- Email: [email protected]
Different sequelae of electrical brain injury — MRI patterns
JBUR 5221 No. of Pages 4
burns xxx (2017) xxx –xxx
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.elsevier.com/locate/burns
Case report
Different sequelae of electrical brain injury — MRI patterns Lukas Grassner a,b,c , Michael Bierschneider a, Martin Strowitzki a, Andreas Grillhösl d, * a
Department of Neurosurgery, Trauma Center Murnau, Germany Center for Spinal Cord Injuries, Trauma Center Murnau, Germany c Institute of Molecular Regenerative Medicine, Spinal Cord Injury and Tissue Regeneration Center Salzburg, Paracelsus Medical University Salzburg, Austria d Section of Neuroradiology, Trauma Center Murnau, Germany b
article info
abstract
Article history:
Purpose: Electrical injury to the central nervous system may lead to neurologic compromise
Accepted 14 March 2017
via pleiotropic mechanisms. It may cause current-related, thermal or nonthermal damage
Available online xxx
followed by secondary mechanisms. Methods: We herein report a case of a 20-year old man, who experienced a low-voltage electric
Keywords: Electrical injury Brain
of pathophysiologic features including thermal, nonthermal and hypoxic cerebral lesions. Conclusion: The capability of MRI assessing a variety of lesions for diagnostic and potentially
MRI Diagnosis
1.
injury due to an occupational accident. Results: Magnetic resonance imaging (MRI) one week after the insult allowed differentiation
prognostic reasons is presented.
Introduction
Electrical injury may affect multiple organ systems. Neurologic compromise may present in different ways including cerebral or spinal cord injury as well as peripheral nerve injuries. The clinical manifestation might be acute or delayed [1]. Depending on the entry site, the nervous system might be affected via a pleiotropic route of action resulting in direct thermal-induced or current related insults as well as secondary injuries such as disruption of transmembrane ion gradients due to electroporation of proteins [2]. Therefore
© 2017 Elsevier Ltd and ISBI. All rights reserved.
cells with a relatively large surface – like neurons – are most likely more susceptible to electric injury [3]. Nowadays MRI may allow the objective differentiation between several pathophysiological mechanisms after severe electric injury to the central nervous system.
2.
Case report
A previously healthy 20-year-old man experienced a low voltage electric injury (400V, 70A) in an occupational accident with loss of consciousness and cardiac arrest followed by
* Corresponding author at: Section of Neuroradiology, Trauma Center Murnau, Professor Küntscher Straße 8, 82418 Murnau, Germany. Fax: +49 8841 48 2160. E-mail address: [email protected] (A. Grillhösl). http://dx.doi.org/10.1016/j.burns.2017.03.012 0305-4179/© 2017 Elsevier Ltd and ISBI. All rights reserved.
