LIGHTNING INJURY. Berezutsky V.I.
Dnepropetrovsk Medical Academy, Dnepr, Ukraine
The statistics shows that about 6,000-24,000 persons die as result of the lightning injury, with 10-fold higher number of disability cases. In the developing countries the mortality from atmospheric electricity trauma did not change during the previous century (30-50 %). 64 persons died after the lightning stroke in Bangladesh in May 2016 [1]. In the developed countries the mortality from the lightning varies within 10-25 %, and it inevitably decreases owing to the technical safeguards, the increasing awareness among the population and improvement in specialized medical care [2]. For example, there were 24.6 % of the lethal outcomes among 12,000 cases of the lighting injury [3].
The long term studies of the relationship between the thunderstorm activity and the climate changes have given the prognosis about the increasing amount of lightning injuries at the background of global warming [4]. The high mortality and frequent severe complications after the atmospheric electricity injury can be decreased by means of timely and goal-oriented actions of specialists dealing with the treatment of patients: emergency physicians, neuropathologists, cardiologists. The efficiency of such actions highly depends on knowledge of the features of pathogenesis, the clinical manifestations, diagnostics and treatment of lightning injuries. All these factors determine the high importance of collection, generalization, analysis and popularization of the experience with management of the lightning injury.
The objective of the study was to analyze the scientific literature reflecting the problems of pathogenesis, diagnosis and treatment of lightning injuries.
The knowledge of the physical properties of the lightning is required for proper understanding of pathogenesis of the changes in the human body after the lightning injury. Although the lightning is one of the most common nature events, it has not been studied properly. Even the question of the lightning initiation inside the thunder storm clouds and its spreading for many kilometers has received the scientific explanation only recently. The research of the lightning and the associated events is conducted in relationship between multiple sections of physics: from atmospheric physics to plasma and physics and quantum electrodynamics. It is known that the lighting discharge distributes through the high conductivity thermic ionized channel (lightning leader), which consists of combination of subsequent electric discharge flows (streamers). Streamers are shifted in time and space (one to one). As result of movement of electrons along subsequently developing streamers, the leader’s channel heats to several thousand degrees and the lightning discharge travels over the great distances between the sky and the ground. When the lightning strikes the ground, the reverse leader appears with direction from upwards to downwards. It lasts for centiseconds and is characterized by speed up to 100,000 kilometers per second, current rate of several thousand amperes and the temperature up to 30,000°C [5]. As result, the combination of high speed, current rate and temperature is mediated by six wounding mechanism, and the features of their combination determine the type and severity of injuries in each individual case.
The first wounding mechanism – straight lightning stroke. It happens during direct contacting between a victim and atmospheric electricity in open territory. Its proportion is not more than 5 % of all cases of the lightning stroke. For this type of hitting the outcome can be fatal, because a victim is affected by the maximal electrical discharge [6]. Even if the direct lightning stroke does not affect the vital organs, it manifests the high destructive power. There is an interesting case of rupture of the metal femoral implant in the femoral neck region after the direct lightning stroke. It is noteworthy that the fracture was a single consequence of atmospheric electrical injury: no cardiologic and neurological changes were found [7].
The second mechanism – contacting with atmospheric electricity through the current-conducting objects, when the lightning strikes an object contacting with the human. It can be a water pipe, metal fencing or phone cable. In this case the electrical discharge distributes in the human body from the entry point to the basis (earth). The frequency of such cases does not exceed 5 %. There is a case of trifacial neuralgia under the influence of atmospheric electricity through the phone device: a woman was talking on the phone at the moment when the lightning struck her house [8].
The third wounding mechanism – “lateral flash” of the lightning. This mechanism realizes, when the lightning strikes an object near the human and “overjump” to him/her. A usual “reflector” of the electrical discharge is a tree or a building. The electrical discharge is separated between two or three nearest objects with inverse dependence on their sum resistance (impedance). A “flash” can jump from one person to another. It is the most common mechanism of with proportion of 30-35 %. There is a case of the typical stroke by “lateral flash” of the lightning in a 17-year boy. It resulted in the heart arrest. After the successful resuscitation the extensive myocardial infarction and death happened [9].
