- Email: [email protected]
Survival after severe intrathoracic electrical injury
burns 36 (2010) e61–e64
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/burns
Case report
Survival after severe intrathoracic electrical injury A.R. Schleich a,*, H. Schweiger c, A. Becsey c, C.W. Cruse b a
Mississippi Premier Plastic Surgery, East Medical Tower, St. Dominic Hospital, Suite 315, 971 Lakeland Drive, Jackson, MS 39216, USA Division of Plastic Surgery, University of South Florida College of Medicine, USA c Division of Critical Care Medicine, University of South Florida College of Medicine, USA b
article info Article history: Accepted 18 June 2009
1.
Introduction
Electrical injuries account for 2–5% of admissions to specialized burn centers [1–3]. Most often affected are young males suffering work related accidents, such as electricians, crane operators and roofers. The severity of injury and risk of mortality increases with voltage, being highest in lightning injuries, followed by high voltage injuries (arbitrarily defined as exposure to current of more than 1000 V) and low voltage injuries (exposure to less than 1000 V). Fatality rates of 17.6%, 5.3% and 2.8%, respectively, have been reported for these groups [4]. In absolute numbers more than 2000 deaths were attributable to electrical occupational injuries in the US over a 6-year period [5] rendering electrical injury the fifth leading cause of occupational injury death in the United States. The causative mechanism of injury is dissipation of energy in the form of heat along the path of the current resulting in tissue damage proportional to the tissue’s resistance in case of a contact injury and direct thermal injury by flame or electrical arc in the case of non-contact injuries. Whereas the latter is amenable to conservative wound care or excision and skin grafting the former results in diffuse and widespread injury of muscles and neurovascular structures in proximity of long bones, which diffuse most of the energy. Radical surgical excision posing complex reconstructive problems or amputations, particularly of the upper extremities, contribute significantly to the burden of care and disease [6].
Additionally, central neurological injury, cataracts and damage to the myocardium and its conduction system pose immediate and long term clinical problems. Reports about visceral injuries are infrequent. Larger series report 0% [6] to 1.7% [7]. It may be speculated that this low incidence just reflects lack of survivability of a major intrathoracic or intraabdominal electrical injury, much in the same way fatalities from electrocution sustain brain stem and myocardial damage incompatible with life. Isolated lung parenchymal injuries secondary to high voltage accidents only appear in isolated case reports [8,9] attesting to the likely high mortality of transthoracic current flow.
2.
Case report
We present the case of a 23-year-old white male electrician sustaining a high voltage work related contact injury when a power line carrying 70 kV made contact with a truck the patient was holding on to. Upon admission to the intensive care unit of the Tampa Bay Regional Burn Center his sole injuries were found to be third degree burns to his right temporal area neck, lower abdomen and bilateral anterior thighs. Cardiac and hemodynamic monitoring, mechanical ventilation and fluid resuscitation were initiated. Massive myoglobinemia was treated with urine alkalinization and preload augmentation to maintain an hourly urine output of at least 1 ml/kg. Initial emergency department chest X-rays did not reveal lung pathology. Early excision and grafting of the abdomen and both thighs totaling 8% total body surface area was performed on injury day 2. The respective deep fascia in both areas was found to be intact and the thigh compartments where soft to palpation by the senior surgeon (CWC).
* Corresponding author. E-mail address: [email protected] (A.R. Schleich). 0305-4179/$36.00 # 2009 Elsevier Ltd and ISBI. All rights reserved. doi:10.1016/j.burns.2009.06.207
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Fig. 3 – CT scan interpreted as recurrent pulmonary embolism with right lower lobe pneumonia.
Fig. 1 – CT scan interpreted as pulmonary embolism with elements of dependent atelectasis.