Please cite this article in press as: L. Grassner, et al., Different sequelae of electrical brain injury — MRI patterns, Burns (2017), http://dx. doi.org/10.1016/j.burns.2017.03.012
JBUR 5221 No. of Pages 4
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successful cardiopulmonary resuscitation. The suspected entry point of the current was the left ear with development of extensive necrosis thereafter. Exit wounds were localized predominantly at the right body site. The intubated and ventilated patient was transported to the local hospital. On arrival initial brain CT (multisclice CT with reconstructions) demonstrated a slightly decreased density of the white matter of the left temporal lobe. Follow-up brain CT on day 3 revealed a sharply demarcated crescent-shaped (16mm55mm39mm) hypodense lesion of the cortex and the subcortical white matter of the left temporal lobe and decreased density of the left temporo-parieto-occipital white matter. Anticonvulsants were started on day 3 due to seizures. Follow-up brain CT on day 6 revealed progressing brain edema of the left hemisphere and a 5mm midline-shift to the right. Due to extensive burning in the area of the left ear and increased intracranial pressure, the patient was further transferred to our trauma center for multidisciplinary management in our intensive care unit. On day 7 after the injury multiplanar multisequence MRI of the brain with administration of a contrast agent was performed including axial SE T1-weighted (T1w), TSE T2w, FFE T2*w, EPI-DWI (with ADC-correlate) and sagittal 3-D FLAIR (with multiplanar reconstructions) sequences. Imaging data were acquired on a 1.5T system (Philips Achieva, Eindhoven, The Netherlands). A 8-channel SENSE Head coil was used. Firstly axial T1w contrast-enhanced and axial DWI MRI showed diffuse enhancement and cytotoxic edema in the central region (Fig. 1A–C). Secondly axial T1w and axial T1w contrast-enhanced MRI demonstrated hyperintense lesions of the cortex in the left temporal gyri (Fig. 2A,B). In addition, cortex and subcortical white matter of the left temporal gyri were also hyperintense in T2w MRI and FLAIR, indicating ongoing edema in the cortex (Fig. 2C,D). Thirdly axial DWI and ADC-correlate showed cytotoxic edema in the white matter of both hemispheres with the exception of the right frontotemporal region (Fig. 2E,F). The clinical condition deteriorated throughout the next 8 days. The serum level of the neuron specific enolase (NSE) was markedly increased. The patient passed away 15days
after the accident without regaining consciousness. Any prior neurosurgical intervention was denied by the parents according to the patient’s most probable wish.
3.
Discussion
Electrical injuries are increasing and occur almost exclusively in young men as a result of occupational hazards and in children [4]. There are several pathways by which electricity may cause injury: thermal and nonthermal mechanisms as well as event-associated injuries, for example trauma and hypoxic injuries due to ventricular fibrillation [4]. The International Electromechanical Commission defines high voltage as above 1000V for alternating current [5]. In general, high-voltage electric injury is thought to be more dangerous as low-voltage electric injury, because the former is associated with more severe tissue destruction and higher mortality. However, in low voltage electric trauma, immediate death may occur either from current induced-ventricular fibrillation or from respiratory arrest, and victims who survive may remain in a persistent vegetative state as a result of global hypoxia [6]. Our patient suffered cardiac arrest followed by successful cardiopulmonary resuscitation. MRI revealed typical findings for global hypoxia [7]: Axial T1w contrast-enhanced and axial DWI MRI showed diffuse enhancement and cytotoxic edema in the cortex of the central region (Fig. 1A–C). Although the severity of thermal injuries is determined primarily by the voltage, low-voltage injuries can be just as dangerous as high voltage ones under certain conditions for instance in coexisting high electric field strength (70A in our case). According to Joule’s law, the power (heat) is defined as amperage squared times resistance [8]. However, in the majority of previously published reports information about the amperage is missing. In our patient thermal injury was assumed due to the extensive burning in the area of the left ear and the sharply demarcated hypodense lesion of the cortex and the subcortical white matter of the left temporal lobe in the follow-up CT. In thermal injury, electricity generates heat, the amount of which
