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Compartment syndrome on a patient's forearm related to carbon monoxide poisoning
American Journal of Emergency Medicine (2012) 30, 2104.e1–2104.e4
www.elsevier.com/locate/ajem
Case Report Compartment syndrome on a patient's forearm related to carbon monoxide poisoning Abstract Carbon monoxide (CO) is a colorless, odorless, nonirritating, toxic gas produced by the incomplete oxidation of hydrocarbons. Common sources of CO include motor vehicles, house fires, furnaces/heaters, and wood-burning stoves. It is a serious health problem resulting in approximately 50 000 visits to the emergency department and is responsible for 3500 deaths annually in the United States. Besides accidental exposure, CO is also one of the leading causes of death by suicide. In the present study, we discuss compartment syndrome caused by CO poisoning in a 15-year-old boy. To our knowledge, this is the first CO poisoning case causing compartment syndrome. Carbon monoxide (CO) is one of the most common causes of fatal poisoning by either intentional (suicidal) or accidental exposure and may be the most common worldwide cause of fatal poisoning [1]. Despite a great deal of clinical experience and randomized trials, there remains a lot of controversy about the ideal approach to managing CO exposure. Exact statistics for CO poisoning are difficult to ascertain, mainly because of incomplete reporting and misdiagnosis [2,3]. Carbon monoxide may be the cause of more than one-half of the fatal poisonings reported in many countries; fatal cases also are grossly underreported or misdiagnosed by medical professionals. Therefore, the precise number of individuals who have experienced CO intoxication is not known. The health effects associated with exposure to CO range from the more subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO. The symptoms, signs, and prognosis of acute CO poisoning correlate poorly with the level of carboxyhemoglobin measured at the time of hospital admission; however, because CO poisoning is a diagnosis frequently overlooked, the importance of measuring carboxyhemoglobin in suspicious settings cannot be overstated. The early symptoms (headache, 0735-6757/$ – see front matter. Published by Elsevier Inc.
dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Complications occur frequently in CO poisoning. Neurologic manifestation of acute CO poisoning includes disorientation, confusion, and coma. In conclusion, CO poisoning occurs frequently; has severe consequences, including immediate death; involves complications and late sequelae; and often is overlooked. However, compartment syndrome (CS) has not been reported in the literature before now. Efforts for prevention and both public and medical education should be encouraged [1,4]. In the present study, CS is discussed as a complication of acute CO poisoning. The 15-year-old boy patient was found lying on his back and unconscious after staying approximately 6 hours in an enclosed room with a coal stove and brought to the emergency service. His preliminary evaluation was as follows: unconscious, Glasgow Coma Scale 9 (M4, V3, E2), blood pressure 125/65 mm Hg, pulse 120 beats per minutes, temperature 36.5°C, and SpO2 value 89%. In the subsequent examinations, his white blood cell count was found to be 28.9 103/µL, hemoglobin 18.2 g/dL, creatine kinase 1558 U/L, creatine- kinase MB isoenzyme 143 U/L, troponin T 0.123 ng/mL, creatinine 1.18 mg/dL, and urea 40 mg/dL. Swelling and rash were detected on the left forearm in the patient's system examinations; radial and ulnar pulses could be detected by hand. No history of trauma or being underweight for the left arm was found in the patient's anamnesis. The left shoulder, humerus, forearm, and hand-wrist graphing performed were evaluated as normal. Cardiac and respiratory system examinations were normal. Carbon monoxide intoxication was considered for the patient with a history of heating using a stove. Hyperbaric oxygen therapy was planned for the patient, whose CO level was determined to be 25% after a pulse oxymetrical measurement performed using a signal extraction pulse COoximeter device (Masimo Corporation, Irvine, CA, USA). The patient completely regained consciousness after 1 session of hyperbaric oxygen therapy that lasted 2 hours, with 2.5 to 3 atmosphere-pressurized air. In the evaluation performed 10 hours after the initial admission to the emergency service, it was detected that the swelling of the
