dysrhythmia risk but high risk for immediate loss of consciousness and respiratory paralysis. Current passing through the thorax can directly depolarize the myocardium or disrupt the cardiac autonomic nervous system. Lower extremity contact or ground pathway contact has lower mortality but still carries significant morbidity from tissue destruction.

• Immediate loss of consciousness with electrical injuries: Unconsciousness at the time of injury reflects either direct effects of current on the brain (depolarization of cerebral neurons) or secondary hypoxia from respiratory muscle paralysis and cardiac dysrhythmia. The degree of consciousness impairment does not correlate well with eventual neurological outcome, as some patients with initial profound coma recover completely while others with mild initial alterations develop significant delayed neurological complications. Lightning strike victims are more likely to have immediate loss of consciousness compared to low-voltage injury victims. In awake patients, confusion, disorientation, and altered mental status can occur from direct cerebral effects or hypoxic injury.

• Cardiac dysrhythmias and hemodynamic compromise: Ventricular fibrillation (VF) is the most common immediately life-threatening dysrhythmia in low-voltage injuries, occurring particularly when current crosses the chest during the vulnerable period of ventricular repolarization. In contrast, high-voltage and lightning injuries more often produce asystole, a finding that paradoxically carries better prognosis than VF because the heart may resume organized rhythm spontaneously if ventilation and perfusion are maintained. Other dysrhythmias include sinus tachycardia (universal in electrical injuries due to sympathetic stimulation), atrial fibrillation, and various conduction abnormalities. Some patients develop dysrhythmias with a delay of hours after injury despite initial normal rhythm, necessitating extended cardiac monitoring. Coronary artery vasospasm can occur, rarely causing acute myocardial infarction even in young patients without atherosclerotic disease.

• Respiratory compromise from muscle paralysis or airway injury: Tetanic contraction of the diaphragm and intercostal muscles prevents normal respiration, creating respiratory arrest despite intact brainstem respiratory centers. This is the primary life-threatening consequence in many lightning strike victims. Severe burns to the mouth, pharynx, or anterior neck can cause edema that progressively obstructs the airway over hours. Inhalation of combustion products (from ignited clothing or surrounding materials) can cause chemical pneumonitis. Hypoxia can be profound and prolonged if ventilation is not rapidly restored, particularly in patients with continued loss of consciousness or unable to protect their airway.

• Severe burns with distinctive patterns: The "contact burn" (entry wound) typically appears as a small, well-demarcated charred area at the site of electrical contact, often located on the fingertips or palm in contact injuries or on the head/neck in lightning strikes. The "arc burn" results from electrical arcing across joints or skin surfaces, creating linear or branching burn patterns. "Flash burns" from the radiant heat of electrical arcing can cause superficial burns remote from the contact area. The distinctive "Lichtenberg figures" (feathery, branching erythematous patterns resembling lightning) can appear on the skin of lightning strike victims within hours, representing capillary dilation from sympathetic discharge and are usually transient. Deep tissue destruction may be extensive despite minimal skin involvement, as the small contact area concentrates current density while deeper tissues along the current pathway are heated to lethal temperatures.

• Rhabdomyolysis with myoglobinuria: Massive muscle necrosis from electrical injury releases myoglobin into the circulation, visible as dark brown or cola-colored urine when plasma myoglobin concentration exceeds the renal threshold. The presence of myoglobinuria without significant hematuria (distinguishing it from hemoglobinuria) indicates severe muscle injury. Patients may present with flank or extremity pain from compartment syndrome, weakness, and swelling of affected limbs. The rhabdomyolysis can be disproportionate to visible skin injury, as deep muscle groups along the current pathway are destroyed while overlying skin appears relatively intact. Peak creatine kinase levels often exceed 10,000 IU/L and may reach levels >100,000 IU/L, with higher levels correlating with greater risk for acute kidney injury.

• Traumatic injuries from muscle contracture and falls: The flexor muscles, being stronger than extensor muscles, dominate the muscle contraction induced by electrical current, producing characteristic injuries. Posterior shoulder dislocation from traction of the subscapularis muscle is a classic finding in high-voltage injuries and is frequently missed on initial radiographs obtained in the anteroposterior projection (requires axillary or scapular-Y view to visualize). Vertebral compression fractures occur from massive axial loading during tetanic contraction of paraspinal muscles. Long bone fractures of the extremities result from the mechanical force of tetanic contraction overcoming skeletal strength. Falls from heights during or immediately after electrical contact can cause blunt trauma to multiple organ systems, including head injuries with epidural or subdural hematomas.

• Ophthalmologic injuries: Cataracts can develop acutely or with a delay of months to years after significant electrical injury, particularly with lightning strikes or current passing through the head. The exact mechanism is uncertain but likely involves direct heat injury to the lens epithelium. Arc burns to the eyes can cause corneal ulceration and anterior uveitis with severe photophobia and vision-threatening complications. Flash burns create superficial corneal abrasions that are painful but usually resolve without sequelae.

