BURN Case Report: Risk of Electric Injury on Delayed Initial Treatment Abstract: Electric Injury is a very aggressive burn injury with severe functional and aesthetic consequences caused by progressive and prolonged Ulfa Elfiah tissue necrosis. Necrosis that attacks the skeletal muscle can lead to Dissa Yulianita Suryani rhabdomyolysis which results in complications if not treated properly. A complicated case of electric injury in Dr. Soebandi Jember General Hospital, a 26 years old man came to the emergency room with complaints of severe shortness of breath and urinary disorders. The patient had a history of having an electric shock in his right hand when turning on the fan a week prior of admission. The examination showed that the patient had bilateral pulmonary effusion, generalized edema and acute tubular necrosis (ATN) which was characterized by oliguria and even anuria accompanied by hematuria. Other symptoms experienced by patients are anterior , subconjunctival hemorrhage, and hematemesis.

lectric injury, a relatively common form 60% - 70% were caused by low voltage of mechanical trauma, can occure as a electricity and sometimes caused by short E result of lightning strikes, low voltage or circuits from car batteries in America and high voltage electric shock, and is often China.3 associated with high morbidity and mortality. In Indonesia, there are not many Almost all electric injuries occur accidentally collective data on electric injury, one of and cannot be prevented. If the patient is not epidemiological research on electric injury treated immediately, fatal damage to electric patients in the Burn Unit, Cipto injury can result in multiple organ or tissue Mangunkusumo General Hospital in 2009 – dysfunction.1 2010 shows that as many as 11,8% patients This phenomenon of electric injury is treated at Burn Unit were electric injury in relatively rare. Although this case is rare, the origin4. A study by Martina and Wardhana in morbidity and mortality from this incident is the Burn Unit, Cipto Mangunkusumo General very high. In the United States, the American Hospital from January 2011 – Desember 2012 Burn Association estimates that 4.400 people explained that as many as 76 adult patients have been injured in electric accidents and 400 died from burns, and 14% of the dead patients have died from electric injury each year, most were caused by electricity.5 Other data, based are related to work (miners, electricians, dan on the results of a preliminary study obtained construction workers). The average victim is a from the Dr. Soebandi Jember General Hospital young adult or teenager, who is often injured in March 2016 – September 2017, there were as a result of outdoor adventure activities 11 patients admitted due to elecric injury.6 (such as climbing electric poles, exploration of In the case of electric injury, survived dangerous places) and children involved in patients often experience body function household accidents.2 In a study done by Liu it disorder and some require reconstructive was found that 0,5% of deaths were related to surgeries.7 Fatal complications caused by electrical injuries, and among these deaths, electric injury, especially in cardiac such as arrhythmias and respiratory arrest may cause death. The final result of electric injury Disclosure: The authors herely declare they have depends on the intensity or voltage of no financial interest in the information discussed exposure, the direction of electric current in this article entering the body, the state of the body, and

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immediate and adequate therapy. Immediate palpation obtained from the right pulmonary and precise diagnosis is influenced by fremitus decreased, percussion obtained a dim selective laboratory results. Proper handling sound in the basal right and left lung, and treatment reduce and even eliminate the auscultation showed a decreased vesicular losses especially caused by complications on sound and there was crackles in the basal right electric injury. and left lung. Physical examination of the abdominal CASE PRESENTATION region and genitalia, inspection slightly A 26 years old male came to Dr. distended abdomen and scrotal edema with Soebandi General Hospital complained of positive translumination, the percussion was severe shortness of breath. He also shifting dullness positive. The initial urine can complained that his left eye was rather blurred be obtained 150 mL/24 hours with cloudy and very little urine. The patient was exposed yellow color. to an electric shock in his right hand when holding a damaged wall fan cable one week prior to admission. Electric shock lasted for more or less 5 minutes and the patient was unconscious. According to the patient’s family, the voltage of his house is 220 volt. When he arrived at emergency room at the private hospital, the patient regained consciousness and complained of dizziness, nausea and blood with the remaining food twice. The patient was only treated for 2 days. Furthermore, the patient at his own request asked to be treated at home. During home care, patient get 4.5 litres of fluid therapy in 4 days under the supervision of a nurse. Since being treated at home, patient complained of little amount of urine. On the 7th days after the incident, the patient felt difficulty in breathing, so the patient came to Dr. Soebandi Jember General Hospital. When arrived at Dr. Soebandi Jember General Hospital, patient complained of Figure 1. Clinical photograph of burns entered shortness of breath and continuous hiccups. due to electric injury. Hemodynamic was stable with blood pressure 144/90 mmHg, pulse 95 bpm regular and Physical examination of the extremities strong, respiratory rate 32 bpm with SpO2 was found at burns entry of the former electric 96% and axillary temperature 36 °C. There shock only at the right hand as necrotic in was no prior history of . digiti II as high as the middle and distal The sign of anemia was found at physical phalang, bone exposed at digiti I with tendon, examination of the head and neck. In addition, tendon exposed at digiti III with a granulation palpebral edema and redness of the of at the edge of the wound. Exit burns in this the both eyes, and turbidity in the of patient were not found (Figure 1). Pitting the patient’s left eye. edema was found in the examination of both Physical examination of the thoracic lower extremities. region starting from the inspection found retraction and lagging of the right lung motion,