The fourth mechanism – step voltage. The ground is electrized as result of the lightning stroke. Step voltage is the difference in the potentials between two ground points over a distance of a step between them. The value of step voltage can reach 1,500 V during the lightning stroke. The higher distance between the human feet, the higher difference in the potentials: the safest position is feet together. Transient inferior paraplegia caused by the light stroke and accompanied by the full loss of sensitivity and the spinal cord motion activity below Th12. The lightning stroke the ground near a man and gave the electric discharge, which entered the body through one foot and came out the second foot (it was evident according to the electrical marks on the planta) [10].
The fifth mechanism – affection from the ascendant streamer. The ascendant streamer is low energetic in comparison with the main stroke, but it can initiate the current rate of several hundreds of amperes. The victim is the channel for conduction of one of the multiple stepwise decreasing streamers of the inverse leader. This mechanism is associated with 10-15 % of cases. There is a case, when the forensic expertise considered the weak ascendant streamer as a cause of death after excluding all other five mechanisms [11].
The sixth mechanism – a blunt injury. The blast wave appears after rapid heating air to 30,000°C. It can cause the mechanical injuries to the internal organs such as myocardial infarction, lung or big vessels rupture, eardrum rupture, eye injuries, esophagus or intestinal perforations. The blast wave can throw a man over the significant distance. Moreover, electric current causes twitching. As result of release of high amount of mechanical and heat energy, the victim’s body is exposed to the direct pressure of 200-500 Kpa, resulting in tissue ruptures [12]. There is a case of fatal injury in a 41-old woman, with a lung injury complicated by the air entering the mediastinum cavity [13]. The human can get injuries as caused by the blast wave and objects destructed by the lightning (for example, building constructions). This injury mechanism includes the cases of fatal shrapnel wounds caused by metal pieces [14].
Most victims of the lightning stroke do not die, and they usually have only poor external manifestations of electric injury (in view of burns) in the contact point with atmospheric electricity. However the externally indeterminate internal organs injuries can be quite significant and diverse, especially in concurrent influence of several injury mechanisms. Even the minimal amount of the lightning damage factors causes the multiple organ pathology, since electrical current damages all tissues during its way through the human body. The neural and vascular tissues demonstrate the lowest resistance in the human body. It is explained by frequent development of neurologic and cardiologic complications. The immediate cause of death after the lightning stroke is fatal disorders of cardiac rhythm or cerebral lesion [15].
Neurologic complications develop in approximately 85 % of cases of the lightning stroke. When electrical current goes through the neural tissue, it changes the permeability of the cell membranes, disorder of the electrochemical balance between the intra- and extracellular spaces and protein denaturation that leads to potential irreversible vasogenic edema. The brain, the cerebral cord and the peripheral nervous system are affected in almost similar manner. The most common manifestations of CNS are tetra- and hemiplegia or tetra- and hemiparesis. Such injury is described with a specific term – keraunoparalysis. But the disorders can be limited with only sensitivity disorders. Such disorders are often accompanied by disordered proprioceptive sense with manifestations in view of postural instability (inability to support the balancing state). The disorders of motion activity are often determined by development of posttraumatic (electric) myelopathy. However the cause can be cerebral strokes or infarction (both ischemic and hemorrhagic) under influence of atmospheric electricity [16]. The respiratory arrest happens in respiratory center injury; tetanus or respiratory muscles paralysis are possible. Neurologic complications appear both in short term and long term periods.
There are two theories of delayed neurologic complications after the lightning stroke. The first theory is based on the destructive effects of oxidative stress, the second – on the events of electroporation. In neurologic complications of vascular origin, the free radicals (caused by oxidative stress) can gradually destroy the endothelial cells in the spinal cord vessels resulting in death of spinal neurons. The key link in pathogenesis of the structural injury to vascular and nervous tissue after lightning-associated oxidative stress is the high level of cortisol as result of electrically-mediated excessive stimulation of glutamate receptors. It initiates the increasing amount of free radicals destroying the capillary endothelium adjacent to the spinal cord. Moreover, free radicals accumulate in lipid-enriched myelin and impair the myelinic cellular membrane [17]. Also the mechanism of nervous tissue injury is associated with electroporation: under the influence of electricity, the transmembrane potential increases rapidly and reorganization of the cellular membrane lipids to the pores appears. The significant increase in membrane permeability is accompanied by high energy losses with depleting the reserves of energetic metabolic substrates in the cells. In the conditions of energy deficiency the ion pumps (driven by ATP energy) cannot compensate rapid ion diffusion through the injured cellular membrane resulting in inevitable cell death. Nervous cells are very amenable to electroporation, because their size is directly related to the transmembrane potential in such cells. The electrophysiological findings of existence of both mechanisms in pathogenesis of late electric injury to the peripheral nervous system have been identified [18]. The long term neurologic complications of the lightning stroke can be without any clinical manifestations, even in a cerebral lesion. There is a case of hemispheric leukoencephalopathy after the lightning stroke without any clinical signs and with confirmation after the tomographic examination [19].