2104.e2
Case Report
left arm had continued to increase and the radial and ulnar pulses had weakened. Paresthesia, paralysis, and pallor were detected, along with pain in the arm during passive movements. Widespread intramuscular hemorrhage and edema in subcutaneous tissues were observed, whereas flow was present in the axillary artery, brachial artery, proximal radial artery, and proximal ulnar artery; no blood flow in the distal radial artery or distal ulnar artery was reported in colored Doppler examination of the upper left extremity. The findings on Doppler examination resulted in the diagnosis of CS. Fasciotomy was performed after this diagnosis. During the operation, fasciotomy was applied on 4 compartments after a curved incision ranging from the medial thenar section to the cubital area on the volar side of the left forearm (Fig. 1). It was observed that the ulnar and radial pulses returned after fasciotomy. A skin graft was administered on the excision site 10 days after fasciotomy (Fig. 2), and the patient was discharged on the 25th day after his admission. Motor and sensorial examination revealed normal results 45 days after fasciotomy (Fig. 3). Acute CS is a surgical emergency in which decompression is required to restore perfusion, and the exact incidence of CS in the emergency department is unknown. If untreated, the condition can result in irreversible nerve and muscle injury with permanent loss of function and extremity contracture [5,6]. Compartment syndrome has been well described, usually as a consequence of trauma; approximately 3 quarters of cases are associated with fractures [5]. Frequently sited locations for CS include the leg, hand, forearm, arm, shoulder, back, buttocks, thigh, and foot [7]. Compartment syndrome develops when there is increased pressure within a closed tissue space, such as muscle compartments bound by dense fascial sheaths. This increased pressure compromises the flow of blood through vessels supplying the contained muscles and nerves [7]. Although CO binds with hemoglobin in the blood, because it binds to myoglobin and cytochrome in tissues, and because it binds instead of oxygen in structures such as N-adenosine diphosphate that contains a heme ring, oxidative phosphorylation deteriorates at the mitochondrial level. The half-life of CO bound with nonhemoglobin structures is longer than carboxyhemoglobin, and its effects
Fig. 1
Seventy-two hours postfasciotomy.
Fig. 2
Skin graft was performed 10 days postfasciotomy.
are best seen on the heart. In our case, we consider that the influence on nonhemoglobin structures and free radicals composed thereof caused damage to the muscle tissue, resulting in intramuscular hemorrhage and widespread edema in subcutaneous tissues. As a result, CS developed. Moreover, we also consider that the oxygen therapy applied under high pressure might have increased this influence. There are studies that support this hypothesis. It was reported by Grace [8] that ischemia-reperfusion injury was mediated by the interaction of oxygen-derived free radicals, endothelial factors, and neutrophils. Furthermore, Duran et al [9] explained that oxygen-derived free radicals could peroxidate the lipid component of cell membranes, leading to enhanced capillary permeability and causing CS. Hyperbaric oxygen therapy corrected the patient's neurologic findings in our case but could not prevent the occurrence of CS. However, we have no idea why CO intoxication induced CS that only developed in the left forearm in our case. The fact that the patient was found lying on his back and no lesions were found due to pressure on the arm has led us to think that the development of CS was not induced by pressure resulting from compression. In this respect, we consider the event in our case to be a nontraumatic CS. Many cases have been reported regarding nontraumatic CS in the literature. Nontraumatic causes of CS include ischemia-reperfusion events after arterial injury, thrombosis, burns, bleeding disorders, blunt injury [5,6,10], and soft tissue injuries without fracture [5,11]. Iatrogenic
Fig. 3
Control figure 45 days postfasciotomy.