The immediate postoperative period was complicated by sudden onset, hemodynamically significant atrial fibrillation, rhabdomyolysis and sepsis. A CT angiogram on injury day 3 was interpreted by a radiologist as pulmonary embolism at the level of segmental bronchi in the right lower lobe. Systemic anticoagulation with a heparin drip was titrated to aPTT of 50– 70 s. On injury day 8, an inferior vena cava filter was inserted (Figs. 1 and 2). Sepsis treatment was instituted according to standard guidelines [10] including the insertion of a Swan– Ganz catheter to guide the hemodynamic management of a state of low systemic vascular resistance with concomitantly elevated pulmonary artery pressures, steroids for adrenal insufficiency, enteral nutrition, treatment for rhabdomyolysis, and empiric and culture specific antibiotics directed at pathogens obtained by bronchoscopic sampling. An open tracheostomy was performed in anticipation of long term mechanical ventilation on injury day 21 at bedside. Despite severe medical instability 90% take of the skin grafts was achieved and areas of graft loss healed secondarily under conservative wound care with silvadene followed by wet to dry dressing changes. Repeat skin grafting was not necessary.
Fig. 2 – Filling defects noted in the right lower and middle pulmonary artery.
Fig. 4 – CT scan prior to thoracotomy showing cavitations subsequent to necrosis of lung tissue predominantly in the lower lobe.
Failure to improve despite maximum medical therapy was attributed to persistent right lung pathology manifesting itself as a persistent infiltrate on chest X-ray with recurrent pleural effusions, which were aspirated twice and eventually treated with insertion of a small chest tube. Gas exchange was markedly impaired and the patient exhibited shunt related hypoxia, which showed short lived improvement after daily bronchoscopic suctioning of the right lower and middle lobe. Airway pressure release ventilation was employed as a ventilator strategy to maintain oxygenation. Serial CT scanning (on injury days 7, 10, 16, 19, 24) failed to show resolution of the right lower lobe pathology and eventually exhibited cavitation of the lung parenchyma, which prompted an exploratory thoracotomy on day 27 with subsequent resection
burns 36 (2010) e61–e64
of the right lower lobe and parts of the middle lobe to remove macroscopically necrotic and infected lung tissue (Figs. 3 and 4). Immediate improvement was slowed by postoperative hemorrhage from the line of lung resection requiring an emergent return to the operating room on day 34. A bronchopleural fistula persisted and required prolonged drainage with a thoracostomy tube for 3 weeks. Ultimately all life threatening issues resolved and rehabilitation was begun enabling the patient to literally walk out of the intensive care unit when he was transferred to a rehabilitation center 2 months after his initial injury, from where he was discharged home to achieve functional societal integration.
3.
Discussion
The consequences of high voltage electrical injury are usually obvious ranging from extensive soft tissue loss, non-viability of extremities, neurovascular damage and compartment syndrome to brain death or intractable cardiac arrest. However, intrathoracic injury due to the passage of current resulting in necrosis of lung tissue while maintaining enough working myocardium to produce a hyperdynamic state seems to be a very unlikely event. In this young patient no underlying lung or chest wall injuries were evident. The working diagnosis of early nosocomial pneumonia was initially supported by a bronchoscopically obtained positive microbiologic specimen, which is more than 90% sensitive and specific for the presence of pneumonia. The lack of any meaningful response to maximal, microbiologically directed therapy and patterns of vascular change inconsistent with an acute inflammatory process may be taken as an argument against the pneumonia hypothesis. Similarly, we provided maximum medical and surgical treatment for presumed pulmonary embolism by instituting systemic anticoagulation and later inserting an inferior vena cava filter basing the diagnosis on a study which is ascribed a specificity of at least 89% [11]. The clinical course of persistent pulmonary hypertension, respiratory distress and unchanging and eventually worsening findings on serial CT scans in the face of maximum therapy is not the likely course of a pulmonary embolism and led to the consideration of the CT scans as a false positive finding. Electrical current does result in direct vascular damage, which is non-selective. We opine that due to this nonselectivity a scenario of damaged bronchial circulation in the face of a pulmonary vasculature conducive to flow is pathophysiologically unlikely so that our findings cannot be explained by an embolus occluding the remaining patent vasculature and leading to distal ischemia. Axial computed tomography with intravenous contrast is not able to assess the vasculature beyond segmental branching vessels limiting its usefulness for the evaluation of smaller peripheral thrombi, but also smaller vessels such as the bronchial circulation. Comparing the results of the initial CT scan on the right side with areas of atelectasis on the left, from which blood is shunted away, we find less contrast enhancement and thus greater relative ischemia on the right without clear signs of filling of bronchial vessels.