Fig. 1 – Cranial MRI of hypoxic injury. Axial SE T1-weighted (TE 15ms, TR 704ms) contrast-enhanced (7ml Gadovist i.v.) cMRI (A) shows diffuse enhancement in the central region. Axial diffusion-weighted (B-value 1000) imaging (B) and ADC-correlate (C) show cytotoxic edema in the central region. Please cite this article in press as: L. Grassner, et al., Different sequelae of electrical brain injury — MRI patterns, Burns (2017), http://dx. doi.org/10.1016/j.burns.2017.03.012
JBUR 5221 No. of Pages 4
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e3
Fig. 2 – Cranial MRI showing thermal and current-related electric injury. Axial SE T1-weighted (TE 13ms, TR 615ms) MRI (A) and axial SE T1-weighted (TE 15ms, TR 704ms) contrast-enhanced (7ml Gadovist i.v.) cMRI (B) show the hyperintense temporal lesion due to thermal injury. This lesion is also hyperintense in axial TSE T2-weighted (TE 100ms, TR 5252) MRI (C) and axial FLAIR (3D-FLAIR, TE 318ms, TR 4800) (D). Axial diffusion-weighted (B-value 1000) imaging (E) and ADC-correlate (F) show cytotoxic edema in the white matter due to current flow. is proportional to tissue resistance. The tissue resistance of bone is the highest, so the temporal calvarium nearby the suspected entry point of the current might have generated the most heat [9]. MRI showed the already described hyperintense lesions of the underlying left temporal cortex in the T1w and T1w contrast-enhanced MRI (Fig. 2A,B) with hyperintensity of the cortex and the subcortical white matter in T2w MRI and FLAIR (Fig. 2C,D). Noteworthy, thermal injury may also give rise to vasoconstriction of cerebral blood vessels with intimal injury and subsequent thrombosis [9]. Low-voltage current tends to spread through tissues with low resistance, such as vessels and nervous tissue. This explains why low currents may induce fatal injuries, such as ventricular fibrillation and cardiac arrest [10]. In our patient axial diffusion weighted imaging and ADCcorrelate showed cytotoxic edema in the white matter. This can be interpreted as nonthermal injury causing direct as well as indirect destruction of cells (Fig. 2E,F) [11]. The sodium– potassium-ATPase pump, which normally operates at 90mV of direct current, is disrupted by higher-voltage alternating current. Breakdown of cell membranes and electroporation of cellular membranes are the consequence [9]. In electric injury prompt cranial computed tomography is indicated to rule out event-associated injuries, for example intracranial hemorrhage [12]. In prolonged unconscious patients MR-imaging should be performed to detect the extent of brain damage for therapeutic and prognostic reasons. Moreover MRI is best suited for differentiating hypoxic,
thermal and nonthermal mechanisms of electric injury contributing to the cerebral damage: Hypoxia is characterized by cytotoxic edema in the cortex of the central region and the basal ganglia. In thermal injuries MR-imaging shows T1w- and T2w-hyperintense lesions of the brain parenchyma (grey and white matter) near the superficial burns. And last but not least nonthermal mechanisms of electric injury are revealed by cytotoxic edema of the white matter.
4.
Conclusion
Electric injury may affect the central nervous system. MRI is capable to assess a variety of cerebral lesions for diagnostic and potentially prognostic reasons.
Acknowledgment/Disclosure statement/Grant support Dr. Grassner reports no disclosures. Dr. Bierschneider has received speakers’ honoria from AO Foundation, he has no specific conflicts relevant to this work. Associate Professor Strowitzki has received speakers’ honoria from AFOR, he has no specific conflicts relevant to this work. Dr. Grillhösl has received speakers’ honoria from Deutsche Gesellschaft für Neurowissenschaftliche Begutachtung and from AO Foundation, he has no specific conflicts relevant to this work.