Case Report factors such as tight pneumatic antishock garments or casts can also cause CS [5,6,7,10]. Bacterial and viral infections such as cellulitis, thrombophlebitis, myositis, and lymphangitis [12,13] are rarely associated with acute CS [14,15]. On the other hand, rhabdomyolysis is associated with influenza [16,17], human immunodeficiency virus [18], spider bites [12], and enteroviruses [19], which have all been described as atypical causes of CS. No cases regarding the development of CO intoxication–induced CS has been reported in the literature; from this perspective, our case is the first of its kind. In our case, early findings related to CS (swelling, reddening, confusion, disorientation, and visual disturbances) were noticed when the patient was found (after 6 hours). However, diagnosis of CS and the decision was made to carry out fasciotomy in the 18th hour. This length of time is not higher than the periods reported in the literature. Ramos et al [20] identified the development of CS in 2 cases of nontraumatic children 24 hours after the incident. Because of early diagnosis and the timely application of fasciotomy in our case, tissue necrosis induced by late intervention, organ failure (such as renal failure), organ amputation necessity, and Volkmann ischemic contracture were avoided. However, because of our compartment pressure measuring device was not ready, unlike in many cases reported in the literature, the diagnosis of CS was only made clinically. It was determined that this diagnosis was correct after fasciotomy. It has been reported by Perron et al [21] that early diagnosis and treatment of acute CS is of the utmost importance, as delay can lead to tissue necrosis, and ultimately severe, permanent disability, as with Volkmann ischemic contracture. Untreated CS usually leads to muscle necrosis, limb amputation, and if severe, in large compartments, renal failure, and death. Alertness, clinical suspicion of the possibility of CS, and occasionally, intracompartmental pressure measurement are required to avoid a delay in diagnosis or missed diagnosis. Open fasciotomy, by incising both skin and fascia, is the most reliable method for adequate CS therapy [21]. As a conclusion, without trauma, patients with headache, dizziness, weakness, nausea, confusion, disorientation, visual disturbance, or coma may admit with pain, edema, paresthesia, paralysis, pallor, or necrosis in their leg, hand, forearm, arm, shoulder, back, buttocks, thigh, or foot. Emergency physicians should be alert to these circumstances, and they should keep CS in mind as a consequence of CO poisoning for these patients. Delayed diagnosis and intervention may result in irreversible nerve and muscle injury with permanent loss of function and extremity contracture.
Behçet Al MD Emergency Department of Medicine School in Gaziantep Üniversitesi, Turkey E-mail address: [email protected]
2104.e3 Mehmet Subası MD Ortopedy Department of Medicine School in Gaziantep Üniversitesi, Turkey Burçin Karsli Ortopedy Department of Gaziantep Avukat Cengiz State Hospital, Turkey Pınar Yarbil Emergency Department of Gaziantep Sehitkamil State Hospital, Turkey Suat Zengin Emergency Department of Medicine School in Gaziantep Üniversitesi, Turkey http://dx.doi.org/10.1016/j.ajem.2012.03.011
References [1] Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoning—a public health perspective. Toxicology 2000;145:1-14. [2] Centers for Disease Control and Prevention: unintentional non-fire related carbon monoxide exposures—United States, 2001-2003. MMWR Morb Mortal Wkly Report 2005;54:36. [3] Centers for Disease Control and Prevention: epidemic carbon monoxide poisoning despite a CO alarm law: Mecklenberg County, NC, December 2002. MMWR Morb Mortal Wkly Report 2004;53:189. [4] Maloney G. Carbon Monoxide. In: Tintinalli JE, editor. Tintinalli's Emergency Medicine Section 16 Chapter 217 Environmental Injuries, 7th edNew York: The McGraw-Hill Companies, Inc.; 2010. p. 1410-4. [5] Kostler W, Strohm PC, Sudkamp NP. Acute compartment syndrome of the limb. Injury 2004;35:121-1227. [6] Seiler JG, Olvey SP. Compartment syndromes of the hand and forearm. J Am Soc