e63
Pulmonary infarction has been reported in the differential diagnosis of pulmonary embolism [12,13] on the basis of imaging data without consistent histological verification of infarction. The clinical and radiological course in our case is not consistent with pulmonary infarction as a consequence of pulmonary artery occlusion [14], but appears more compatible with wide spread vascular insult in all pulmonary vascular beds [15] supporting our hypothesis of electrical injury to the lung. While we cannot discount the possibility of a combined insult we consider the development of thrombosis in an electrically damaged pulmonary artery (and not embolism) by far more likely, again supporting a high likelihood of electrical lung injury. With the patient’s physiology being consistent with a persistent septic focus we think that the microbiologic spectrum of nosocomial gram negative bacteria isolated from the right lower lobe was more consistent with a region of infected necrosis caused by the electrical injury than a necrotizing lung infection. Similar to other reports [8] we found a macroscopically infected necrotic and infected block of lung tissue. Histologically, necrosis with secondary changes such as abscess formation and liquefaction were confirmed. The diagnosis was considered and thoracotomy was performed as early as on the third day post-injury in the case described in [8], which lacked some of the characteristics of our patient, most notably the early positive microbiological specimens acquired by techniques thought to represent the diagnostic gold standard and the CT angiographic findings consistent with pulmonary embolism, which is simply more prevalent in any population of postoperative patients than other causes of cessation of flow to an area of lung. Some questions remain open, though. One concerns the supposed path of current from the right temporal region through neck skin and right lung to the lower abdomen and right thigh without causing any visceral injury except to the right lung. The other relates to the persistent rhabdomyolysis which only improved after lung resection. While we may speculate that the current followed the path of least resistance at the time of injury resulting in this peculiar injury pattern, the airways and lung certainly do not possess enough muscle cells containing enough myoglobin to maintain significantly elevated laboratory values over several weeks.
4.
Conclusion
Reports of intrathoracic electrical injury appear sporadically in the literature [8,9] attesting to the difficulty at arriving at the correct diagnosis in the setting of a very low prevalence of survivors of electrical injuries of this kind. It is also very unlikely to find the tissue changes required to produce the clinical picture presented here in any postmortem specimens of electrocutions, as the initial damage is thought to be electroporation of the cell membrane without even specific ultrastructural changes prior to the death of the organism [16]. We thus think that parenchymal lung damage by high voltage current remains a clinical diagnosis of exclusion with a list of differential diagnosis encompassing the entire spectrum of frequent lung problems in critical care.
e64
burns 36 (2010) e61–e64
Surviving this injury despite a significant delay in diagnosis attests to the power of modern strategies in maximum supportive medical therapy but also to the age old surgical adage that the patient only gets better once all necrotic tissue has been removed.
Conflict of interest None declared.
Acknowledgements We wish to thank Dr. Mark J. Alkire and Dr. John C. Brock for their participation in the care of this patient.
references
[1] Tredget EE, Shankowsky HA, Tilley WA. Electrical injuries in Canadian burn care. Annals of the New York Academy of Sciences 1999;888:75–87. [2] Ge S, Yang Y, Bai G. Treatment of severe electrical burns. Annals of the New York Academy of Sciences 1999;888: 60–74. [3] Koumbourlis AC. Electrical injuries. Critical Care Medicine 2002;30(Suppl. 1):S424–30. [4] Arnoldo BD, Purdue GF, Kowalske K, Helm PA, Burris A, Hunt JL. Electrical injuries: a 20 year review. Journal of Burn Care and Rehabilitation 2004;25:479–84. [5] Cawley JC, Homce GT. Occupational electrical injuries in the United States, 1992–1998, and recommendations for safety research. Journal of Safety Research 2003;34:241–8.
