INTRODUCTION

Malaysia is among the countries with the highest density of lightning flashes [1]. Lightning represents an uncommon but potentially devastating cause of trauma. Injuries from lightning strikes are characterized by unique symptoms and can lead to long-term morbidity, yet they are consistently underreported [2]. Although electrical injuries and lightning injuries differ in various aspects, they have historically been assessed together in the literature due to their similar clinical presentations, management principles, and outcomes [2]. This discussion aims to compare these two types of injuries through the examination of presented cases involving a lightning injury and an electrical burn injury.

CASE REPORTS

Case 1

A 12-year-old boy was found unconscious on an outdoor football field on a rainy day. He was taken to a local community hospital and subsequently referred to our center. Witnesses confirmed that he had been struck by lightning while playing football with his friends. Eyewitnesses also reported flashes of light and thunderclaps at the time of the incident.

Upon arrival at the emergency department, the patient regained consciousness. Initially, he reported only weakness and pain in both shoulders. We later observed transient paralysis of his bilateral lower limbs, which spontaneously resolved after a few hours, followed by pain in his right calf. He had no recollection of the incident. The primary survey indicated that he was in mild distress, with sinus tachycardia and hypertension. The secondary survey revealed multiple erythematous macular skin lesions in a feathering pattern across his chest and bilateral lower limbs (Fig. 1). These nonblanching macules faded over several hours and completely disappeared within a day, leaving no residual skin changes.

The patient was admitted to the burn unit for close observation due to concerns about rhabdomyolysis. Initial venous blood tests revealed leukocytosis with a white cell count of 18,000/mm³, a high creatine kinase level at 6,270 U/L, an elevated lactate level of 8 mmol/L, and acidosis with a pH of 7.3. Although his amber-colored urine tested positive for myoglobin, no renal impairment was identified. Following 4 days of aggressive fluid replacement therapy, all laboratory values returned to normal.

The ophthalmology, otorhinolaryngology, and orthopedic teams concurred on the absence of lightning-related complications. The patient was discharged after 4 days of admission, and subsequent clinic consultations revealed no long-term sequelae of the lightning injury.

Case 2

A 27-year-old technician sustained an electrical burn injury at his workplace. He was standing on a metal ladder 3 m above the ground while attempting to repair an electric cable. Eyewitnesses reported that he held the cable with his left hand for approximately 5 seconds before falling. He lost consciousness for 40 minutes and was subsequently transported to the hospital by a colleague.

Upon regaining consciousness, the patient reported pain and numbness in his left hand, left thigh, and right shin. Initially, he presented with hypertension and sinus tachycardia, which resolved following fluid resuscitation. Physical examination revealed full-thickness burns on his left hand, left inner thigh, and right leg (Fig. 2). Thrombosis of the great saphenous veins was noted in the left thigh and right leg. The presumed electrical exit wound was identified on the mid-right tibia, presenting as a periosteum-free defect measuring approximately 3×2 cm. Movement in the left hand and both legs was limited. Additionally, the examination showed multiple scalp lacerations and bruises on the posterior trunk.

The patient was treated for rhabdomyolysis, as indicated by a positive urine myoglobin test and an elevated serum creatine kinase level (8,307 U/L) upon admission, which resolved within a week. All other blood parameters were within the normal range. During his hospital stay, he underwent multiple tangential excisions of his burn wounds; these were eventually covered with autologous skin grafts, while the exposed tibia was covered by a random transpositional flap (Fig. 2). After a month of inpatient treatment, this patient was discharged.

Ethics statement

Written informed consents for publication of the research details and clinical images were obtained from the patients (for case 1, informed consent was obtained from the patient's parents).

DISCUSSION

Malaysia ranks among the top three countries for high lightning density, with an annual mean ground flash density of 13.9 flashes per square kilometer [1]. Factors such as geographical position, a marked increase in factories, deforestation, and other developmental activities contribute to an increase in the earth’s heat, which in turn heightens the severity and frequency of thunderstorms [1]. The global mortality rate due to lightning strikes is estimated to be between 0.2 and 1.7 deaths per million people annually [3]. A recent study in Malaysia found that lightning strikes resulted in fatalities for 1 in every 10 victims, with a total of 235 injuries recorded between 2008 and 2015 [1].