Surg Hand 2003;3:184-9. [7] Hoover TJ, Siefert JA. Soft tissue complications of orthopedic emergencies. Emerg Med Clin N Am 2000;18:116-39. [8] Grace PA. Ischaemia-reperfusion injury. Br J Surg 1994;81:637-47. [9] Duran W, Takenaka H, Hobson R. Microvascular pathophysiology of skeletal muscle ischaemia-reperfusion. Semin Vasc Surg 1998;11:203-14. [10] Pearse MF, Harry L, Nanchahal J. Acute compartment syndrome of the leg. Br J Med 2002;325:557-8. [11] Susuki T, Moirmura N, Kawai K, et al. Arterial injury associated with acute compartment syndrome of the thigh following blunt trauma. Injury 2005;36:151-9. [12] Andreasen T, Green S, Childers BJ. Massive infectious soft tissue injury: diagnosis and management of necrotizing fasciitis and purpura fulminans. Plast Reconstr Surg 2001;107:1025-34. [13] Falagas ME, Vergidis PI. Narrative review: diseases that masquerade as infectious cellulitis. Ann Intern Med 2005;142:47-56. [14] Harrington P, Scott B, Chetcuti P. Multifocal streptococcal pyomyositis complicated by acute compartment syndrome: a case report. J Pediatr B Orthop 2001;10:120-2. [15] Bibbo C, Patel DV, Mackessy RP, et al. Pyomyositis of the leg with early neurologic compromise. Pediatr Emerg Care 2000;16:352-4. [16] Swaringer JC, Seiler JG, Bruce RW. Influenza A—induced rhabdomyolysis resulting in extensive compartment syndrome. ClinOrthop 2000;375:243-9. [17] Lam R, Lin PH, Alankar S, et al. Acute limb ischemia secondary to myositis-induced compartment syndrome in a patient with human immunodeficiency virus infection. J Vasc Surg 2003;37:1103-5.
2104.e4 [18] Cohen J, Bush S. Case report: compartment syndrome after a suspected black widow spider bite. Ann Emerg Med 2005;45: 414-6. [19] Bhattacharyya T, Vrahas MS. The medical-legal aspects of compartment syndrome. J Bone Joint Surg Am 2004;86:864-8.
Case Report [20] Ramos C, Whyte CM, Harris BH. Nontraumatic compartment syndrome of the extremities in children. J Pediatr Surg 2006;41: 5-7. [21] Perron AD, Brady WJ, Keats TE. Orthopedic Pitfalls in the ED: acute compartment syndrome. Am J Emerg Med 2001;19:413-6.
www.elsevier.com/locate/ajem
Case Report Compartment syndrome on a patient's forearm related to carbon monoxide poisoning Abstract Carbon monoxide (CO) is a colorless, odorless, nonirritating, toxic gas produced by the incomplete oxidation of hydrocarbons. Common sources of CO include motor vehicles, house fires, furnaces/heaters, and wood-burning stoves. It is a serious health problem resulting in approximately 50 000 visits to the emergency department and is responsible for 3500 deaths annually in the United States. Besides accidental exposure, CO is also one of the leading causes of death by suicide. In the present study, we discuss compartment syndrome caused by CO poisoning in a 15-year-old boy. To our knowledge, this is the first CO poisoning case causing compartment syndrome. Carbon monoxide (CO) is one of the most common causes of fatal poisoning by either intentional (suicidal) or accidental exposure and may be the most common worldwide cause of fatal poisoning [1]. Despite a great deal of clinical experience and randomized trials, there remains a lot of controversy about the ideal approach to managing CO exposure. Exact statistics for CO poisoning are difficult to ascertain, mainly because of incomplete reporting and misdiagnosis [2,3]. Carbon monoxide may be the cause of more than one-half of the fatal poisonings reported in many countries; fatal cases also are grossly underreported or misdiagnosed by medical professionals. Therefore, the precise number of individuals who have experienced CO intoxication is not known. The health effects associated with exposure to CO range from the more subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO. The symptoms, signs, and prognosis of acute CO poisoning correlate poorly with the level of carboxyhemoglobin measured at the time of hospital admission; however, because CO poisoning is a diagnosis frequently overlooked, the importance of measuring carboxyhemoglobin in suspicious settings cannot be overstated. The early symptoms (headache, 0735-6757/$ – see front matter. Published by Elsevier Inc.
dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Complications occur frequently in CO poisoning. Neurologic manifestation of acute CO poisoning includes disorientation, confusion, and coma. In conclusion, CO poisoning occurs frequently; has severe consequences, including immediate death; involves complications and late sequelae; and often is overlooked. However, compartment syndrome (CS) has not been reported in the literature before now. Efforts for prevention and both public and medical education should be encouraged [1,4]. In the present study, CS is discussed as a complication of acute CO poisoning. The 15-year-old boy patient was found lying on his back and unconscious after staying approximately 6 hours in an enclosed room with a coal stove and brought to the emergency service. His preliminary evaluation was as follows: unconscious, Glasgow Coma Scale 9 (M4, V3, E2), blood pressure 125/65 mm Hg, pulse 120 beats per minutes, temperature 36.5°C, and SpO2 value 89%. In the subsequent examinations, his white blood cell count was found to be 28.9 103/µL, hemoglobin 18.2 g/dL, creatine kinase 1558 U/L, creatine- kinase MB isoenzyme 143 U/L, troponin T 0.123 ng/mL, creatinine 1.18 mg/dL, and urea 40 mg/dL. Swelling and rash were detected on the left forearm in the patient's system examinations; radial and ulnar pulses could be detected by hand. No history of trauma or being underweight for the left arm was found in the patient's anamnesis. The left shoulder, humerus, forearm, and hand-wrist graphing performed were evaluated as normal. Cardiac and respiratory system examinations were normal. Carbon monoxide intoxication was considered for the patient with a history of heating using a stove. Hyperbaric oxygen therapy was planned for the patient, whose CO level was determined to be 25% after a pulse oxymetrical measurement performed using a signal extraction pulse COoximeter device (Masimo Corporation, Irvine, CA, USA). The patient completely regained consciousness after 1 session of hyperbaric oxygen therapy that lasted 2 hours, with 2.5 to 3 atmosphere-pressurized air. In the evaluation performed 10 hours after the initial admission to the emergency service, it was detected that the swelling of the
2104.e2
Case Report
left arm had continued to increase and the radial and ulnar pulses had weakened. Paresthesia, paralysis, and pallor were detected, along with pain in the arm during passive movements. Widespread intramuscular hemorrhage and edema in subcutaneous tissues were observed, whereas flow was present in the axillary artery, brachial artery, proximal radial artery, and proximal ulnar artery; no blood flow in the distal radial artery or distal ulnar artery was reported in colored Doppler examination of the upper left extremity. The findings on Doppler examination resulted in the diagnosis of CS. Fasciotomy was performed after this diagnosis. During the operation, fasciotomy was applied on 4 compartments after a curved incision ranging from the medial thenar section to the cubital area on the volar side of the left forearm (Fig. 1). It was observed that the ulnar and radial pulses returned after fasciotomy. A skin graft was administered on the excision site 10 days after fasciotomy (Fig. 2), and the patient was discharged on the 25th day after his admission. Motor and sensorial examination revealed normal results 45 days after fasciotomy (Fig. 3). Acute CS is a surgical emergency in which decompression is required to restore perfusion, and the exact incidence of CS in the emergency department is unknown. If untreated, the condition can result in irreversible nerve and muscle injury with permanent loss of function and extremity contracture [5,6]. Compartment syndrome has been well described, usually as a consequence of trauma; approximately 3 quarters of cases are associated with fractures [5]. Frequently sited locations for CS include the leg, hand, forearm, arm, shoulder, back, buttocks, thigh, and foot [7]. Compartment syndrome develops when there is increased pressure within a closed tissue space, such as muscle compartments bound by dense fascial sheaths. This increased pressure compromises the flow of blood through vessels supplying the contained muscles and nerves [7]. Although CO binds with hemoglobin in the blood, because it binds to myoglobin and cytochrome in tissues, and because it binds instead of oxygen in structures such as N-adenosine diphosphate that contains a heme ring, oxidative phosphorylation deteriorates at the mitochondrial level. The half-life of CO bound with nonhemoglobin structures is longer than carboxyhemoglobin, and its effects
Fig. 1
Seventy-two hours postfasciotomy.