[6] Hussmann J, Kucan JO, Russell RC, Bradley T, Zamboni WA. Electrical injuries—morbidity, outcome and treatment rationale. Burns 1995;21:530–5. [7] Haberal M, Ucar N, Bayraktar U, Oner Z, Bilgin N. Visceral injuries, wound infections and sepsis following electrical injuries. Burns 1996;22:158–61. [8] Masanes MJ, Gourbiere E, Prudent J, Lioret N, Febvre M, Prevot S, et al. A high voltage electrical burn of lung parenchyma. Burns 2000;26:659–63. [9] Goldenberg DC, Bringel RW, Fontana C, Teixeira TL, de Almeida PC, de Faria JC, et al. Pulmonary lesion in electrical injury: report of a case. Revista do Hospital das Clinicas 1996;51:15–7. [10] Surviving Sepsis Campaign Management Guidelines Committee. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Critical Care Medicine 2004;32:858–73. [11] Eng J, Krishnan JA, Segal JB, Bolger DT, Tamariz TJ, Streiff MB, et al. Accuracy of CT in the diagnosis of pulmonary embolism: a systematic literature review. American Journal of Roentgenology 2004;183:1819–27. [12] Revel MP, Triki R, Chatellier G, Couchon S, Haddad N, Hernigou A, et al. Is it possible to recognize pulmonary infarction on multisection CT images? Radiology 2007;244(3):875–82. [13] He H, Stein MW, Zalta B, Haramati LB. Pulmonary infarction: spectrum of findings on multidetector helical CT. Journal of Thoracic Imaging 2006;21(1):1–7. [14] Remy J, Deschildre F, Artaud D, Remy-Jardin M, Copin MC, Bordet R, et al. Bronchial arteries in the pig before and after permanent pulmonary artery occlusion. Investigative Radiology 1997;32(4):218–24. [15] Jandik J, Endrys J, Rehulova E, Mraz J, Sedlacek J, De Geest H. Bronchial artereis in experimental pulmonary infarction. Angiographic and morphometric study. Cardiovascular Research 1993;27(6):1076–83. [16] Lee RC, Astumian AD. The physicochemical basis for thermal and nonthermal burn injuries. Burns 1996;22:509–19.
available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/burns
Case report
Survival after severe intrathoracic electrical injury A.R. Schleich a,*, H. Schweiger c, A. Becsey c, C.W. Cruse b a
Mississippi Premier Plastic Surgery, East Medical Tower, St. Dominic Hospital, Suite 315, 971 Lakeland Drive, Jackson, MS 39216, USA Division of Plastic Surgery, University of South Florida College of Medicine, USA c Division of Critical Care Medicine, University of South Florida College of Medicine, USA b
article info Article history: Accepted 18 June 2009
1.
Introduction
Electrical injuries account for 2–5% of admissions to specialized burn centers [1–3]. Most often affected are young males suffering work related accidents, such as electricians, crane operators and roofers. The severity of injury and risk of mortality increases with voltage, being highest in lightning injuries, followed by high voltage injuries (arbitrarily defined as exposure to current of more than 1000 V) and low voltage injuries (exposure to less than 1000 V). Fatality rates of 17.6%, 5.3% and 2.8%, respectively, have been reported for these groups [4]. In absolute numbers more than 2000 deaths were attributable to electrical occupational injuries in the US over a 6-year period [5] rendering electrical injury the fifth leading cause of occupational injury death in the United States. The causative mechanism of injury is dissipation of energy in the form of heat along the path of the current resulting in tissue damage proportional to the tissue’s resistance in case of a contact injury and direct thermal injury by flame or electrical arc in the case of non-contact injuries. Whereas the latter is amenable to conservative wound care or excision and skin grafting the former results in diffuse and widespread injury of muscles and neurovascular structures in proximity of long bones, which diffuse most of the energy. Radical surgical excision posing complex reconstructive problems or amputations, particularly of the upper extremities, contribute significantly to the burden of care and disease [6].