The electrical current involved in lightning strikes is a unidirectional, massive current impulse akin to direct current (DC), in contrast to the alternating current (AC) that typically causes household and industrial electric injuries [3,4]. The amount of DC delivered by a lightning strike ranges from approximately 30,000 to 50,000 A, which exceeds that of AC [3]. However, the exposure duration from lightning is brief, lasting only about 10 to 100 milliseconds, which is insufficient to cause Joule heating. Instead, it results in muscle and nerve damage through a mechanism known as electroporation [3]. Electroporation involves an imposed transmembrane potential that causes the reorganization of lipids in the cell membrane, forming pores that increase membrane permeability. When cellular metabolic energy stores cannot maintain transmembrane concentration gradients, cell death occurs. Skeletal muscle and nerve cells are particularly vulnerable to electroporation due to their length, which is directly proportional to the transmembrane potential. Some authors have suggested that the delayed onset of neurological sequelae following a lightning injury is largely attributable to the cumulative effects of electroporation over time [3].

The mechanisms of lightning injury include side flash, direct strike, contact injury, ground current, upward streamer, and blast injury [3,4]. Case 1 patient likely sustained his lightning injury through a side flash, where the current jumped from a fatal direct strike received by his nearby friend. Humid air is often implicated in the side flash mechanism [3]. Alternatively, the patient may have been affected by ground current when the lightning struck the field, with his late friend being closer to the strike point and thus receiving a stronger current. Contact injury and blast injury are unlikely mechanisms in this case. Primary blast injury typically results in ruptured tympanic membranes, while tertiary blast injury is usually characterized by blunt trauma, occurring when the victim is thrown by the intense opisthotonic contraction induced by the lightning strike [3].

Electricity can be transmitted either directly or indirectly [2]. Case 2 patient sustained a direct contact injury with the cable through his left hand, which served as the entry point, while the exit points were located on the left thigh and right leg. Entry points, whether in direct or indirect contact with the power source, may or may not exhibit burns; this is partly due to variations in skin resistance [2]. Duff and McCaffrey [2] observed that the exit point often exhibits extensive damage, similar to case 2 in our study. They further noted that the route of the electrical current through the body follows the path of least resistance, typically through nerves and blood vessels, as the current seeks a ground. When electricity encounters tissue resistance, it generates heat [3,5]. The cable that the case 2 patient touched likely carried AC, as indicated by the “no let-go” phenomenon exhibited by his left hand. This involuntary response was due to tetanic spasm caused by the AC, which led to continuous muscle contractions in the hand, preventing the patient from releasing the cable [2]. In cases involving AC, the exit point can also become a re-entry point [5]. AC is generally considered more hazardous than DC because it prolongs the duration of electrical contact; additionally, the cardiorespiratory system appears more susceptible to the effects of AC [2].

Fatality has been recorded with contact at voltages as low as 25 V [2]. In addition to voltage, the severity of an electrical injury is determined by factors including the type of current, the pathway of the current through the body, the resistance of tissues along this pathway, the amperage of the current, the duration of contact, and environmental factors such as weather and humidity [4,5]. Most patients affected by electrical or lightning injuries are male, as men and boys often predominate within relevant occupational environments and outdoor activities [4,5]. The average age of victims of electrical and lightning incidents is 34.8 years [2].

Feathering lesions are one of the skin manifestations resulting from lightning strikes. They are not thermal injuries, as the epidermis and dermis typically appear normal. Lichtenberg figures are associated with this type of lesion and are pathognomonic for lightning injuries [3,6]. These lesions consist of blood extravasation in the subcutaneous tissue. Feathering skin lesions are usually transient and disappear without residual impacts. Another skin lesion related to lightning is linear burns, which occur due to the vaporization of water from the skin surface where there is a high concentration of sweat. Punctate burns are closely spaced circular injuries that can sometimes result in full-thickness burns, but they rarely require grafting due to their limited surface area. Thermal injury may also occur if clothing ignites or from metal objects worn by the patient. Generally, cutaneous burns in lightning injuries are minor and less extensive, unlike electrical burns, which typically involve extensive tissue necrosis at various depths from the skin to the bone [3]. These wounds are often functionally disabling, necessitating aggressive treatment—including serial tangential excision and early coverage—to preserve vital structures [5]. Denatured nerves, tendons, joints, and bones may partially regenerate if covered with vascularised skin [5]. Compartment syndrome is a rare complication of lightning injuries; however, fasciotomy is indicated if it occurs [3].

Okafor [4] reported that between 3% and 15% of individuals who experience a major lightning injury might develop acute kidney injury. Prompt and aggressive fluid resuscitation prevented the development of acute kidney injury in patients of both cases, who were presented with rhabdomyolysis and myoglobinuria. The electrical current from lightning and electrical injuries devitalizes tissue as it travels through the body, leading to rhabdomyolysis and subsequent myoglobinuria. Excess circulating myoglobin can precipitate in the kidneys, causing intratubular cast formation. The breakdown of intratubular myoglobin releases free iron, which catalyzes the production of free radicals in ischemic injury. This is postulated to exert toxic effects on tubular epithelial cells and may induce intrarenal vasoconstriction by inhibiting nitric oxide bioactivity, leading to later ischemic reperfusion injury. Okafor [4] suggests that urine alkalinization, achieved by adding bicarbonate to intravenous fluids, can prevent the dissociation of myoglobin into nephrotoxic ferrihemate.

