TY - JOUR
AU - Wiktor, Arek, J
AB - Abstract We present the case of a man who suffered a high-voltage electrical injury followed by a delayed presentation of an epidural hematoma. CT of the brain demonstrated hyper dense material along the anterior and frontal region consistent with an epidural hematoma at the vertex. The patient underwent serial computed tomography scans of his brain which demonstrated stability of the hematoma and no operative intervention was required. This appears to be the first case report of such an injury. CASE REPORT High-voltage electrical injury is commonly associated with a myriad of injuries such as burns, rhabdomyolysis, and cataracts, but rarely intracranial hemorrhage. We present the case of a man who suffered a high-voltage electrical injury to the head followed by a delayed presentation of an epidural hematoma, 2 weeks later. We hypothesize that damage to the sagittal sinus due to heat/electrical current, may have led to a delayed bleed of the epidural hematoma. Presentation of Case A 39-year-old male with a history of bipolar disorder was transferred to the hospital after suffering an electrical injury while working inside a high-voltage switch box. The patient reported that he was working in the metal box when his head and left shoulder came in contact with 12,000 volts. Upon receiving the shock, the patient was unable to break contact with the box for approximately 1 minute until his coworkers used a nonconductive piece of equipment to detach him from the electrical panel. He subsequently fell to the ground and started having seizure like activity. Per witness report, he did not injure his head, and the patient had no recollection of the incident. He arrived to the emergency department alert, oriented, and slightly confused, but without any focal neurological deficits. He complained of pain in his head and left shoulder. He exhibited decreased range of motion, strength, tenderness, and pain in his left upper extremity. A CT scan of his head, chest, abdomen, pelvis, and spine, demonstrated no acute abnormalities. The results of his laboratory studies, including CBC, comprehensive metabolic panel, and electrolytes were all within normal limits. His creatinine kinase was mildly elevated on admission at 848 ng/ml. It peaked at 5937 ng/ml on hospital day #2, and then began to trend downward. The patient’s physical exam was notable for a full thickness scalp burn that measured 6 × 12 cm (Figure 1), as well as a full thickness L shoulder burn that measured 6 × 6.5 cm (Figure 2). Figure 1. View largeDownload slide Scalp wound. Figure 1. View largeDownload slide Scalp wound. Figure 2. View largeDownload slide Left shoulder wound. Figure 2. View largeDownload slide Left shoulder wound. Over the course of the next 2 weeks, the patient recovered well on the burn unit, and underwent multiple operative debridements of his wounds. Notably, the patient was on DVT prophylaxis during his hospitalization with subcutaneous enoxaparin at a dose of 30 mg twice per day. He was working with physical therapy on hospital day #14 when he reported gait instability. He complained of his knees buckling and his legs feeling weak. In addition, he reported short-term memory loss, problems with balance, and emotional lability. Given his myriad of symptoms, the neurology service was consulted. Neurology concluded his symptoms appeared consistent with his electrical injury, and recommended an magnetic resonance imaging. The patient, however, was unable to undergo an magnetic resonance imaging due to negative pressure dressings in place over his wounds. As a result, the patient underwent a CT scan of the brain and cervical spine. The CT of the brain was notable for a new finding of a nonenhancing hyperdense material layering over the anterior frontal region at the vertex, left greater than right, consistent with an epidural hematoma. The epidural hematoma measured approximately 10 mm in thickness, extending superior to the expected course of the superior sagittal sinus (Figure 3). Neurosurgery was consulted and recommended serial CT scans to ensure stability and, ultimately, no operative intervention. Repeat CT scans were obtained at 6 and 24 hours later which demonstrated stability of the hematoma. Enoxaparin was briefly held after the initial brain CT until stability was verified. A final follow-up scan was obtained on hospital day #17, the day of discharge, which showed no changes to the epidural hematoma. Figure 3. View largeDownload slide CT image demonstrating vertex epidural hematoma. Figure 3. View largeDownload slide CT image demonstrating vertex epidural hematoma. DISCUSSION Between 1992 and 2010, workers suffered 66,748 nonfatal electrical injuries that resulted in days away from work in North America according to the Electrical Safety Foundation International, a non-profit organization that promotes electrical safety at home and in the workplace.1 Overall, the number of nonfatal electrical injuries are downtrending, peaking at 6018 nonfatal electrical injuries in 1994 down to 1890 in 2010.1 The nonfatal injury electrical injury incidence rate is 0.2 per 10,000 workers.1 Despite the downtrend in the number of