Additionally, central neurological injury, cataracts and damage to the myocardium and its conduction system pose immediate and long term clinical problems. Reports about visceral injuries are infrequent. Larger series report 0% [6] to 1.7% [7]. It may be speculated that this low incidence just reflects lack of survivability of a major intrathoracic or intraabdominal electrical injury, much in the same way fatalities from electrocution sustain brain stem and myocardial damage incompatible with life. Isolated lung parenchymal injuries secondary to high voltage accidents only appear in isolated case reports [8,9] attesting to the likely high mortality of transthoracic current flow.
2.
Case report
We present the case of a 23-year-old white male electrician sustaining a high voltage work related contact injury when a power line carrying 70 kV made contact with a truck the patient was holding on to. Upon admission to the intensive care unit of the Tampa Bay Regional Burn Center his sole injuries were found to be third degree burns to his right temporal area neck, lower abdomen and bilateral anterior thighs. Cardiac and hemodynamic monitoring, mechanical ventilation and fluid resuscitation were initiated. Massive myoglobinemia was treated with urine alkalinization and preload augmentation to maintain an hourly urine output of at least 1 ml/kg. Initial emergency department chest X-rays did not reveal lung pathology. Early excision and grafting of the abdomen and both thighs totaling 8% total body surface area was performed on injury day 2. The respective deep fascia in both areas was found to be intact and the thigh compartments where soft to palpation by the senior surgeon (CWC).
* Corresponding author. E-mail address: [email protected] (A.R. Schleich). 0305-4179/$36.00 # 2009 Elsevier Ltd and ISBI. All rights reserved. doi:10.1016/j.burns.2009.06.207
e62
burns 36 (2010) e61–e64
Fig. 3 – CT scan interpreted as recurrent pulmonary embolism with right lower lobe pneumonia.
Fig. 1 – CT scan interpreted as pulmonary embolism with elements of dependent atelectasis.
The immediate postoperative period was complicated by sudden onset, hemodynamically significant atrial fibrillation, rhabdomyolysis and sepsis. A CT angiogram on injury day 3 was interpreted by a radiologist as pulmonary embolism at the level of segmental bronchi in the right lower lobe. Systemic anticoagulation with a heparin drip was titrated to aPTT of 50– 70 s. On injury day 8, an inferior vena cava filter was inserted (Figs. 1 and 2). Sepsis treatment was instituted according to standard guidelines [10] including the insertion of a Swan– Ganz catheter to guide the hemodynamic management of a state of low systemic vascular resistance with concomitantly elevated pulmonary artery pressures, steroids for adrenal insufficiency, enteral nutrition, treatment for rhabdomyolysis, and empiric and culture specific antibiotics directed at pathogens obtained by bronchoscopic sampling. An open tracheostomy was performed in anticipation of long term mechanical ventilation on injury day 21 at bedside. Despite severe medical instability 90% take of the skin grafts was achieved and areas of graft loss healed secondarily under conservative wound care with silvadene followed by wet to dry dressing changes. Repeat skin grafting was not necessary.
Fig. 2 – Filling defects noted in the right lower and middle pulmonary artery.
Fig. 4 – CT scan prior to thoracotomy showing cavitations subsequent to necrosis of lung tissue predominantly in the lower lobe.
Failure to improve despite maximum medical therapy was attributed to persistent right lung pathology manifesting itself as a persistent infiltrate on chest X-ray with recurrent pleural effusions, which were aspirated twice and eventually treated with insertion of a small chest tube. Gas exchange was markedly impaired and the patient exhibited shunt related hypoxia, which showed short lived improvement after daily bronchoscopic suctioning of the right lower and middle lobe. Airway pressure release ventilation was employed as a ventilator strategy to maintain oxygenation. Serial CT scanning (on injury days 7, 10, 16, 19, 24) failed to show resolution of the right lower lobe pathology and eventually exhibited cavitation of the lung parenchyma, which prompted an exploratory thoracotomy on day 27 with subsequent resection
burns 36 (2010) e61–e64
of the right lower lobe and parts of the middle lobe to remove macroscopically necrotic and infected lung tissue (Figs. 3 and 4). Immediate improvement was slowed by postoperative hemorrhage from the line of lung resection requiring an emergent return to the operating room on day 34. A bronchopleural fistula persisted and required prolonged drainage with a thoracostomy tube for 3 weeks. Ultimately all life threatening issues resolved and rehabilitation was begun enabling the patient to literally walk out of the intensive care unit when he was transferred to a rehabilitation center 2 months after his initial injury, from where he was discharged home to achieve functional societal integration.