A peripheral nervous injury is usually presented by plexitis and neuritis, which are often transient and are accompanied by evident dysfunction of the vegetative nervous system [20]. A typical post-lightning injury adrenergic dysfunction is a case with a 24-old man with vegetative nervous system disorders in view of sinus tachycardia and arterial hypertension, which were considered as the manifestations of hypersympathicotonia of central origin after the neurologic examination [21].
The reversibility of post-lightning neurologic disorders is associated with vasospasm of the small vessels feeding the nerves. The disorders can persist from several minutes to several weeks or months [22]. There is a case of temporary (one week) tetraparesis in a patient after a stroke of the lightning which reflected from a building [23].
The authors of the study Peripheral nervous system involvement in lightning strike — the devil in disguise wanted to accentuate the difficulties of diagnostics and the significance of consequences of the atmospheric electrical damage of the peripheral nervous system. The study described a case of a lightning damage of the right brachial plexus accompanied by long term hemiparesis [24]. There is a case of the right brachial plexus neurapraxia in a young man who suffered from the lightning. Hemiplegia and the sensitivity disorders were persistent during 5 weeks at the background of intensive care with steroids. The efficiency of the treatment with steroids is one of the arguments of the electroporation theory of the peripheral nervous system injury caused by atmospheric electricity: steroids recover the membrane potential of neurons which is disordered by electroporation after the lightning stroke [25]. However there are some cases, when too high current rate and high voltage caused the structural changes in the nervous system after the lightning stroke. Humeral plexopathy in the upper and middle stem was irreversible after the lightning stroke in a 53-old man [26].
Cognitive and mental disorders are seen even in the situation, when the way of electric current does not cross the brain, with absent structural injury to the nervous and vascular systems organs. Synergism between the effects of increasing cortisol and agitation of glutamate receptors makes the negative influence on the memory through the mechanism of long term potentiating. The clinical experience shows that such disorders remain within several months or years in absence of specific rehabilitation. The use of early cognitive training in the complex rehabilitation for patients after the lightning injury significantly increases the efficiency of neurorehabilitation and promotes more rapid elimination of neurologic disorders [27]. There is a case of mass casualty, when the lightning hit a tent with 26 juvenile age girls, 2 adults and 7 dogs. 4 girls and 4 dogs died immediately after cerebral injury. The adults were without injuries. All children, except for 3, were seriously injured. Some neurologic and ophthalmologic disorders remained during several weeks, and mental disorders (emotional lability, depression, sleep disorders and cognitive impairment) – within several months [28].
Cardiovascular disorders appear in 46 % of cases after the lightning stroke. Most mechanisms of cardiovascular events are explained by current passage: coronary arterial spasm, hypercatecholaminia, direct thermic injury, disorders in the cardiac conducting system. The direct effects of the lightning injury include asystolia, ventricular fibrillation and respiratory center injury which are the main cause of death. It was found that ventricular fibrillation or cardiac arrest appear when the lightning strikes during the myocardial repolarization phase [29].
Most cases of arrhythmia happen immediately after the lightning stroke, but sometimes ventricular arrhythmia develops within subsequent 12 hours. There is a case of a lightning injury that caused cardiac and respiratory arrest and lesion of the upper motional neuronal way with quadriplegia [30]. When the atmospheric electrical discharge passes through the cardiac conducting system, some organic and functional disorders appear: from safe sinus arrhythmia to fatal necrosis of the cardiac muscle. A 35-old man suffered from the lightning stroke. He experienced the clinical death and died from myocardial infarction in 4 days. The autopsy confirmed the cause of his death [31]. Another case with a 7-old girl sowed the significant ST-segment elevation without concurrent Q wave and without any dynamic changes during 5 years of the follow-up. The changes in ECG were not accompanied by the increasing blood level of troponin and disorders of contractile myocardial function during transthoracic angiography. Therefore, the changes were considered as events of coronary vasospasm [32]. There is a case of myocardial infarction in a 44-old man after a lightning injury. The man died on the day 5. The diagnosis was confirmed by the clinical, electrocardiographic and biochemical data and the autopsy. Vital coronography showed the complete patency in all branches of the coronary arteries [33].