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Table 1. Results of laboratory test.

HB 10,3 gr/dl WBC 15,4 109/L HCT 29,6 % Thrombocyte 316 109/L Albumin 3,1 gr/dl Glucose 64 mg/dl Natrium 110,6 mmol/L Kalium 3,82 mmol/L Chlorida 78,0 mmol/L Calcium 1,87 mmol/L Creatinin 16,0 mg/dl BUN 135 mg/dl Urea 288 mg/dl Urid Acid 12,9 mg/dl

Urinalysis Color Cloudy yellow Figure 2. Thorax x-ray (2A) and manus dextra pH 5,0 Density 1,015 (2B) Protein +1 (25 mg/dL) Glucose Normal Leucosyte macro Negative Blood macro Negative Eritrocyte 2-5 Leucocyte 0-2 Epitel Squamous 0-2 Yeast Positive

Result of thoracic marker USG showed Figure 3. Normal ECG result. that the intensity of echo fluid in both pleural cavity, (Figure 4). Abdominal USG results Investigation was carried out by showed right kidney: normal size, echo cortex laboratory test, ECG, x-ray photos of the chest intensity increased, sinus cortex line unclear. and manus dextra. ECG results in the form of a Left kidney: normal size, echo cortex intensity sinus rhythm and no abnormalities were increased, sinus cortex line unclear, visible found (Figure 3). On thorax x-ray, extra pleural stone in the middle pole size 0,87 cm. effusion is obtained, whereas manus dextra x- Emerging intensity of echo fluid in both ray is not found abnormalities (Figure 2). abdominal cavity and bilateral thoracic cavity Laboratory results showed anemia, increased (Figure 5). leukocytes, increase in serum creatinine and hyponatremia and hypoglycemia. Whereas in the urinalysis proteinuria and erythrocytes are found (Table 1).

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Figure 4. Results of thoracic marker USG

Based on physical examination and workup results, patients diagnosed by kidney failure with pulmonary edema as a result of acute tubular necrosis accompanied by anterior uveitis, subconjunctival hemorrhage, and hematemesis as a result of electric injury with inappropriate initial treatment.

Patient Management Figure 5. Results of abdominal USG. Based on patient’s history and physical examination, management is given to improve Eye complaints are defined as uveitis general conditions with correction of anterior ocular sinistra (OS) and hypoglycemia, hyponatremia, administration subconjunctival ocular dextra dan of antibiotics and ranitidine. sinistra (ODS) due to electrical mechanical Severe shortness of breath due to trauma. Management by opthelmologist was uremia and bilateral pleural effusion are given statrol ed 5x1 drops of OS, ocuftan ed treated through hemodialysis. After 24 hours 5x1 drops of OS, and methylprednisolone oral post hemodialysis the results of renal function 3x4 mg for 7 days. examination improved (Table 2), and pleural Wound management with puncture immediately in patients the results debridement and reconstruction of right hand were obtained 150 mL clear yellow color at with abdominal flap 3 days after pleural right pleural puncture and no fluid was found puncture. at left pleural puncture.