Electrical and lightning injuries clinically exhibit multiorgan derangements, particularly cardiogenic and neurogenic dysfunction [3]. Upon arrival at the emergency department, both of our patients presented with sinus tachycardia and hypertension, which were attributed to vasoconstriction from the massive release of catecholamines during injury [3]. The primary cause of death following a lightning strike is cardiac arrest due to asystole or ventricular fibrillation [7,8]. Patients with lightning injuries should be treated as if they have sustained high-energy blunt trauma [3]. The American Heart Association recommends vigorous resuscitative measures, even for those who appear deceased upon initial evaluation, as victims may respond well to resuscitation [3]. Continuous cardiac monitoring for the first 24 hours is not advocated if the initial electrocardiogram is normal, as subsequent cardiac dysrhythmias are unlikely [9]. Lightning-related central nervous system injuries are classified into four categories: immediate and transient, immediate and prolonged or permanent, possible delayed neurological syndromes, and trauma from falls or blasts [2,3,10]. Here, case 1 patient experienced immediate and transient neurological effects, which included loss of consciousness, amnesia, weakness, and keraunoparalysis. Keraunoparalysis is a unique presentation of lightning injury; it is characterized by transient paralysis and loss of sensation, most commonly affecting the bilateral lower limbs [3]. Other classifications of central nervous system deficits may be evident on radiological imaging [3]. Victims of electrical or lightning injuries often sustain more than one type of injury due to the thermoacoustic effect [2].

Residual or delayed functional, neurologic, ocular, otovestibular, or neuropsychological deficits following an injury should be assessed accordingly [3,11]. An otolaryngology assessment is crucial to exclude conditions such as tympanic membrane rupture, sensorineural deafness, vestibular injury, transient vertigo, tinnitus, basilar skull fracture, burns to the external auditory canal, or bilateral perilymphatic fistulas [3,11]. Tympanic membrane rupture occurs in about 50% of lightning strike survivors [12]. An ophthalmology consultation is important to evaluate a range of eye injuries, including lightning cataract, corneal burns, intraocular hemorrhage or thrombosis, uveitis, chorioretinitis, iridocyclitis, hyphema, and orbital fracture [3]. Delayed and progressive neurologic sequelae may manifest more than 48 hours after the injury, including involuntary movement disorders, basal ganglia disorders, seizures, spinal cord signs, and myelopathy [13]. Reduced visual acuity and sleep disturbances are the most frequently reported symptoms. Neuropsychological sequelae such as depression, anxiety, chronic fatigue, and sleep disturbances may also present later following the injury.

Ultimately, electrical and lightning injuries can cause harm in various ways, and each exhibits distinct characteristics. Patients who have experienced lightning injury should be managed similarly to those who have sustained high-energy blunt trauma. Treatment is typically conservative; however, surgical intervention may be necessary for some patients, particularly those with severe cutaneous burns or compartment syndrome. These individuals must also be assessed for other lightning-related conditions, including neurological, ocular, otovestibular, and neuropsychological disorders, all of which warrant long-term follow-up. Understanding lightning safety is essential for community protection during such events. Prevention is crucial, and individuals who work in high-risk settings or participate in outdoor activities during the thunderstorm season should exercise a high degree of caution.

ARTICLE INFORMATION

Author contributions

Conceptualization: YL; Investigation: all authors; Methodology: all authors; Project administration: all authors; Visualization: all authors; Writing–original draft: all authors; Writing–review & editing: all authors; All authors read and approved the final manuscript.

Conflicts of interest

The authors have no conflicts of interest to declare.

Funding

The authors received no financial support for this study.

Data availability

Data sharing is not applicable as no new data were created or analyzed in this study.

Fig. 1.

Clinical photographs of case 1 patient. Multiple erythematous macular skin lesions are arranged in a feathering pattern on his (A, B) bilateral legs, (C) right medial thigh, and (D) chest.

Fig. 2.

Clinical photographs of case 2 patient. (A, B) The entry point with full-thickness burn wounds on the left hand, subsequently resurfaced with full-thickness skin grafts. (C) The exit point with full-thickness burn wounds on the left inner thigh. (D) The left thigh wound is approximated primarily after tangential excision. (E) The exit point with full-thickness burn wounds on the right leg with exposed tibia. (F) The right leg wound covered with random transpositional flap and split-thickness skin grafts.

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References

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