The standard approaches to therapy of rhythm disorders after a lightning injury is efficient in some cases. A 28-year old man was hit by the lightning while he was working in the field. Atrial fibrillation happened. The electric points of the input (on the elbow) and the output (on both plantae) of current showed that the electrical discharge went through the heart. Electric cardioversion was conducted for unstable hemodynamics. The recurrent ECG examination showed the presence of WPW-syndrome. The conductance was able to recover after radiofrequency ablation [34]. In other case, post-lightning injury atrial fibrillation was treated with pharmaceutical antiarrhythmic therapy [35].
The principles of the treatment for victims of electric trauma (including injury from atmospheric electricity) have been studied. The cardiac monitoring (during 7 days) was conducted for estimating the probable late myocardial complications of electric trauma in 169 patients. There were not any significant cardiac disorders even in the patients who suffered from high voltage. The researchers concluded the absence of necessity for cardiac monitoring for patients with electric trauma and absent clinical signs of complications [36].
The modern studies showed the efficiency of controlled hypothermia for patients with cardiac arrest or cerebral injury after the lightning stroke. Multiple mechanisms of a lightning injury are associated with cerebral hypoxia. Cerebral ischemia appears as result of disordered cardiac rhythm or decreasing myocardial contractile function. Cerebral perfusion is disordered after atmospheric electricity impaction, blast wave or high temperature. Cerebral hypoxia appears at the background of hyperadrenergetic condition after a lightning injury. The various pathogenetical mechanisms cause the cerebral ischemia with selective death of some neurons and apoptosis of others. The neuroprotective effect of hypothermia significantly reduces the risk of neurological complications in such patients: decreasing the body temperature by 1 degree slows down the metabolism of neurons and decreases their energetic requirements by 6-7 %. Therapeutic hypothermia stabilizes the cellular membranes, minimizes the formation of toxic free radicals (caused by electric trauma) and inhibits the nervous demyelination. Moreover, hypothermia decreases the intensity of cerebral edema at the background of neurons death, vascular necrosis and disorder of hematoencephalic barrier, decreases the glutamate detent and prevents the release of the inflammatory cytokines [37].
Skin lesions take place in each third person after lightning trauma. The pathogenesis of lightning burns is based on both electric damages of skin vessels and direct influence of high temperature. Burns can be superficial that is determined by extremely low impaction time of the damaging factors [38]. According to the same reason, burns after atmospheric electricity impact are characterized by relatively favorable outcomes [39]. Metal objects on the body attract the electric discharge and retain it on the skin surface. Moreover, they heat greatly that causes contact burns [40].
Lichtenberg figures (named after Georg Cristoph Lichtenberg, a German scientist) are common for lightning trauma. These are the marks of fern shape that appear on the skin after high voltage impact. It is supposed that such figures are result of rupture of subcutaneous blood vessels: the skin is a good insulator, with dielectric destruction caused by the flow of electrons in the skin. Red blood cells go through the destructed capillaries to the superficial skin layers with formation of bizarre figures. The figures can appear several hours or even days after the lightning stroke and disappear completely in several days. Lichtenberg figures may appear in any type of contact with atmospheric electricity: in direct lightning stroke, in stroke with lateral flash or stepwise voltage. There is a case when the figures appeared in 1 hour after lateral flash from the lightning entering a building. They remained during 1 week [41].
Eye injury in the lightning stroke is accompanied by disordered permeability of the phacocyst petrous, protein coagulation from electric current, worsening alimentation of the phacocyst petrous after iritis and mechanical damage of its fibers that leads to formation of cataract. The first case of cataract after the lightning stroke was described in 1699 [42]. Cataract develops in 5-6 % of cases after a lightning injury. The pathological process usually affects an eye, which is the nearest to the point of electrical discharge. Because of high level of melanin in pigment epithelium, the macula is highly sensitive to thermic injuries. There is a case of a lightning injury to both anterior and posterior eye chamber with development of cataract affecting the anterior and posterior parts of eye lens, and a macular cyst that required a surgical intervention [43]. Another common complication is retinopathy [44].