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Table 2. Post hemodialysis laboratory results. The severity and complications of Natrium 133,8 mmol/L electric injury depend on the amount of stress, Kalium 3,60 mmol/L resistance, type of current, current path and Chlorida 99,6 mmol/L duration of contact. There are three main Calcium 2,65 mmol/L mechanisms for the occurrence of electric Creatinin 6,2 mg/dl injury, they are: (1) electrical energy causes BUN 67 mg/dl direct tissue damage, alters the potential of Urea 144 mg/dl resting membrane cells, and generates muscle Urid Acid 5,5 mg/dl tetany; (2) conversion of electrical energy into

heat energy, causing large tissue damage and coagulative necrosis; (3) mechanical injury with direct trauma resulting from falls or severe muscle contractions.9 This case is classified as electric injury low voltage (<1000) because the voltage is 220 V. Although low voltage, this electric injury can cause the patient to become unconscious, the appearance of tissue necrosis, myoglobinuria, and hemoglobinuria.10 In this case, the patient Figure 5. Post abdominal flap surgery was unconscious and progressive tissue necrosis occurred in his right hand. The case Surgical actions on entry wound include examined by Buja et. Al stated that they also debridement, digiti II phalang distal-media treated patients with amputation not only amputation and defect closure with abdominal from the fingers but also on the forearm, which flap (Figure 5). was caused by low voltage.10 Blood vessels, muscles, and nerves DISCUSSION contain high levels of electrolytes and water so Electricity is the flow of electrons (outer that resistance is low, and electricity particles negatively charged from an atom) conductors are the best compared to bone, fat, through a conductor. The object that collects and skin. Hard skin areas are very good electrons become negative, and when resistors, while moderate amounts of water or electrons flow away from this object through a sweat on the skin surface can significantly conductor, an electric current is created, reduce resistance.9 measured in amperes. The power that causes Electric current can flow through two electrons to flow is called voltage, and is types of currents, namely direct current (DC / measured in volts. Anything that blocks the direct current) or alternating current (AC / flow of electrons through a conductor creates alternating current), where the flow of resistance, which is measured in ohms. electrons changes direction in rhythmic mode. Electric injury will occur when a person comes Alternating current is the most common type into contact with the current produced by a of electricity in homes and offices, source. These sources can be man-made (for standardized to a frequency of 60 example, power lines in utility companies) or cycles/second (Hz). The case of this patient's natural, such as lightning strikes.8 In this case, electric injury was a type of air conditioner the patient is exposed to an electric shock from because it happened at home. Alternating household appliances in the form of a fan, but current voltage with the same voltage as DC is an electric shock comes from a fan cable considered to be about 3 times more connected to the home electric current so that dangerous, because the cyclic flow of electrons the current voltage is 220 V. causes the tetani muscle to extend the victim's exposure to the source. Tetani muscle occurs

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when fibers are stimulated at 40-110 Hz; in which the is the most sensitive tissue to standard electric current 60 Hz is in the range. electricity and heat generated in the eye If the source of contact is the hand, when there followed by low-resistance parts of the eye is a tetanic muscle contraction, contraction of such as the and . Whereas in the extremity flexor will cause the victim the case of electric injury, the unilateral produce continuous prolonged contact with mechanism of uveitis (inflammation of the the source. Conversely, high DC voltage often and ) after an electrical injury is causes large muscle contractions and causes unknown. Electric current may have spread the victim to bounce due to the short duration only to the left eye as well, the heat generated of contact with the source stream.9 by the flow of current through the eyes can In its flow through the body, the electric cause a variety of cellular or interullular current always looks for the shortest and changes that may result in uveitis.14 fastest route to the exit point. There are Management of anterior uveitis in these several main lines of electric shock cases that patients is categorized as severe anterior are most common in the community, namely: uveitis based on symptoms and physical (1) the first line is the electric current through examination. The principle of handling is to the hand holding an electric conductor then maintain visual acuity, relieve ocular pain, the current flows to find the shortest route to eliminate ocular inflammation, and prevent the neutral conductor in the form of soil synechiae formation.15 through the foot; (2) The second path is the Most occurs obliq path, most likely the electric current spontaneously. However, this bleeding can passes through the heart organ which has its also occur spontaneously due to trauma, own electrical system, the electric current that postoperative bleeding, systemic diseases passes through this organ then interferes with such as hypertension, and clotting the heart's electrical process; (3) The third factor disorders. Subconjunctival bleeding is path occurs when the contralateral hand holds bright red or dark red sclera. The an electrical conductor, then the electric inflammatory process can occur, but is usually current from the hand will flow to the not severe. Bleeding can also expand in the contralateral hand holding the conductor.11 first 24 hours, but afterwards it starts to In this case, burn wound was found only decrease due to the absorption process. The at the source contact point (entry wound), but absorption process takes place within 1-2 no ground contact points were found (exit weeks. wounds). Entrance and exit wounds do not Gastrointestinal can also always appear together, sometimes only entry occur in electric injury. This is associated with wounds, sometimes also just wounds come out a sequel's "stress response" which increases or both appear together.12 Descriptive the secretion of stomach acid and peptic acid. research conducted by Guntheti et. al stated The pathogenesis of "curling's ulcers" and from 62 patients, there were 13 (20.96%) stress ulcer is a change in the quality and cases where no entry or exit wounds were quantity of mucosubstantion stomach, loss of found, only 25 (40.32%) of the wounds were integrity of mucous barrier, bile acid reflux included, only 2 (3.23%) out cases and 22 and digestive enzymes, acid hypersecretion, (38.48%) cases.13 hypoproteinemia or negative nitrogen The pathophysiology of electrically balance, mucosal ischemia during opening of induced ocular injuries is complex. Electrically submucosal arteriovenous shunts, local induced ocular injuries have been associated vasoconstriction or the development of with many pathological changes such as microvascular after intravascular , , edema, . Gastrointestinal lesion can epithelial corneal , uveitis, and occur within 5 hours after the incident. Within pupillary abnormalities. Among other things, 72 hours, many cases develop gastroduodenal cataracts are the most common complication