Please cite this article in press as: L. Grassner, et al., Different sequelae of electrical brain injury — MRI patterns, Burns (2017), http://dx. doi.org/10.1016/j.burns.2017.03.012
JBUR 5221 No. of Pages 4
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burns xxx (2017) xxx –xxx
REFERENCES
[8] [1] Farrell DF, Starr A. Delayed neurological sequelae of electrical injuries. Neurology 1968;18(6):601–6. [2] Lee RC, Kolodney MS. Electrical injury mechanisms: electrical breakdown of cell membranes. Plast Reconstr Surg 1987;80 (5):672–9. [3] Arevalo JM, Lorente JA, Balseiro-Gomez J. Spinal cord injury after electrical trauma treated in a burn unit. Burns 1999;25 (5):449–52. [4] Johansen CK, Welker KM, Lindell EP, Petty GW. Cerebral corticospinal tract injury resulting from high-voltage electrical shock. AJNR Am J Neuroradiol 2008;29(6):1142–3, doi: http://dx.doi.org/10.3174/ajnr.A1009. [5] International Standard IEC 60038:1983.. [6] Yeong EK, Huang HF. Persistent vegetative state in electrical injuries: a 10-year review. Burns 2008;34(4):539–42, doi:http:// dx.doi.org/10.1016/j.burns.2007.06.011. [7] Hirsch KG, Mlynash M, Jansen S, Persoon S, Eyngorn I, Krasnokutsky MV, Wijman CAC, Fischbein NJ. Prognostic value of a qualitative brain MRI scoring system after cardiac
[9]
[10]
[11]
[12]
arrest. J Neuroimaging 2015;25:430–7, doi:http://dx.doi.org/ 10.1111/jon.12143. Hunt JL, Mason Jr. AD, Masterson TS, Pruitt Jr. BA. The pathophysiology of acute electric injuries. J Trauma 1976;16 (5):335–40. Ackerman LL, Ryken TC, Kealey GP, Traynelis VC. Onset of symptomatic hydrocephalus requiring emergency cerebrospinal fluid diversion following high-voltage electrical burn injury. J Neurosurg 2010;112(2):394–8, doi:http://dx.doi. org/10.3171/2009.7.JNS09578. 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(2):277–81, doi:http://dx.doi.org/ 10.5535/arm.2014.38.2.277. Scholz T, Rippmann V, Wojtecki L, Perbix W, Rothschild MA, Spilker G. Severe brain damage by current flow after electrical burn injury. J Burn Care Res 2006;27:917–22, doi:http://dx.doi. org/10.1097/01.BCR.0000245646.80680.26. Liao WC, Lin JT. High-voltage electrical brain injury. J Trauma 2008;64(3):843–5, doi:http://dx.doi.org/10.1097/01. ta.0000234739.14621.3e.
Please cite this article in press as: L. Grassner, et al., Different sequelae of electrical brain injury — MRI patterns, Burns (2017), http://dx. doi.org/10.1016/j.burns.2017.03.012
burns xxx (2017) xxx –xxx
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.elsevier.com/locate/burns
Case report
Different sequelae of electrical brain injury — MRI patterns Lukas Grassner a,b,c , Michael Bierschneider a, Martin Strowitzki a, Andreas Grillhösl d, * a
Department of Neurosurgery, Trauma Center Murnau, Germany Center for Spinal Cord Injuries, Trauma Center Murnau, Germany c Institute of Molecular Regenerative Medicine, Spinal Cord Injury and Tissue Regeneration Center Salzburg, Paracelsus Medical University Salzburg, Austria d Section of Neuroradiology, Trauma Center Murnau, Germany b
article info
abstract
Article history:
Purpose: Electrical injury to the central nervous system may lead to neurologic compromise
Accepted 14 March 2017
via pleiotropic mechanisms. It may cause current-related, thermal or nonthermal damage
Available online xxx
followed by secondary mechanisms. Methods: We herein report a case of a 20-year old man, who experienced a low-voltage electric
Keywords: Electrical injury Brain
of pathophysiologic features including thermal, nonthermal and hypoxic cerebral lesions. Conclusion: The capability of MRI assessing a variety of lesions for diagnostic and potentially
MRI Diagnosis
1.
injury due to an occupational accident. Results: Magnetic resonance imaging (MRI) one week after the insult allowed differentiation
prognostic reasons is presented.
Introduction
Electrical injury may affect multiple organ systems. Neurologic compromise may present in different ways including cerebral or spinal cord injury as well as peripheral nerve injuries. The clinical manifestation might be acute or delayed [1]. Depending on the entry site, the nervous system might be affected via a pleiotropic route of action resulting in direct thermal-induced or current related insults as well as secondary injuries such as disruption of transmembrane ion gradients due to electroporation of proteins [2]. Therefore
© 2017 Elsevier Ltd and ISBI. All rights reserved.
cells with a relatively large surface – like neurons – are most likely more susceptible to electric injury [3]. Nowadays MRI may allow the objective differentiation between several pathophysiological mechanisms after severe electric injury to the central nervous system.
