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Lightning Injuries Clinical Presentation

  • Author: Mary Ann Cooper, MD; Chief Editor: Joe Alcock, MD, MS  more...
 
Updated: Jun 06, 2016
 

History

Lightning injuries are obvious if they occur in a group setting with witnesses present. However, lightning injuries can be difficult to diagnose if the person presents without witnesses, is unable to relate the details of his or her injury, or is found dead in a field, mountain side, or street.[83]

Often, the person can relate what happened. However, it is common for the person to have anterograde amnesia or confusion.[23] While the person may be able to carry on a reasonably coherent social conversation, giving demographic and billing data, the examiner may also observe that he or she repeats the same questions multiple times or may not remember events in the emergency department (ED). More disturbing symptoms such as not recognizing a family member should draw suspicion for malingering or other litigious behavior.

Next

Physical Examination

Each patient must receive a complete physical examination, including a neurologic assessment and a thorough examination of the skin for wounds and burns. Physical presentation may vary from mild disorientation with no immediate physical signs to cardiac arrest (the only direct cause of death) and anoxic brain injury. Conscious patients most often complain of muscle aches, dysesthesias, headaches, weakness, or other neurologic/musculoskeletal problems.[10, 23]

Indications of lightning injury noted on physical examination include the following:

  • Cold, pulseless extremities - A sign of vasomotor instability
  • Confusion, amnesia, paralysis, and loss of consciousness
  • Temporary hearing loss or tympanic membrane rupture - Caused by concussive shock wave
  • Hypotension - Usually from vasomotor instability and spasm but spinal cord injuries and other more common causes should be ruled out
  • Prolonged paresis or paralysis of the extremities - Indicates possible spinal cord injuries
  • Fixed and dilated pupils - Typically a result of transient autonomic disturbances, not serious head injuries; pupillary areflexia and dilatation therefore cannot be used as a reason to stop resuscitation
  • Lichtenberg figures - Rare but pathognomonic of lightning injury; also known as ferning pattern or keraunographic markings [96] or other singeing of hair or clothing
  • Clothing that is singed, shredded, or blown apart; shoes that appear to be exploded from the inside; magnetized watches, zippers, or other metal objects; streaming and cuprification of brass grommets or zippers.

Hypothermia

Because lightning injuries occur most commonly outdoors, often in wilderness or where the person may lie exposed for a period, hypothermia should be ruled out.

Cardiorespiratory symptoms

Cardiorespiratory arrest is the only known direct cause of death. Lightning may send the heart into momentary asystole, from which the heart often spontaneously recovers. Autonomic nervous system control of cardiac rhythm has been shown to be affected by lightning. In some cases, respiratory arrest may last longer than the initial cardiac arrest and a secondary cardiac arrest from hypoxia, from more serious brain injury prolonging the respiratory arrest, or from other unknown causes may occur.[10, 17, 18, 23]

QT prolongation is the most common electrocardiogram (ECG) abnormality, which generally resolves over several months and does not commonly require treatment. Other ECG abnormalities should receive standard treatments.[10, 17, 18, 19]

Neurologic symptoms

The immediate effect of the electrical current of a lightning strike on the CNS is an altered level of consciousness that varies from disorientation with retrograde amnesia to loss of consciousness. In the most severe cases, paralysis of the respiratory center may occur and cause sudden death or significant anoxic brain injury if the person is resuscitated. Rarely, the injury is so devastating that rapid onset of cerebral edema with brainstem herniation occurs. If the patient is unconscious, suspect and investigate anoxic brain injury or underlying brain injury. Contusion and intracranial hemorrhage have been reported.[32, 82, 88]

Cerebral edema should be managed in the standard way.