• Neurological deficits (acute and delayed): Transient loss of consciousness is common and usually associated with good recovery, but persistent altered mental status suggests significant injury with poor prognosis. Some patients develop spinal cord injury from direct thermal injury (particularly with current passing through the thoracic spine) or from traumatic injury secondary to falls or muscle contraction-induced vertebral fractures. Respiratory center paralysis from direct current effects on the medulla can occur, sometimes with delayed onset over hours. Peripheral nerve injuries can result from direct thermal injury along current pathways or from compartment syndrome-induced ischemia. Delayed spinal cord dysfunction developing days to months after the initial injury (even without acute neurological deficits) can occur from progressive necrosis along the current pathway.

• Clinical history with attention to injury characteristics: The diagnosis begins with detailed history of the electrical exposure, including voltage of the source (household vs industrial vs lightning), duration of contact, whether contact was direct or through water, and environmental conditions (wet vs dry, indoors vs outdoors during thunderstorm). The mechanism of contact (grasping vs hand-to-hand contact vs lightning strike) helps predict the current pathway and risk for dysrhythmia. Associated trauma history (fall from height, blunt impact) must be documented. Timing of symptom onset and progression helps distinguish immediate effects (dysrhythmia, respiratory paralysis) from delayed complications (compartment syndrome, rhabdomyolysis recognition). Witness accounts are crucial since the patient may be unconscious or unable to recall details.

• Physical examination for entry/exit wounds and hidden burns: The examiner must perform a systematic skin examination looking for entry wounds (typically small, circumscribed, charred contact points, often on hands/fingers in contact injuries or scalp in lightning) and exit wounds (usually larger and more irregular, often on the feet or lower extremities). The absence of visible burns does NOT exclude significant underlying tissue injury, as deep muscle damage can occur with minimal skin involvement. Careful examination for Lichtenberg figures (pathognomonic transient erythematous branching patterns) should be documented in suspected lightning injuries, recognizing that these are frequently not present even in confirmed lightning strikes. Extremities must be examined for compartment firmness suggesting developing compartment syndrome, with particular attention to the compartments of the forearms and lower legs that are most commonly involved. Neurological examination including cranial nerves, strength, sensation, and reflexes should be documented as baseline for comparison given the risk of delayed neurological complications.

• Electrocardiography and cardiac monitoring: 12-lead ECG should be obtained immediately in all electrical injury victims, specifically looking for signs of myocardial injury (ST-segment elevation or depression, T-wave inversions), conduction abnormalities (prolonged QT interval, bundle branch block), and dysrhythmias. The ECG may appear normal despite significant cardiac injury, and a normal initial ECG does not exclude the possibility of delayed dysrhythmia. Patients with any sign of cardiac involvement (symptomatic dysrhythmia, abnormal ECG, syncope, loss of consciousness, chest pain, or high-voltage exposure) require continuous cardiac monitoring for a minimum of 24 hours. Troponin levels should be measured to assess for myocardial injury, though troponin elevation may be falsely negative in the immediate post-injury period and serial measurements may be more sensitive than single measurements.

• Laboratory studies including electrolytes, creatine kinase, and renal function: Creatine kinase (CK) level should be measured immediately to assess the degree of muscle injury, recognizing that CK rises progressively over 24-48 hours and peak levels correlate with risk of acute kidney injury. CK levels >10,000 IU/L

Immediate stabilisation (scene and first minutes)

• Scene safety and source de-energisation: rescuers must not touch the patient until the circuit is confirmed off; downed high-voltage lines create ground-current gradients. Lightning victims carry no residual charge and are safe to touch immediately.
• ACLS with a lightning-specific twist: per the AHA Guidelines for CPR and Emergency Cardiovascular Care (special circumstances of resuscitation), reverse triage applies to multiple lightning casualties — treat the apneic/pulseless victims first, because asystole often self-terminates and death results from prolonged respiratory arrest. Defibrillate ventricular fibrillation/pulseless VT; for asystole/PEA give a vasopressor (epinephrine 1 mg IV/IO every 3–5 minutes) and ventilate. Prolonged resuscitation is justified, particularly in young lightning victims.
• Airway and trauma survey: intubate early for facial/oral burns or depressed consciousness. Follow ATLS (ACS Committee on Trauma) principles with cervical spine precautions, since tetany and falls cause occult fractures.

Fluid resuscitation and rhabdomyolysis

• Isotonic crystalloid (lactated Ringer's) is first-line. The American Burn Association's Advanced Burn Life Support teaching is that surface-area formulas such as Parkland underestimate requirements in electrical injury because burn depth is invisible; titrate instead to urine output, targeting a substantially higher output (roughly 75–100 mL/hr in adults) while pigmented urine persists.
• Urinary alkalinisation with sodium bicarbonate and osmotic diuresis with mannitol are second-line adjuncts of uncertain benefit; they are not a substitute for volume and risk hypocalcemia and alkalosis.
• Hyperkalemia from muscle lysis is treated conventionally (calcium, insulin/dextrose, dialysis if refractory).