2.
Case report
A previously healthy 20-year-old man experienced a low voltage electric injury (400V, 70A) in an occupational accident with loss of consciousness and cardiac arrest followed by
* Corresponding author at: Section of Neuroradiology, Trauma Center Murnau, Professor Küntscher Straße 8, 82418 Murnau, Germany. Fax: +49 8841 48 2160. E-mail address: [email protected] (A. Grillhösl). http://dx.doi.org/10.1016/j.burns.2017.03.012 0305-4179/© 2017 Elsevier Ltd and ISBI. All rights reserved.
Please cite this article in press as: L. Grassner, et al., Different sequelae of electrical brain injury — MRI patterns, Burns (2017), http://dx. doi.org/10.1016/j.burns.2017.03.012
JBUR 5221 No. of Pages 4
e2
burns xxx (2017) xxx –xxx
successful cardiopulmonary resuscitation. The suspected entry point of the current was the left ear with development of extensive necrosis thereafter. Exit wounds were localized predominantly at the right body site. The intubated and ventilated patient was transported to the local hospital. On arrival initial brain CT (multisclice CT with reconstructions) demonstrated a slightly decreased density of the white matter of the left temporal lobe. Follow-up brain CT on day 3 revealed a sharply demarcated crescent-shaped (16mm55mm39mm) hypodense lesion of the cortex and the subcortical white matter of the left temporal lobe and decreased density of the left temporo-parieto-occipital white matter. Anticonvulsants were started on day 3 due to seizures. Follow-up brain CT on day 6 revealed progressing brain edema of the left hemisphere and a 5mm midline-shift to the right. Due to extensive burning in the area of the left ear and increased intracranial pressure, the patient was further transferred to our trauma center for multidisciplinary management in our intensive care unit. On day 7 after the injury multiplanar multisequence MRI of the brain with administration of a contrast agent was performed including axial SE T1-weighted (T1w), TSE T2w, FFE T2*w, EPI-DWI (with ADC-correlate) and sagittal 3-D FLAIR (with multiplanar reconstructions) sequences. Imaging data were acquired on a 1.5T system (Philips Achieva, Eindhoven, The Netherlands). A 8-channel SENSE Head coil was used. Firstly axial T1w contrast-enhanced and axial DWI MRI showed diffuse enhancement and cytotoxic edema in the central region (Fig. 1A–C). Secondly axial T1w and axial T1w contrast-enhanced MRI demonstrated hyperintense lesions of the cortex in the left temporal gyri (Fig. 2A,B). In addition, cortex and subcortical white matter of the left temporal gyri were also hyperintense in T2w MRI and FLAIR, indicating ongoing edema in the cortex (Fig. 2C,D). Thirdly axial DWI and ADC-correlate showed cytotoxic edema in the white matter of both hemispheres with the exception of the right frontotemporal region (Fig. 2E,F). The clinical condition deteriorated throughout the next 8 days. The serum level of the neuron specific enolase (NSE) was markedly increased. The patient passed away 15days
after the accident without regaining consciousness. Any prior neurosurgical intervention was denied by the parents according to the patient’s most probable wish.
3.