Patients who are awake are usually able to carry on reasonably appropriate social conversation. Later, they may develop disabling neurocognitive deficits similar to those of people with concussive or blunt brain injury, which may not be apparent until survivors attempt to return to their previous work and are unable to process new information, organize their activities, and multitask.[10, 97]

Acute pain, numbness, or other dysesthesias may be reported. Chronic pain syndromes may develop from lightning injuries and may be due to nerve injury, sympathetic nervous system injury, spinal cord injury, or other causes.[10]

Sympathetic nervous system injury may acutely cause vascular spasm; temporary paralysis and mottling of an extremity (keraunoparalysis); transient self-limited hypertension; and late problems with positive tilt test results, vertigo or dizziness, hypertension, and pain syndromes.[10, 89, 90]

Mechanical trauma from a fall after a lightning strike can also account for neurologic sequelae. Rarely, lightning may cause the victim to fall or be thrown with sufficient force to cause skull fracture and intracranial hemorrhage. Because a comatose or semicomatose state may follow the lightning strike, it is often difficult to distinguish coma resulting from electrical shock from intracranial hematoma until lateralizing signs develop.

Burns

Because lightning contact with the skin is brief, deep burns are typically rare.[16, 98] If burns occur, they should be treated like any other high-voltage injury, including investigating for myoglobinuria. Discrete entry and exit points are rarely seen with lightning injury.

The following types of burns are caused by lightning:

  • Feathering (Lichtenberg figures, keraunographic markings)
  • Linear
  • Punctate - Multiple, closely spaced, discrete, circular, usually full-thickness burn that results from current passing through dry skin; a few millimeters to a centimeter in diameter and resembles a cigarette burn
  • Thermal - Results when lightning ignites or melts clothing; can be a full-thickness burn
  • Contact - Occurs when metal, such as jewelry, zippers, or belt buckles, contacts the skin during a lightning strike; can be a full-thickness burn or can actually "tattoo" metal, such as a necklace, into the skin
  • Flash - Superficial burn that results in brown discoloration of the skin

An almost pathognomonic cutaneous feature known as feathering or lightning prints consists of linear, fernlike, superficial skin markings (also called keraunographic marks) that usually disappear after several days.[99] These cutaneous manifestations of lightning injury usually consist of erythematous streaks that do not blanch on diascopy. Erythema begins to fade in 4-6 hours with no residual skin changes. Keraunographic markings are probably related to the flashover phenomenon, from the transmission of electricity along the superficial vasculature. Recognition of this sign may save the life of an unaccompanied, comatose patient and should signal the need for immediate resuscitation if a victim is not breathing and has no pulse.

Linear burns are usually partial-thickness, 1-4 cm wide, that occur on sweat/rain-covered areas of the body, such as beneath the breasts or midchest, and in the midaxillary line. These burns present minutes to hours after the lightning strike and result from vaporization of sweat or rainwater into steam on the patient's body. These can be treated as any other superficial burn.

Although full-thickness burns rarely result from lightning in developed countries, lightning occasionally causes a more typical electrical burn from long continuous current flow, with clinical manifestations similar to those from a commercial, high-voltage electrical injury. Rarely, scarring following lightning burns may develop into squamous cell carcinoma (Marjolin ulcer).

Therapy for more severe burn injuries should include cleansing the burn wound with poloxamer 188, followed by treatment with a topical antimicrobial cream containing polymyxin (10,000 U/g), nystatin (4000 U/g), and nitrofurantoin (0.3%). Tetanus prophylaxis is required. Any devitalized skin should be excised and autogenous, split-thickness skin grafts considered.

In developing countries where marginal housing is the norm, keraunoparalysis may prevent victims from escaping subsequent fires, resulting in much more severe thermal injuries that can be managed with standard burn treatments.[100]

Blunt injury

Concomitant myoglobinuria should be considered if blunt injury is present. Fractures are uncommon and occur more rarely in lightning injuries than in high-voltage injuries.

Organ contusions, pulmonary hemorrhage, and cardiac contusions have been reported but are rare. If the patient has a history of a fall or being thrown a distance, investigate for fractures and blunt injuries. A patient may also have experienced explosive trauma and shrapnel effects if he or she was close to an object that has been exploded by lightning.[21]

Musculoskeletal system

Lightning may injure the musculoskeletal system either by mechanical trauma or by passage of the electrical current.[101] Fractures of the skull, ribs, extremities, and spine have been reported but are rare.