Hearing organ injury from the lightning is caused by disordered structure of the inner ear, vascular and neurologic disorders as response to the blast wave, a burn or high voltage current [45]. Ear drum perforation with hearing loss and external ear canal burn is the most common complication after a lightning injury. Hearing nerve damage and hearing loss of mixed origin are rarer. A 19-old woman suffered from a lightning injury with severe burns of the left ear, central perforation of ear drum with hearing loss of 108 dB on the left side, and sensor neural hearing loss on the right side (52 dB) [46]. There is a case of pneumocephalus after bilateral rupture of ear drums caused by the lightning: the air entered the cranium trough an inborn defect in petrous part of the scute. The neurologic disorders persisted within 6 months after the injury [47].
As compared to nervous and vascular tissues, the muscular tissue is slightly less sensitive to atmospheric electricity, but the lightning stroke often causes rhabdomyolysis. A muscular damage is caused both by immediate impact of high voltage electric current and spasm mediated by it. There is a case of severe myoglobinuria not associated with renal pathology. It was caused by massive destruction of the muscular tissue after the lightning injury [48]. The consequences of the lightning injury highly depend on the power of its electrical discharge, a concrete damaging mechanism and on other circumstances [49]. Such dependence is especially evident in cases of mass lightning injury. The lightning flash reflected from a tree and affected nine military men simultaneously. All of them had loss of consciousness, two – ectopic disorders of cardiac rhythm and Lichtenberg figures on the skin, five – temporary hemiplegia and skin burns, one – a clavicle fracture [50].
CONCLUSION
The combined mechanism of the lightning injury determines the multisystem pattern of the injury and requires for the interdisciplinary approach to diagnosis and treatment. Such approach can be efficiently realized only on the basis of close relationship between high amount of specialists: emergency physicians, intensivists, neuropathologists, cardiologists, combustiologists, otolaryngologists, ophthalmologists, traumatologists. The promotion of the experience and the increasing awareness about the features of pathogenesis and the clinical signs of the lightning injury are able to significantly increase the efficiency of care for victims.
REFERENCES:
1. Holle RL and Islam, AKMS Lightning Fatalities in Bangladesh in May 2016. In: Proceedings of the 8th Conference on the Meteorological Applications of Lightning Data. 2017 American Meteorological Society Annual Meeting, Seattle, Washington, 22-26 January 2017
2. Holle RL. A Summary of Recent National-Scale Lightning Fatality Studies. Weather, Climate, and Society. 2016; 8(1): 35-42
3. Zack F, Puchstein S, Büttner A. Letalität von Blitzunfällen. Rechtsmedizin. 2016; 26(1): 9-11
4. Saha U, Siingh D, Kamra AK, Galanaki E, Maitra A, Singh RP et al. On the association of lightning activity and projected change in climate over the Indian sub-continent. Atmospheric Research. 2017; 183(1): 173-190
5. Mazur V. Lightning initiation – the most difficult issue of lightning physics. Principles of Lightning Physics. 2016
6. Sumangala C, Kumar MP. Lightning Death: A Case Report. Journal of Indian Academy of Forensic Medicine. 2015; 37(1): 93-95
7. Lizano-Díez X, Alentorn-Geli E, León-García A, Marqués-López F. Fracture of the Femoral Component after a Lightning Strike Injury: A Case Report. Acta Orthopaedica et Traumatologica Turcica. 2017; 51(1): 84-87
8. Lopez A, Cheshire W. Trigeminal neuralgia following a telephone-mediated lightning injury. The Journal of Pain. 2015; 16(4): 29