Fig. 2
Skin graft was performed 10 days postfasciotomy.
are best seen on the heart. In our case, we consider that the influence on nonhemoglobin structures and free radicals composed thereof caused damage to the muscle tissue, resulting in intramuscular hemorrhage and widespread edema in subcutaneous tissues. As a result, CS developed. Moreover, we also consider that the oxygen therapy applied under high pressure might have increased this influence. There are studies that support this hypothesis. It was reported by Grace [8] that ischemia-reperfusion injury was mediated by the interaction of oxygen-derived free radicals, endothelial factors, and neutrophils. Furthermore, Duran et al [9] explained that oxygen-derived free radicals could peroxidate the lipid component of cell membranes, leading to enhanced capillary permeability and causing CS. Hyperbaric oxygen therapy corrected the patient's neurologic findings in our case but could not prevent the occurrence of CS. However, we have no idea why CO intoxication induced CS that only developed in the left forearm in our case. The fact that the patient was found lying on his back and no lesions were found due to pressure on the arm has led us to think that the development of CS was not induced by pressure resulting from compression. In this respect, we consider the event in our case to be a nontraumatic CS. Many cases have been reported regarding nontraumatic CS in the literature. Nontraumatic causes of CS include ischemia-reperfusion events after arterial injury, thrombosis, burns, bleeding disorders, blunt injury [5,6,10], and soft tissue injuries without fracture [5,11]. Iatrogenic
Fig. 3
Control figure 45 days postfasciotomy.
Case Report factors such as tight pneumatic antishock garments or casts can also cause CS [5,6,7,10]. Bacterial and viral infections such as cellulitis, thrombophlebitis, myositis, and lymphangitis [12,13] are rarely associated with acute CS [14,15]. On the other hand, rhabdomyolysis is associated with influenza [16,17], human immunodeficiency virus [18], spider bites [12], and enteroviruses [19], which have all been described as atypical causes of CS. No cases regarding the development of CO intoxication–induced CS has been reported in the literature; from this perspective, our case is the first of its kind. In our case, early findings related to CS (swelling, reddening, confusion, disorientation, and visual disturbances) were noticed when the patient was found (after 6 hours). However, diagnosis of CS and the decision was made to carry out fasciotomy in the 18th hour. This length of time is not higher than the periods reported in the literature. Ramos et al [20] identified the development of CS in 2 cases of nontraumatic children 24 hours after the incident. Because of early diagnosis and the timely application of fasciotomy in our case, tissue necrosis induced by late intervention, organ failure (such as renal failure), organ amputation necessity, and Volkmann ischemic contracture were avoided. However, because of our compartment pressure measuring device was not ready, unlike in many cases reported in the literature, the diagnosis of CS was only made clinically. It was determined that this diagnosis was correct after fasciotomy. It has been reported by Perron et al [21] that early diagnosis and treatment of acute CS is of the utmost importance, as delay can lead to tissue necrosis, and ultimately severe, permanent disability, as with Volkmann ischemic contracture. Untreated CS usually leads to muscle necrosis, limb amputation, and if severe, in large compartments, renal failure, and death. Alertness, clinical suspicion of the possibility of CS, and occasionally, intracompartmental pressure measurement are required to avoid a delay in diagnosis or missed diagnosis. Open fasciotomy, by incising both skin and fascia, is the most reliable method for adequate CS therapy [21]. As a conclusion, without trauma, patients with headache, dizziness, weakness, nausea, confusion, disorientation, visual disturbance, or coma may admit with pain, edema, paresthesia, paralysis, pallor, or necrosis in their leg, hand, forearm, arm, shoulder, back, buttocks, thigh, or foot. Emergency physicians should be alert to these circumstances, and they should keep CS in mind as a consequence of CO poisoning for these patients. Delayed diagnosis and intervention may result in irreversible nerve and muscle injury with permanent loss of function and extremity contracture.