Definitive and surgical management

• Fasciotomy for compartment syndrome and escharotomy for circumferential eschar; serial debridement and, not uncommonly, amputation of nonviable limbs.
• Burn centre transfer is an American Burn Association referral criterion for all high-voltage and lightning injuries.
• Tetanus toxoid–containing vaccine per CDC/ACIP.

Contraindicated/avoid

• Prophylactic systemic antibiotics for burn wounds (topical agents only).
• Succinylcholine beyond roughly the first 24 hours after major burn/muscle injury — acetylcholine receptor upregulation causes hyperkalemic arrest; use a nondepolarising agent such as rocuronium.

Emergencies — recognise within minutes to hours

• Ventricular fibrillation / pulseless VT or asystole: direct myocardial depolarisation during the vulnerable T-wave period, or global depolarisation with high-voltage/lightning. Signalled by pulselessness; the only intervention that changes outcome is prompt defibrillation for VF/pulseless VT and ventilation plus CPR for asystole.
• Compartment syndrome: intracompartmental edema from membrane pore formation and myocyte lysis exceeds perfusion pressure. Signalled by pain out of proportion, pain on passive stretch, and a tense compartment — not by loss of pulses, which is a late and unreliable sign. Requires emergent fasciotomy.
• Airway obstruction: progressive edema from oropharyngeal or anterior neck burns; signalled by hoarseness, stridor, or singed perioral tissue. Intubate before the airway is lost.
• Delayed labial artery hemorrhage: the classic toddler who bites an electrical cord develops an oral commissure burn; brisk bleeding occurs roughly 5–14 days later as the eschar separates. Parents must be explicitly counselled.
• Hyperkalemia and myoglobinuric acute tubular necrosis: potassium and myoglobin released from necrotic muscle; signalled by peaked T waves and cola-coloured urine with a urine dipstick positive for blood but few red cells on microscopy.

Subacute and delayed

• Progressive tissue necrosis and limb loss: endothelial injury causes delayed vascular thrombosis, so the demarcation line advances over days — the reason initial assessment underestimates severity.
• Wound sepsis: devitalised deep muscle is an ideal culture medium; signalled by fever, rising leukocytosis, and graft failure.
• Cataracts: lens epithelial thermal injury, presenting months to years later, classically after current through the head.
• Tympanic membrane rupture from the lightning shock wave, and neuropsychiatric sequelae (memory deficits, chronic pain, PTSD).

Treatment-related

• Over-resuscitation causing pulmonary edema, extremity or abdominal compartment syndrome.
• Bicarbonate-induced hypocalcemia, worsened by calcium sequestration in injured muscle.
• Succinylcholine-triggered hyperkalemic arrest after receptor upregulation.

• Low voltage causes VF; high voltage and lightning cause asystole: the exam tests this pair directly. Asystole after lightning paradoxically has the better prognosis because the sinus node may resume automaticity — provided ventilation is supported through the period of respiratory-muscle paralysis.
• Reverse triage in lightning mass casualties: per the AHA's special-circumstances resuscitation guidance, treat the apparently dead first. This inverts the usual triage rule and is the single most commonly tested lightning fact.
• Fixed, dilated pupils after lightning are not a reason to stop resuscitation — they reflect transient autonomic disruption, not brain death. This is the classic distractor.
• Keraunoparalysis: transient blue, pulseless, insensate lower extremities after lightning from vasospasm and sympathetic overactivity; resolves over hours. Do not mistake it for spinal cord transection or arterial occlusion.
• Lichtenberg figures (feathery, branching erythema) are the buzzword for lightning; they are transient capillary phenomena, not true burns, and require no wound care.
• Cola-coloured urine with dipstick positive for blood but no RBCs on microscopy = myoglobinuria. The single best next step is aggressive isotonic crystalloid titrated to urine output, plus CK and potassium — not a bicarbonate drip, and not diuretics.
• The skin lies: minimal-appearing entry and exit wounds can overlie massive deep muscle necrosis, because current tracks along low-resistance vessels and nerves. Surface-area burn formulas therefore underestimate fluid needs (American Burn Association).
• Posterior shoulder dislocation is the classic tetany-related orthopedic injury and is missed on the AP film — order an axillary or scapular-Y view.
• Disposition: an asymptomatic patient after a low-voltage household exposure with a normal ECG and normal examination generally does not require prolonged monitoring; high-voltage exposure, loss of consciousness, arrhythmia, or an abnormal ECG mandates admission with continuous cardiac monitoring.