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ulcerations which result in large bleeding, or the right lung has more fluid. Right pleural perforation.16 puncture results obtained clear yellow liquid Initial administration of oral or enteral and included the type of transudate based on food that starts within 6 hours after the the light’s criteria. Pleural effusion is incident is an effective supplement in influenced by a balance between fluid preventing stress-induced ulceration. Early production, fluid absorbance, and several feeding reduces the incidence and severity of defense forces such as plasma osmolality, bacterial translocation by maintaining the hydrostatic pressure, venous pressure, and integrity of the mucosal barrier. The use of permeability of capillary walls.18 Pleural antacids, and H2 receptor blockers has effusion in this case can be due to increased become an established practice in an effort to permeability of the capillary wall due to the prevent bleeding. H2 receptor blockers, for electroporation process and due to the example Ranitidine, administered at a dose of process of rhabdomyolysis which causes 150 mg twice a day for about 3-6 weeks, is a Acute Tubular Necrosis (ATN). normal practice today, with the idea of Patients in this case experience acute reducing acid secretion by blocking histamine renal failure or commonly known today as H2 receptors on parietal cells of the gastric Acute Kidney Injury (AKI) which occurs after mucosa.16 burns are mostly caused by reduced cardiac Electric shock can also cause disruption output, which is mainly caused by fluid loss. of cell membrane permeability due to This is usually caused by delayed or electroconformational denaturation of inadequate fluid resuscitation but can also be proteins (macromolecules). When electrified, caused by muscle damage or substantial it means that there is direct contact between hemolysis. Reducing urine output even though the current source and the conductor (body adequate fluid administration is usually the surface tissue), there is an electron first sign of AKI. This will be followed by an displacement as well as the process of increase in serum creatinine and urea transferring ions in the solution. At that time, concentrations.19 AKI after electric injury the process of electrolysis and exothermal which increases creatinine and potassium reaction, electrochemistry, followed by levels is an indication for hemodialysis. Blood changes in pH, oxygen concentration, and urea is not a useful independent indicator release of toxic substances into the because it increases in non-kidney conditions surrounding tissue. Electric current through such as dehydration and high protein diets.20 the cell layers shows a phenomenon called the Oliguria in this case is caused by the electroporation process. The process takes presence of ATN which occurs due to the place in the cell membrane; Negatively process of rhabdomyolysis into myoglobinuria charged membrane proteins denaturate. on electric injury causing fluid accumulation Protein denaturation especially occurs around throughout the body in the form of anarchic the location of cell lines and gates (location of edema and bilateral pleural effusion. This sodium pumps, calcium pumps, and potassium edema and bilateral pleural effusion occurs channels). These cell membrane proteins lose because the kidneys are unable to function as their three-dimensional structure, experience excretory organs. While rhabdomyolysis is a distortion or form intramembrane pores so syndrome in which pain occurs and necrosis of that the intracellular components are easily skeletal muscle by releasing muscle enzymes mixed with extracellular components; the into the circulation. process takes place so fast.17 The amount of Rhabdomyolysis can result in elevated intracellular fluid to extracellular will form levels of myoglobulin, creatinine edema. phosphokinase (CK), lactatdehydrogenase Complaints of shortness of breath in (LDH). The symptoms range from moderate patients due to uremia and the presence of increases in muscle enzymes to life- pleural effusion in both lungs of patient where threatening diseases associated with extreme