Behçet Al MD Emergency Department of Medicine School in Gaziantep Üniversitesi, Turkey E-mail address: [email protected]
2104.e3 Mehmet Subası MD Ortopedy Department of Medicine School in Gaziantep Üniversitesi, Turkey Burçin Karsli Ortopedy Department of Gaziantep Avukat Cengiz State Hospital, Turkey Pınar Yarbil Emergency Department of Gaziantep Sehitkamil State Hospital, Turkey Suat Zengin Emergency Department of Medicine School in Gaziantep Üniversitesi, Turkey http://dx.doi.org/10.1016/j.ajem.2012.03.011
References [1] Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoning—a public health perspective. Toxicology 2000;145:1-14. [2] Centers for Disease Control and Prevention: unintentional non-fire related carbon monoxide exposures—United States, 2001-2003. MMWR Morb Mortal Wkly Report 2005;54:36. [3] Centers for Disease Control and Prevention: epidemic carbon monoxide poisoning despite a CO alarm law: Mecklenberg County, NC, December 2002. MMWR Morb Mortal Wkly Report 2004;53:189. [4] Maloney G. Carbon Monoxide. In: Tintinalli JE, editor. Tintinalli's Emergency Medicine Section 16 Chapter 217 Environmental Injuries, 7th edNew York: The McGraw-Hill Companies, Inc.; 2010. p. 1410-4. [5] Kostler W, Strohm PC, Sudkamp NP. Acute compartment syndrome of the limb. Injury 2004;35:121-1227. [6] Seiler JG, Olvey SP. Compartment syndromes of the hand and forearm. J Am Soc Surg Hand 2003;3:184-9. [7] Hoover TJ, Siefert JA. Soft tissue complications of orthopedic emergencies. Emerg Med Clin N Am 2000;18:116-39. [8] Grace PA. Ischaemia-reperfusion injury. Br J Surg 1994;81:637-47. [9] Duran W, Takenaka H, Hobson R. Microvascular pathophysiology of skeletal muscle ischaemia-reperfusion. Semin Vasc Surg 1998;11:203-14. [10] Pearse MF, Harry L, Nanchahal J. Acute compartment syndrome of the leg. Br J Med 2002;325:557-8. [11] Susuki T, Moirmura N, Kawai K, et al. Arterial injury associated with acute compartment syndrome of the thigh following blunt trauma. Injury 2005;36:151-9. [12] Andreasen T, Green S, Childers BJ. Massive infectious soft tissue injury: diagnosis and management of necrotizing fasciitis and purpura fulminans. Plast Reconstr Surg 2001;107:1025-34. [13] Falagas ME, Vergidis PI. Narrative review: diseases that masquerade as infectious cellulitis. Ann Intern Med 2005;142:47-56. [14] Harrington P, Scott B, Chetcuti P. Multifocal streptococcal pyomyositis complicated by acute compartment syndrome: a case report. J Pediatr B Orthop 2001;10:120-2. [15] Bibbo C, Patel DV, Mackessy RP, et al. Pyomyositis of the leg with early neurologic compromise. Pediatr Emerg Care 2000;16:352-4. [16] Swaringer JC, Seiler JG, Bruce RW. Influenza A—induced rhabdomyolysis resulting in extensive compartment syndrome. ClinOrthop 2000;375:243-9. [17] Lam R, Lin PH, Alankar S, et al. Acute limb ischemia secondary to myositis-induced compartment syndrome in a patient with human immunodeficiency virus infection. J Vasc Surg 2003;37:1103-5.
2104.e4 [18] Cohen J, Bush S. Case report: compartment syndrome after a suspected black widow spider bite. Ann Emerg Med 2005;45: 414-6. [19] Bhattacharyya T, Vrahas MS. The medical-legal aspects of compartment syndrome. J Bone Joint Surg Am 2004;86:864-8.
Case Report [20] Ramos C, Whyte CM, Harris BH. Nontraumatic compartment syndrome of the extremities in children. J Pediatr Surg 2006;41: 5-7. [21] Perron AD, Brady WJ, Keats TE. Orthopedic Pitfalls in the ED: acute compartment syndrome. Am J Emerg Med 2001;19:413-6.