3.
Discussion
The consequences of high voltage electrical injury are usually obvious ranging from extensive soft tissue loss, non-viability of extremities, neurovascular damage and compartment syndrome to brain death or intractable cardiac arrest. However, intrathoracic injury due to the passage of current resulting in necrosis of lung tissue while maintaining enough working myocardium to produce a hyperdynamic state seems to be a very unlikely event. In this young patient no underlying lung or chest wall injuries were evident. The working diagnosis of early nosocomial pneumonia was initially supported by a bronchoscopically obtained positive microbiologic specimen, which is more than 90% sensitive and specific for the presence of pneumonia. The lack of any meaningful response to maximal, microbiologically directed therapy and patterns of vascular change inconsistent with an acute inflammatory process may be taken as an argument against the pneumonia hypothesis. Similarly, we provided maximum medical and surgical treatment for presumed pulmonary embolism by instituting systemic anticoagulation and later inserting an inferior vena cava filter basing the diagnosis on a study which is ascribed a specificity of at least 89% [11]. The clinical course of persistent pulmonary hypertension, respiratory distress and unchanging and eventually worsening findings on serial CT scans in the face of maximum therapy is not the likely course of a pulmonary embolism and led to the consideration of the CT scans as a false positive finding. Electrical current does result in direct vascular damage, which is non-selective. We opine that due to this nonselectivity a scenario of damaged bronchial circulation in the face of a pulmonary vasculature conducive to flow is pathophysiologically unlikely so that our findings cannot be explained by an embolus occluding the remaining patent vasculature and leading to distal ischemia. Axial computed tomography with intravenous contrast is not able to assess the vasculature beyond segmental branching vessels limiting its usefulness for the evaluation of smaller peripheral thrombi, but also smaller vessels such as the bronchial circulation. Comparing the results of the initial CT scan on the right side with areas of atelectasis on the left, from which blood is shunted away, we find less contrast enhancement and thus greater relative ischemia on the right without clear signs of filling of bronchial vessels.
e63
Pulmonary infarction has been reported in the differential diagnosis of pulmonary embolism [12,13] on the basis of imaging data without consistent histological verification of infarction. The clinical and radiological course in our case is not consistent with pulmonary infarction as a consequence of pulmonary artery occlusion [14], but appears more compatible with wide spread vascular insult in all pulmonary vascular beds [15] supporting our hypothesis of electrical injury to the lung. While we cannot discount the possibility of a combined insult we consider the development of thrombosis in an electrically damaged pulmonary artery (and not embolism) by far more likely, again supporting a high likelihood of electrical lung injury. With the patient’s physiology being consistent with a persistent septic focus we think that the microbiologic spectrum of nosocomial gram negative bacteria isolated from the right lower lobe was more consistent with a region of infected necrosis caused by the electrical injury than a necrotizing lung infection. Similar to other reports [8] we found a macroscopically infected necrotic and infected block of lung tissue. Histologically, necrosis with secondary changes such as abscess formation and liquefaction were confirmed. The diagnosis was considered and thoracotomy was performed as early as on the third day post-injury in the case described in [8], which lacked some of the characteristics of our patient, most notably the early positive microbiological specimens acquired by techniques thought to represent the diagnostic gold standard and the CT angiographic findings consistent with pulmonary embolism, which is simply more prevalent in any population of postoperative patients than other causes of cessation of flow to an area of lung. Some questions remain open, though. One concerns the supposed path of current from the right temporal region through neck skin and right lung to the lower abdomen and right thigh without causing any visceral injury except to the right lung. The other relates to the persistent rhabdomyolysis which only improved after lung resection. While we may speculate that the current followed the path of least resistance at the time of injury resulting in this peculiar injury pattern, the airways and lung certainly do not possess enough muscle cells containing enough myoglobin to maintain significantly elevated laboratory values over several weeks.