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increases in enzymes, electrolyte imbalances occlusion of renal tubules by formation of (especially hyperkalemia), and continuing into hemoglobin casts, and finally AKI, especially if AKI. The last common pathway for injury to combined with dehydration, acidosis, shock, rhabdomyolysis is an increase in free or endotoxemia. Hemoglobin is freely intracellular ionized cytoplasm and absorbed by degraded tubular epithelium to mitochondrial calcium. This may be caused by globin and hem.20 reduced adenosine triphosphate (ATP), Progressive ischemia in electric injury cellular energy sources, and / or by direct is also a serious complication. Thrombus injury and rupture of the plasma membrane. formation in arterioles, narrowing of vessels ATP depletion causes pump dysfunction Na / decreases blood flow, and tissue necrosis can K-ATPase and Ca 2+ ATPase which are occur.23 This is a factor that contributes to important to maintain the integrity of muscle amputation decisions. Therefore, in this case, cells, resulting in the release of muscle amputation is done in the part that has enzymes in the circulation. The mechanism of necrosis. The main goal in handling electrical myoglobin which causes damaged glomerular injuries on the hand is to restore the function filtration is unknown. Previous studies have of the hand to the maximum. Plastic surgery shown that renal vasoconstriction, direct procedures, such as skin grafts or artificial tubular injury, indirect tubular injury dermis, are useful for first-time surgery, and (ischemic) and intraluminal blockade by regional or free flaps are useful if the injury is myoglobin play a role.21 severe. Case of electric injury with high The importance of detecting ATN signs tension, groin and abdominal flaps are the early, to prevent the continuation of AKI. ATN most commonly used flaps. In this case, signs can be found through clinical or abdominal flaps are performed on low-voltage laboratory. Clinical ATN can be accompanied electrical injuries.23 by oliguria or without oliguria. So that laboratory results are needed to establish the CONCLUSION diagnosis of ATN in the form of urinary Electric injury has complex osmolality <400 mOsm / Kg, amount of urine complications, so that appropriate treatment sodium> 40 mEq / L, creatinine ratio <20, to prevent complications from occurring has a percentage of sodium> 2, and in urine very important role. sediments found renal, granular and muddy This case explains the effect of acute tubular epithelium brown granular casts. tubular necrosis (ATN) which continues to be Management of ATN includes a hemodynamic the acute kidney injury (AKI). The progressive improvement in the form of preventing ischemic effect of electric injury accelerates hypotension which can cause disruption of the rhabdomyolysis. Detecting possible glomerular filtration rate due to the complications on electric injury and good mechanism of renal arterial vasoconstriction. follow-up of patients will minimize the If the weight of the treatment is occurrence of AKI in patients with electric hemodialysis.22 injury. Hematuria in the case of electric injury is the result of denatured protein Reference (pigmenturia) in the form of free hemoglobin 1. Lisa A. Foris; Martin R. Huecker. Electrical released from red blood cells degraded by heat Injuries. StatPearls Publishing LLC: Januari conjugated by haptoglobin and transferred to 2018. the liver. When large amounts of free https://www.ncbi.nlm.nih.gov/books/NBK4 hemoglobin are produced in electric injury, 48087/ non-conjugated free hemoglobin passes 2. Waldmann, Victor, Kumar Narayanan, Nicolas through the glomerulus and is excreted in the Combes, Eloi Marijon. Electrical Injury. BMJ urine causing hematuria. This can cause 2017; 357 doi: https://doi.org/10.1136/bmj.j1418 degenerative changes in tubular cells,