nonfatal electrical injuries, there can be significant morbidity related to these injuries, with a median of 4 days away from work (range 3–10 days during years 1992–2010).1 Cost estimates associated with nonfatal electrical injuries range from $76,694 to $80,023 per incident.2 Injuries related to electrical injury occur via the following three mechanisms: 1) direct injury secondary to the electrical current, 2) thermal injury (both direct contact and arc injuries) leading to superficial and deep burns, and 3) blunt injury related to falls or muscle spasms that occur after the electrical shock. The amount or intensity of the current related to the electrical injury determines the extent of the damage. Ohm’s law states that the current through a conductor is proportional to the voltage and the resistance (V = IR, where V = voltage, I = current, and = resistance). In most cases, the only known variable is the voltage. As a result, electrical injuries are classified into low-voltage (<1000 V) or high-voltage (>1000 V) events. Other factors that contribute to the extent of the injury include duration of contact with the conductor, the pathway of the current, and the resistance of the body. The neurologic complications related to electrical injuries are extremely varied. There can be damage to both the central and peripheral nervous systems even with an absence of an external burn injury. Injuries related to the peripheral nervous system include both motor and sensory deficits that may be patchy in distribution. Other neurologic complications include loss of consciousness, amnesia, seizures, transient paralysis of limbs, headache, and/or cerebral infarction. These complications are likely to appear early (minutes to days) after the initial insult. Additional neurologic complications such as progressive muscular atrophy, myelopathy, neuropathy, and post-traumatic stress syndrome often present late and in a delayed fashion, often days to weeks, or even months after the injury. A less common complication of electrical injury is brain hemorrhage. There have been several case reports of intracerebral hematoma from secondary lightning or other electrical injury.3–6 In one case report, a 54-year-old male patient presented with a normal neurologic exam after contacting his head with a power cable.3 However, his neurologic exam diminished an hour after presentation, prompting a CT scan of his head which demonstrated a left parietal intracerebral hemorrhage, which was managed conservatively. In a second case report, a high-voltage wire touched the head of a 39-year-old male while he was working in the ceiling of a home, leading to loss of consciousness.6 He presented with an 8 cm electrical burn to the parietal region of his head, and was subsequently found to have an intraparenchymal hemorrhage within the left parietal region, requiring evacuation via burr hole. Previous articles have suggested at least four proposed mechanisms to describe bodily and brain injury associated with electrical injuries. The electrostatic theory suggests that electric charges build up in the body (if the patient is not grounded) and subsequently repel each other, leading to a sudden expansive force that can cause significant tissue rupture.7 The vascular theory suggests that electrical injury causes vasoconstriction, with subsequent intimal injury and/or thrombosis.8 This theory may account for delayed presentations of cerebral hemorrhage or ischemia. According to the heat theory, damage occurs to tissues secondary to direct thermal injury.8 The mechanical theory suggests that tissue injury occurs secondary to significant mechanical vibration of the tissue as a result of the electrical current leading to an injury.7 Most likely, it is the combination of all of these theories, as opposed to a single model, that leads to tissue injury after electrical shock. We present a case of a delayed finding of an epidural hematoma, considering that the patient presented with both a normal brain CT scan and a normal clinical exam on admission. Based on previously described theories of tissue injury related to electrical injuries, we hypothesize that the electrical current caused direct injury to the superior sagittal sinus. Prior work by Robson et al. demonstrated elevated circulating levels of thromboxane A2 in blood after electrical injuries.9 Thromboxane A2 is a known mediator of vasoconstriction and promotes thrombosis. These authors postulate that excess thromboxane A2 may cause progressive tissue loss. Additional work by Wang et al. demonstrated cell membrane perforations present in the aorta and pulmonary arterial endothelial cells of electrocution victims. These changes appeared within 24 hours following injury.10 In this experiment, the endothelium had completely disintegrated after 24 hours. As a result, we postulate that the heat transferred during this electrical event led to direct damage to the sagittal sinus. We hypothesize that this led to subsequent endothelial cell disruption, which then led to a delayed presentation. Although epidural hematomas are a relatively common injury following trauma they are usually due to laceration of the middle meningeal