9. Azari A, Bigdelu L, Pishbin E, Rohani A. Acute Myocardial Infarction in a 17-Year-Old Boy Secondary to Lightning Strike. Journal of Cardio-Thoracic Medicine. 2013; 3(1): 104-106
10. Gouse M, Arockiaraj J, Khanapur R, Srinivasan G. Transient paraplegia in an elderly due to lightning injury: an unusual cause. Journal of Emergencies, Trauma, and Shock. 2015; 8(4): 238
11. Cooper MA. A Fifth Mechanism of Lightning Injury. Academic Emergency Medicine. 2002; 9(2): 172–174
12. Blumenthal R. On the sixth mechanism of lightning injury: dissertation. Pretoria: University of Pretoria South Africa. 2015
13. Blumenthal R, Saayman G. Case Report: Lightning-Induced Pneumomediastinum. The American Journal of Forensic Medicine and Pathology. 2017; Jan 21. doi: 10.1097/PAF.0000000000000299. URL: https://www.ncbi.nlm.nih.gov/pubmed/28114174
14. Van Waes OJF, van de Woestijne PC, Halm JA. «Thunderstruck»: Penetrating thoracic injury from lightning strike. Annals of Emergency Medicine. 2014; 63(4): 457–459
15. Tadler M, Rüegg E, Niquille M, Gencer B, Gautschi OP, Pittet-Cuénod B, et al. Multi-organ injuries due to a lightning strike: a case report highlighting the importance of a multi-disciplinary approach. Case Reports in Plastic Surgery and Hand Surgery. 2017; 4(1): 1-4
16. Gruhn KM, Knossalla F, Schwenkreis P, Hamsen U, Schildhauer TA, Tegenthoff M et al. Neurologische Erkrankungen nach Blitzschlag. Der Nervenarzt. 2016; 87(6): 623-628
17. Reisner A. Delayed neural damage induced by lightning and electrical injury: neural death, vascular necrosis and demyelination? Neural Regeneration Research. 2014; 9(9): 907-908
18. Parikh S, Fink J, Feigon M, Plishkin M. Electrical and Lightning Brain Injuries. Acquired Brain Injury: Clinical Essentials for Neurotrauma and Rehabilitation Professionals. Springer Publishing Company, New York, 2016
19. Kruja J, Kuqo A, Grabova S, Rroji A, Vyshka G. Right Hemispheric Leukoencephalopathy as an Incidental Finding Following a Lightning Strike. Open Access Macedonian Journal of Medical Sciences. 2016; 4(4): 692-694
20. Morin A, Lesourd A, Cabane J. Les atteintes extra-cérébrales de la foudre: vignettes cliniques et revue de la littérature. Revue Neurologique. 2015; 171(1): 75-80
21. Parsaik AK, Ahlskog JE, Singer W, Gelfman R, Sheldon SH, Seime RJ et al. Central hyperadrenergic state after lightning strike. Clinical Autonomic Research. 2013; 23(4): 169-173
22. Choi IK., Choi HJ. A Patient of Lightning Injury Combined with Reversible Neurologic Deficits: A Case Report. Journal of the Korean Society of Emergency Medicine. 2015; 26(4): 345-348
23. Biswas S, Karim ME, Chowdhury JA, Sarkar PK, Begum M, Sarkar MM et al. Lightning Injury in Indoor Setting: A Case Report. Journal of Dhaka Medical College. 2016; (1): 79-81
24. Senthilkumaran S, Balamurugan N, Jayaraman S, Sasikumar S, Thirumalaikolundusubramanian P. Peripheral nervous system involvement in lightning strike – the devil in disguise. The American Journal of Emergency Medicine. 2015; 33(11): 1704-1705
25. Patnaik A, Mahapatra A, Jha M. Pan-brachial plexus neuropraxia following lightning: A rare case report. Surgical Neurology International. 2015; 6(3): 110-112
26. Kasundra G, Khichar S, Bhargava A, Bhushan B. Lightning strike-induced brachial plexopathy. Journal of Neurosciences in Rural Practice. 2014; 5(4): 399-400
27. Tánczos T, Zádori D, Jakab K, Hnyilicza Z, Klivényi P, Keresztes L. The role of cognitive training in the neurorehabilitation of a patient who survived a lightning strike. A case study. NeuroRehabilitation. 2014; 35(1): 137-146
28. Silva LMA, Cooper MA, Blumenthal R, Pliskin N. A follow-up study of a large group of children struck by lightning. South African Medical Journal. 2016; 106(9): 929-932