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3. Liu, H., Q. Wang, Z. Zhao, Y. Xie, S. Ding, dan Z. for burn injuries. Ulus Travma Acil Cerrahi Wang. 2016. The Clinical and Medicolegal Derg, March 2015, Vol. 21, No. 2 Analysis of Electrical Shocked Rats: Based on 16. Duman, Rahmi, Sadık Görkem Çevik, Ayşe the Serological and Histlogical Methods. Tüfekçi1. Unilateral uveitis, and Biomed Research International. 2016;1-12. following low-voltage 4. Suzan, R., dan D. E. Andayani. Management of electrical injury. Burns & Trauma. 2015; 3:19 Nutrition in Patient with Burns Electricity. 17. American Optometric Association. Optometric JMJ. 2017;5(1):1-13. Clinical Practice Guideline Care of The Patient 5. Martina, N. R., dan A. Wardhana. Mortality with Anterior Uveitis. AOA: 243 N. Lindbergh Analysis of Adult Burn Patients. Journal of Blvd., St. Louis, MO 63141-7881. 2004. Plastic Reconstruction. 2013;2(2): 96-100. 18. Kumar, Arige Subodh, Gogulapati Venkata 6. Djunaedi, Annisa Sarfina, Ulfa Elfiah. Thesis: Sudhakar. Upper gastrointestinal lesions and Analysis of Rat Vessels Based on Distance of bleed in burn injuries: An endoscopic Post-Exposure Electrical Injuries. Jember evaluation. Indian Journal of Burns: Vol 22 University. 2018. Issue 1. December 2014. 7. Karimi, H., M. Momeni, dan M. Vasigh. Long 19. Moenadjat, Y. Burns: Problems and Term Outcome and Follow Up of Electrical Management. Fourth edition. Jakarta: Hall of Injury. Journal of Acute Disease. 2015;107- Publishers of the Faculty of Medicine 111. Indonesia University. 2009. 8. Koumbourlis, Anastassios C. Electrical 20. Sato, tetsuo. Differential Diagnosis of Effusion injuries. Crit Care Med 2002; 30[Suppl.]:S424 Pleura. 2006. JMAJ 49 (9-10):315-319 –S430. 21. Chauhan, D. C, P. S. Chari, G. K. Khuller, Dalbir 9. Ungureanu M. Electrocutions – treatment Singh. Correlation of renal complications with strategy (case presentation). Journal of extent and progression of tissue damage in Medicine and Life Vol. 7, Issue 4, October- electrical burns. Indian J Plastic Surg Vol 37 December 2014, pp.623-626 Issue 2. July-December 2004. 10. Buja Z., Arifi H., Hoxha E. Electrical Burn 22. Emara S.S., Alzaylai A.A. Renal Failure in Burn Injuries. An Eight-Year Review. Annals of Patients: A Review. Annals of Burns and Fire Burns and Fire Disasters - vol. XXIII - n. 1 - Disasters - vol. XXVI - n. 1 - March 2013. March 2010 23. Naqvi, Rubina, F. Akhtar, E. Ahmed, A. Naqvi, 11. Pudjiastuti, A. Difference in the Frequency of A. Rizvi. Acute Kidney Injury with Wistar Rat Heart Muscles Due to Exposure to Rhabdomyolysis: 25 Years Experience from a Electric Current Directly and through Water Tertiary Care Center. Journal of nephrology: Media. Not Published. Thesis. Semarang: 2015, 5, 67-74. Faculty of Medicine, Diponegoro University. http://dx.doi.org/10.4236/ojneph.2015.530 2009. 11 12. Seng, Khoo Kah, Leong Qi Wen, Bustaman Syamimi, Ho Choon Aik, Lim Chen Hong. Management of an Electrocuted Burn Injury in a District Hospital-A Case Report and Literature Review. Journal of Clinical and Diagnostic Research. May 2018, Vol-12(5): PD11-PD12 13. Guntheti, Bharath Kumar, Sheikh Khaja, Uday .P .Singh. Pattern of Injuries due to Electric Current. J Indian Acad Forensic Med. Jan- March 2012, Vol. 34, No. 1 14. Cushing, Tracy A, Ronald K Wright. Electrical Injuries in Emergency Medicine. https://emedicine.medscape.com/article/77 0179-overview 15. Yasti, Ahmet Çınar, Emrah Şenel, Mutlu Saydam, Geylani Özok, Atilla Çoruh, Kaya Yorgancı. Guideline and treatment algorithm

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