Discussion
Electrical injuries are increasing and occur almost exclusively in young men as a result of occupational hazards and in children [4]. There are several pathways by which electricity may cause injury: thermal and nonthermal mechanisms as well as event-associated injuries, for example trauma and hypoxic injuries due to ventricular fibrillation [4]. The International Electromechanical Commission defines high voltage as above 1000V for alternating current [5]. In general, high-voltage electric injury is thought to be more dangerous as low-voltage electric injury, because the former is associated with more severe tissue destruction and higher mortality. However, in low voltage electric trauma, immediate death may occur either from current induced-ventricular fibrillation or from respiratory arrest, and victims who survive may remain in a persistent vegetative state as a result of global hypoxia [6]. Our patient suffered cardiac arrest followed by successful cardiopulmonary resuscitation. MRI revealed typical findings for global hypoxia [7]: Axial T1w contrast-enhanced and axial DWI MRI showed diffuse enhancement and cytotoxic edema in the cortex of the central region (Fig. 1A–C). Although the severity of thermal injuries is determined primarily by the voltage, low-voltage injuries can be just as dangerous as high voltage ones under certain conditions for instance in coexisting high electric field strength (70A in our case). According to Joule’s law, the power (heat) is defined as amperage squared times resistance [8]. However, in the majority of previously published reports information about the amperage is missing. In our patient thermal injury was assumed due to the extensive burning in the area of the left ear and the sharply demarcated hypodense lesion of the cortex and the subcortical white matter of the left temporal lobe in the follow-up CT. In thermal injury, electricity generates heat, the amount of which
Fig. 1 – Cranial MRI of hypoxic injury. Axial SE T1-weighted (TE 15ms, TR 704ms) contrast-enhanced (7ml Gadovist i.v.) cMRI (A) shows diffuse enhancement in the central region. Axial diffusion-weighted (B-value 1000) imaging (B) and ADC-correlate (C) show cytotoxic edema in the central region. Please cite this article in press as: L. Grassner, et al., Different sequelae of electrical brain injury — MRI patterns, Burns (2017), http://dx. doi.org/10.1016/j.burns.2017.03.012
JBUR 5221 No. of Pages 4
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e3
Fig. 2 – Cranial MRI showing thermal and current-related electric injury. Axial SE T1-weighted (TE 13ms, TR 615ms) MRI (A) and axial SE T1-weighted (TE 15ms, TR 704ms) contrast-enhanced (7ml Gadovist i.v.) cMRI (B) show the hyperintense temporal lesion due to thermal injury. This lesion is also hyperintense in axial TSE T2-weighted (TE 100ms, TR 5252) MRI (C) and axial FLAIR (3D-FLAIR, TE 318ms, TR 4800) (D). Axial diffusion-weighted (B-value 1000) imaging (E) and ADC-correlate (F) show cytotoxic edema in the white matter due to current flow. is proportional to tissue resistance. The tissue resistance of bone is the highest, so the temporal calvarium nearby the suspected entry point of the current might have generated the most heat [9]. MRI showed the already described hyperintense lesions of the underlying left temporal cortex in the T1w and T1w contrast-enhanced MRI (Fig. 2A,B) with hyperintensity of the cortex and the subcortical white matter in T2w MRI and FLAIR (Fig. 2C,D). Noteworthy, thermal injury may also give rise to vasoconstriction of cerebral blood vessels with intimal injury and subsequent thrombosis [9]. Low-voltage current tends to spread through tissues with low resistance, such as vessels and nervous tissue. This explains why low currents may induce fatal injuries, such as ventricular fibrillation and cardiac arrest [10]. In our patient axial diffusion weighted imaging and ADCcorrelate showed cytotoxic edema in the white matter. This can be interpreted as nonthermal injury causing direct as well as indirect destruction of cells (Fig. 2E,F) [11]. The sodium– potassium-ATPase pump, which normally operates at 90mV of direct current, is disrupted by higher-voltage alternating current. Breakdown of cell membranes and electroporation of cellular membranes are the consequence [9]. In electric injury prompt cranial computed tomography is indicated to rule out event-associated injuries, for example intracranial hemorrhage [12]. In prolonged unconscious patients MR-imaging should be performed to detect the extent of brain damage for therapeutic and prognostic reasons. Moreover MRI is best suited for differentiating hypoxic,
thermal and nonthermal mechanisms of electric injury contributing to the cerebral damage: Hypoxia is characterized by cytotoxic edema in the cortex of the central region and the basal ganglia. In thermal injuries MR-imaging shows T1w- and T2w-hyperintense lesions of the brain parenchyma (grey and white matter) near the superficial burns. And last but not least nonthermal mechanisms of electric injury are revealed by cytotoxic edema of the white matter.