As current passes through tissue, electrical energy is converted to heat that can rarely damage muscle tissue. Muscle necrosis causing compartmental syndrome or rhabdomyolysis and renal failure are extremely rare, occurring much less frequently than in commercial electrical injuries.[102]

Eyes and adnexa

Lightning can injure the eye and its adnexa.[103] Nearly every type of eye injury has been reported with lightning injury, including cataracts, macular holes, retinal separation, and iritis.[30] Cataracts may be an early or late sequela of lightning injury, as are chronic pain syndromes, sleep disturbance, and severe headaches.

Disruption of the autonomic nervous system can cause dilated and/or nonreactive pupils. This reaction to lightning strike is usually short-term and should not be used as an indicator of brain death.

Cataracts are the most common intraocular lesions caused by lightning.[104] Two types of cataracts are seen: (1) an ordinary traumatic cataract that develops shortly after the injury from a concussion that results in minute tears of the lens capsule and (2) a type of cataract that is characteristic of an injury from either lightning or high-voltage current. In the latter, a high-voltage current produces anterior subcapsular changes, while lightning causes opacities in the anterior and posterior capsules. The cataract most commonly appears within the first few days or weeks but has been reported as late as 24 months postinjury and is often bilateral. Generally, opacification develops more rapidly after lightning injury than after commercial high-voltage electrical injury.

Retinal involvement after lightning injury is less frequently documented, although chorioretinal atrophy, macular holes, macular cyst, papilledema, hemorrhage, and detachment have been noted. Macular cyst can be diagnosed with optical coherence tomography. Consequently, consider the possibility of retinal damage when evaluating the visual potential of a patient who has developed a cataract following a lightning strike.

Lid lesions caused by lightning vary from a partial-thickness burn to ulcerated necrotic lesions. Conjunctival chemosis frequently occurs, and corneal lesions vary from transitory punctate keratitis to severe interstitial keratitis. Iridocyclitis may be mild and short-lived or more severe and chronic. Paresis of accommodation also may occur following a lightning strike.

Ears

In contrast to direct electrical current accidents, lightning commonly causes ear injuries, occurring in up to half the patients.[10, 11, 85] Direct electrical injury and blast effects can injure the ear. In lightning-damaged ears, substantial ear damage and hearing loss are common, as are tinnitus and other eighth nerve symptoms, including dizziness and unsteadiness.[23]

Temporal bone pathology shows tympanic membrane rupture, middle ear and mastoid effusion of blood, total rupture of the Reissner membrane, degeneration of the stria vascularis and organ of Corti, edema of the intracanalicular portion of the facial nerve, herniation of a portion of cerebellum into the internal auditory meatus, and a possible microfracture of the otic capsule. These lightning-damaged ears often are associated with other injuries (eg, burns of the skin, acromioclavicular joint separation).

Perforation of the tympanic membrane occurs in more than half of patients more severely injured by lightning but should always be sought in lesser injuries as well. This injury is caused by the blast effect, basilar skull fracture, or direct burn damage from lightning. Simple ruptures of the tympanic membranes from lightning usually heal well without surgical intervention.

Occasionally, unilateral hearing loss can occur without other trauma after lightning injury.[42] An audiogram often shows typical nerve-type hearing loss. The tympanic membrane is intact but markedly inflamed. Hearing disability is temporary, and recovery occurs in 9 months.

Almost all lightning survivors report chronic tinnitus as one of their most irritating sequelae.

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Contributor Information and Disclosures
Author

Mary Ann Cooper, MD Professor Emerita, Department of Emergency Medicine, University of Illinois at Chicago College of Medicine; Founding Director, African Centres for Lightning and Electromagnetics

Mary Ann Cooper, MD is a member of the following medical societies: American Meteorological Society

Disclosure: Nothing to disclose.