artery. In contrast, vertex epidural hematomas due to sagittal sinus injury are relatively rare, representing 0 to 8% of case series of all epidural hematomas.11 As a result, the literature on this injury is limited to mostly case reports. Case reports have demonstrated wide variation in the presentation of these injuries, ranging from 1 day to 6 weeks. Some authors have postulated that the delayed onset of symptoms is related to the disruption in cerebral venous drainage and blockage of cerebral spinal fluid absorption.12 In the majority of the case reports, operative intervention was chosen for the management of the vertex epidural hematomas due to worsening clinical neurologic symptoms. However, conservative management of vertex epidural hematomas has been described, especially in patients with less clinically significant symptoms. Based on our research, this is only the second case report of an epidural hematoma associated with an electrical injury. The first case report of an epidural hematoma after a lightning strike was published in the New England Journal of Medicine in 1958. Morgan et al. describe the presentation of a 52-year-old male who had been found unconscious on the floor of a power substation after a lightning strike.13 The description of his presentation is described as responding only to painful stimuli, with normal reflexes, and normal pupils. He was noted to have parietal and temporal bone skull fractures. On hospital day 2, he was noted to have progressive weakness on his left side. As a result, a temporoparietal craniotomy was performed, which revealed a 4 × 15 × 10 cm epidural hematoma secondary to a laceration of the right middle meningeal artery. Clearly, an epidural hematoma after a lightning injury is a rare complication. Those authors, like ourselves, also concluded that unexplained neurologic symptoms should warrant further investigation. Conflict of interest statement. None declared. REFERENCES 1. International ESF (Electrical Safety Foundation) . Workplace electrical injury and fatality statistics, 2003 - 2015 . 2017 , available from http://files.esfi.org/file/Workplace-Fatalities-and-Injuries-2003-2015.pdf 2. Cawley J. Occupational electrical accidents in the U.S., 2003 – 2009 . Electrical Safety Foundation International ; 2015 , available from http://files.esfi.org/file/ESFI-White-Paper-Occupational-Electrical-Accidents-in-the-U-S-2003-2009.pdf 3. You JS , Chung SP . Intracerebral hemorrhage following electrical head injury . J Trauma 2009 ; 67 : E72 – 4 . Google Scholar Crossref Search ADS PubMed 4. Kim HM , Ko YA , Kim JS , Lim SH , Hong BY . Neurological complication after low-voltage electric injury: a case report . Ann Rehabil Med. 2014 ; 38 : 277 – 81 . Google Scholar Crossref Search ADS PubMed 5. Asian S , Yimaz S , Karcioglu O . Lightning: an unusual cause of cerebellar infarction . Emerg Med J 2004 ; 21 : 750 – 1 . Google Scholar Crossref Search ADS PubMed 6. Axayacalt GA , Alejandro CE , Marcos RA , Inocencio RF , Alfredo HG . Brain hemorrhage after electrical burn injury: case report and probable mechanism . Surg Neurol Int. 2016 ; 7 ( Suppl 28 ): S759 – 62 . Google Scholar Crossref Search ADS PubMed 7. Pritchard E . Changes in the central nervous system due to electrocution . Lancet. 1934 ; 1 : 1163 – 7 . Google Scholar Crossref Search ADS 8. Stanley LD , Suss RA . Intracerebral hematoma secondary to lightning stroke: case report and review of the literature . Neurosurgery. 1985 ; 16 : 686 – 8 . Google Scholar Crossref Search ADS PubMed 9. Robson MC , Murphy RC , Heggers JP . A new explanation for the progressive tissue loss in electrical injuries . Plast Reconstr Surg 1984 ; 73 : 431 – 7 . Google Scholar Crossref Search ADS PubMed 10. Wang Y , Liu M , Cheng WB , Li F , Liao Z , Wang Y . Endothelial cell membrane perforation of aorta and pulmonary artery in the electrocution victims . Forensic Sci Int 2008 ; 178 : 204 – 6 . Google Scholar Crossref Search ADS PubMed 11. Miller DJ , Steinmetz M , McCutcheon IE . Vertex epidural hematoma: surgical versus conservative management: two case reports and review of the literature . Neurosurgery. 1999 ; 45 : 621 – 4 ; discussion 624. Google Scholar Crossref Search ADS PubMed 12. Matsumoto K , Akagi K , Abekura M , Tasaki O . Vertex epidural hematoma associated with traumatic arteriovenous fistula of the middle meningeal artery: a case report . Surg Neurol 2001 ; 55 : 302 – 4 . Google Scholar Crossref Search ADS PubMed 13. Morgan ZV Jr , Headley RN , Alexander EA , Sawyer CG . Atrial fibrillation and epidural hematoma associated with lightning stroke; report of a case . N Engl J Med 1958 ; 259 : 956 – 9 . Google Scholar Crossref Search ADS PubMed © American Burn Association 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. 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TI - Delayed Presentation of a Vertex Epidural Hematoma Following High-Voltage Electrical Injury to the Head
JF - Journal of Burn Care & Research
DO - 10.1093/jbcr/irz042
DA - 2019-06-21
UR - https://www.deepdyve.com/lp/oxford-university-press/delayed-presentation-of-a-vertex-epidural-hematoma-following-high-OYATc0TKZq
SP - 517
VL - 40
IS - 4
DP - DeepDyve
ER -