4.
Conclusion
Reports of intrathoracic electrical injury appear sporadically in the literature [8,9] attesting to the difficulty at arriving at the correct diagnosis in the setting of a very low prevalence of survivors of electrical injuries of this kind. It is also very unlikely to find the tissue changes required to produce the clinical picture presented here in any postmortem specimens of electrocutions, as the initial damage is thought to be electroporation of the cell membrane without even specific ultrastructural changes prior to the death of the organism [16]. We thus think that parenchymal lung damage by high voltage current remains a clinical diagnosis of exclusion with a list of differential diagnosis encompassing the entire spectrum of frequent lung problems in critical care.
e64
burns 36 (2010) e61–e64
Surviving this injury despite a significant delay in diagnosis attests to the power of modern strategies in maximum supportive medical therapy but also to the age old surgical adage that the patient only gets better once all necrotic tissue has been removed.
Conflict of interest None declared.
Acknowledgements We wish to thank Dr. Mark J. Alkire and Dr. John C. Brock for their participation in the care of this patient.
references
[1] Tredget EE, Shankowsky HA, Tilley WA. Electrical injuries in Canadian burn care. Annals of the New York Academy of Sciences 1999;888:75–87. [2] Ge S, Yang Y, Bai G. Treatment of severe electrical burns. Annals of the New York Academy of Sciences 1999;888: 60–74. [3] Koumbourlis AC. Electrical injuries. Critical Care Medicine 2002;30(Suppl. 1):S424–30. [4] Arnoldo BD, Purdue GF, Kowalske K, Helm PA, Burris A, Hunt JL. Electrical injuries: a 20 year review. Journal of Burn Care and Rehabilitation 2004;25:479–84. [5] Cawley JC, Homce GT. Occupational electrical injuries in the United States, 1992–1998, and recommendations for safety research. Journal of Safety Research 2003;34:241–8.
[6] Hussmann J, Kucan JO, Russell RC, Bradley T, Zamboni WA. Electrical injuries—morbidity, outcome and treatment rationale. Burns 1995;21:530–5. [7] Haberal M, Ucar N, Bayraktar U, Oner Z, Bilgin N. Visceral injuries, wound infections and sepsis following electrical injuries. Burns 1996;22:158–61. [8] Masanes MJ, Gourbiere E, Prudent J, Lioret N, Febvre M, Prevot S, et al. A high voltage electrical burn of lung parenchyma. Burns 2000;26:659–63. [9] Goldenberg DC, Bringel RW, Fontana C, Teixeira TL, de Almeida PC, de Faria JC, et al. Pulmonary lesion in electrical injury: report of a case. Revista do Hospital das Clinicas 1996;51:15–7. [10] Surviving Sepsis Campaign Management Guidelines Committee. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Critical Care Medicine 2004;32:858–73. [11] Eng J, Krishnan JA, Segal JB, Bolger DT, Tamariz TJ, Streiff MB, et al. Accuracy of CT in the diagnosis of pulmonary embolism: a systematic literature review. American Journal of Roentgenology 2004;183:1819–27. [12] Revel MP, Triki R, Chatellier G, Couchon S, Haddad N, Hernigou A, et al. Is it possible to recognize pulmonary infarction on multisection CT images? Radiology 2007;244(3):875–82. [13] He H, Stein MW, Zalta B, Haramati LB. Pulmonary infarction: spectrum of findings on multidetector helical CT. Journal of Thoracic Imaging 2006;21(1):1–7. [14] Remy J, Deschildre F, Artaud D, Remy-Jardin M, Copin MC, Bordet R, et al. Bronchial arteries in the pig before and after permanent pulmonary artery occlusion. Investigative Radiology 1997;32(4):218–24. [15] Jandik J, Endrys J, Rehulova E, Mraz J, Sedlacek J, De Geest H. Bronchial artereis in experimental pulmonary infarction. Angiographic and morphometric study. Cardiovascular Research 1993;27(6):1076–83. [16] Lee RC, Astumian AD. The physicochemical basis for thermal and nonthermal burn injuries. Burns 1996;22:509–19.