Coauthor(s)

Richard F Edlich, MD, PhD, FACS, FACEP FASPS, Distinguished Professor Emeritus of Plastic Surgery, Biomedical Engineering and Emergency Medicine, University of Virginia Health Care System

Richard F Edlich, MD, PhD, FACS, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Burn Association, American College of Emergency Physicians, American College of Surgeons, American Society of Plastic Surgeons, American Spinal Injury Association, Plastic Surgery Research Council, Society of University Surgeons, Surgical Infection Society, American Surgical Association, American Trauma Society

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Marc D Basson, MD, PhD, MBA Professor, Chair, Department of Surgery, Michigan State University

Marc D Basson, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Gastroenterological Association, Phi Beta Kappa, and Sigma Xi

Disclosure: Nothing to disclose.

H Scott Bjerke, MD, FACS Clinical Associate Professor, Department of Surgery, University of Missouri-Kansas City School of Medicine; Medical Director of Trauma Services, Research Medical Center; Clinical Associate Professor, Department of Surgery, Indiana University School of Medicine

H Scott Bjerke, MD, FACS is a member of the following medical societies: American Association for the History of Medicine, American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Midwest Surgical Association, National Association of EMS Physicians, Pan-Pacific Surgical Association, Royal Society of Medicine, Southwestern Surgical Congress, andWilderness Medical Society

Disclosure: Nothing to disclose.

David B Drake, MD, FACS Associate Professor, Department of Plastic Surgery, Medical Director, DeCamp Burn and Wound Center, Program Director, Hand Fellowship, University of Virginia School of Medicine

David B Drake, MD, FACS is a member of the following medical societies: American Association for Hand Surgery, American Burn Association, American College of Surgeons, American Society for Reconstructive Microsurgery, American Society of Plastic and Reconstructive Surgery, Association for Surgical Education, Southeastern Society of Plastic and Reconstructive Surgeons, and Southern Medical Association

Disclosure: Nothing to disclose.

John Geibel, MD, DSc, MA Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital

John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Other

Edmond A Hooker II, MD, DrPH, FAAEM Assistant Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine

Edmond A Hooker II, MD, DrPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Public Health Association, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

William B Long III, MD, FACS, FASTS President, Trauma Specialists, LLP; Legacy Emanuel Trauma Center, Legacy Emanuel Hospital, Portland, Oregon

William B Long III, MD, FACS, FASTS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, American Thoracic Society, American Trauma Society, and Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

Dennis P Orgill, MD, PhD Professor of Surgery, Harvard Medical School; Associate Chief of Plastic Surgery, Brigham and Women's Hospital

Dennis P Orgill, MD, PhD is a member of the following medical societies: American Medical Association, American Society for Reconstructive Microsurgery, Massachusetts Medical Society, and Plastic Surgery Research Council

Disclosure: Kinetic Concepts, Inc. Grant/research funds Principle Investigator; Brigham and Women's Hospital Royalty None; Kinetic Concepts, Inc. Expert Witness None

Robert L Sheridan, MD Assistant Chief of Staff, Chief of Burn Surgery, Shriners Burns Hospital; Associate Professor of Surgery, Department of Surgery, Division of Trauma and Burns, Massachusetts General Hospital and Harvard Medical School

Robert L Sheridan, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, and American College of Surgeons

Disclosure: Nothing to disclose.

Wayne Karl Stadelmann, MD Stadelmann Plastic Surgery, PC

Wayne Karl Stadelmann, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society of Plastic Surgeons, New Hampshire Medical Society, Northeastern Society of Plastic Surgeons, and Phi Beta Kappa

Disclosure: Nothing to disclose

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

Lars M Vistnes, MD, FRCSC, FACS Professor of Surgery, Emeritus, Stanford University Medical Center

Lars M Vistnes, MD, FRCSC, FACS is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

James Steven Walker, DO, MS Clinical Professor of Surgery, Department of Surgery, University of Oklahoma Health Sciences Center

James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

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