29. Wiater J. Lightning Induced Ventricular Fibrillation risk during wandering. Ðrzegląd elektrotechniczny. 2016; 1(2): 108-113
30. Àbdulla S, Conrad A, Schwemm KP, Stienstra MP, Gorsselink EL, Dengler R , et al. Lesions along the upper motor neuronal pathway with locked-in features after lightning strike and cardiac arrest: A case-review analysis. Brain Injury. 2014; 28(3): 298-303
31. Möhle F, Preuss J, Madea B, Doberentz E. Vier Tage überlebter Blitzschlag nach zunächst erfolgreicher Reanimation. Rechtsmedizin. 2015; 25(6): 561-565
32. Akın A, Bilici M, Demir F, Gözü-Pirinççioğlu A, Yıldırım A, Bilici M, et al. ST-segment elevation following lightning strike: case report and review of the literature. The Turkish journal of pediatrics. 2015; 57: 186-188
33. Karadas S, Vuruskan E, Dursun R, Sincer I, Gonullu H, Akkay E. Myocardial infarction due to lightning strike. J Pak Med Assoc. 2013; 63(9): 1186-1188
34. Leiria TLL, Pires LM, Kruse ML, de Lima GG. Struck by lightning: a case of nature-induced pre-excited atrial fibrillation. Circulation: Arrhythmia and Electrophysiology. 2013; 6(2): 20-21
35. Ocak Ò, Duran A, Yaylali Ç, Özlü MF. Yıldırım Çarpması ile Oluşan Atriyal Fibrilasyon: Olgu Sunumu. Kocatepe Medical Journal. 2014; 15(1): 65-70
36. Krämer C, Pfister R, Boekels T, Michels G. Cardiac monitoring always required after electrical injuries? Medizinische Klinik – Intensivmedizin Und Notfallmedizin. 2016; 111(8): 708-714
37. Scantling D, Frank B, Pontell ME, Medinilla S. Inducing therapeutic hypothermia in cardiac arrest caused by lightning strike. Wilderness & Environmental Medicine. 2016; 27(3): 401-404
38. Russell KW, Cochran AL, Mehta ST, Morris SE, McDevitt MC. Lightning burns. Journal of Burn Care & Research. 2014; 35(6): 436-438
39. Shih JG, Shahrokhi S, Jeschke MG. Review of adult electrical burn injury outcomes worldwide. Journal of Burn Care & Research. 2017; 38(1): 293-298
40. Adil MT, Rahman R, Das S. Patterned charring along the contact points of a metallic locket due to lightning strike. Clinical Case Reports. 2016; 4(6): 618-619
41. Dutta B. Lichtenberg figure and lightning. Indian Journal of Dermatology. 2016; 61(1): 109-111
42. Flockerzi E, El-Husseiny M, Löw U, Daas L, Seitz B. Historische Beschreibung der Kataraktentwicklung nach Blitzschlagverletzung. Der Ophthalmologe. 2017; 2: 1
43. Chakraborti C. Lightning induced ocular complications: A case report. Pak J Ophthalmol. 2014; 30(1). 49-52
44. Liu TYA, See C, Singman E, Han IC. Delayed onset of intraretinal cystoid abnormalities in lightning retinopathy. JAMA Ophthalmology. 2016; 134(7): 840-842
45. Kılıç E, Genç H, Aydın Ü, Aşık B, Satar B. Variations in otological presentations of lightning strike victims: clinical report of 3 Patients. Turkish Journal of Trauma and Emergency Surgery. 2017; 23(2): 163-166
46. Turan M, Kalkan F, Bozan N, Özçalimli İ, Zeki Erdem M, Yalınkılıç A et al. Isolated sensorineural hearing loss as a sequela after lightning strike. Case Reports in Otolaryngology. 2015: 1-4
47. Yarnell PR, Weiland D. Pneumocephalus in lightning injury with additional neurologic sequelae. Trauma. 2016; 9: 146040861665968
48. Aldana NN. Severe rhabdomyolysis without renal injury associated with lightning strike. Journal of Burn Care & Research. 2014; 35(1): 120-123
49. Argüelles Argüello AB, Rodríguez KB, González JP, León Spesny CS, Umaña Brenes AA, Arguedas CV. Fisiopatología, manifestaciones sistémicas y secuelas de la fulguración en seres humanos. Medicina Legal de Costa Rica. 2015; 32(1): 138-145
50. Nagesh IV, Bhatia P, Mohan S, Lamba NS, Sen S. A bolt from the blue: Lightning injuries. Medical Journal Armed Forces India. 2015; 71(1): 134-137