4.
Conclusion
Electric injury may affect the central nervous system. MRI is capable to assess a variety of cerebral lesions for diagnostic and potentially prognostic reasons.
Acknowledgment/Disclosure statement/Grant support Dr. Grassner reports no disclosures. Dr. Bierschneider has received speakers’ honoria from AO Foundation, he has no specific conflicts relevant to this work. Associate Professor Strowitzki has received speakers’ honoria from AFOR, he has no specific conflicts relevant to this work. Dr. Grillhösl has received speakers’ honoria from Deutsche Gesellschaft für Neurowissenschaftliche Begutachtung and from AO Foundation, he has no specific conflicts relevant to this work.
Please cite this article in press as: L. Grassner, et al., Different sequelae of electrical brain injury — MRI patterns, Burns (2017), http://dx. doi.org/10.1016/j.burns.2017.03.012
JBUR 5221 No. of Pages 4
e4
burns xxx (2017) xxx –xxx
REFERENCES
[8] [1] Farrell DF, Starr A. Delayed neurological sequelae of electrical injuries. Neurology 1968;18(6):601–6. [2] Lee RC, Kolodney MS. Electrical injury mechanisms: electrical breakdown of cell membranes. Plast Reconstr Surg 1987;80 (5):672–9. [3] Arevalo JM, Lorente JA, Balseiro-Gomez J. Spinal cord injury after electrical trauma treated in a burn unit. Burns 1999;25 (5):449–52. [4] Johansen CK, Welker KM, Lindell EP, Petty GW. Cerebral corticospinal tract injury resulting from high-voltage electrical shock. AJNR Am J Neuroradiol 2008;29(6):1142–3, doi: http://dx.doi.org/10.3174/ajnr.A1009. [5] International Standard IEC 60038:1983.. [6] Yeong EK, Huang HF. Persistent vegetative state in electrical injuries: a 10-year review. Burns 2008;34(4):539–42, doi:http:// dx.doi.org/10.1016/j.burns.2007.06.011. [7] Hirsch KG, Mlynash M, Jansen S, Persoon S, Eyngorn I, Krasnokutsky MV, Wijman CAC, Fischbein NJ. Prognostic value of a qualitative brain MRI scoring system after cardiac
[9]
[10]
[11]
[12]
arrest. J Neuroimaging 2015;25:430–7, doi:http://dx.doi.org/ 10.1111/jon.12143. Hunt JL, Mason Jr. AD, Masterson TS, Pruitt Jr. BA. The pathophysiology of acute electric injuries. J Trauma 1976;16 (5):335–40. Ackerman LL, Ryken TC, Kealey GP, Traynelis VC. Onset of symptomatic hydrocephalus requiring emergency cerebrospinal fluid diversion following high-voltage electrical burn injury. J Neurosurg 2010;112(2):394–8, doi:http://dx.doi. org/10.3171/2009.7.JNS09578. 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(2):277–81, doi:http://dx.doi.org/ 10.5535/arm.2014.38.2.277. Scholz T, Rippmann V, Wojtecki L, Perbix W, Rothschild MA, Spilker G. Severe brain damage by current flow after electrical burn injury. J Burn Care Res 2006;27:917–22, doi:http://dx.doi. org/10.1097/01.BCR.0000245646.80680.26. Liao WC, Lin JT. High-voltage electrical brain injury. J Trauma 2008;64(3):843–5, doi:http://dx.doi.org/10.1097/01. ta.0000234739.14621.3e.
Please cite this article in press as: L. Grassner, et al., Different sequelae of electrical brain injury — MRI patterns, Burns (2017), http://dx. doi.org/10.1016/j.burns.2017.03.012