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Congenital spine deformities: a new screening indication for blunt cerebrovascular injuries after cervical trauma?
Journal of Pediatric Surgery (2010) 45, 2444–2446
www.elsevier.com/locate/jpedsurg
Congenital spine deformities: a new screening indication for blunt cerebrovascular injuries after cervical trauma? Christine Capone, Sathyaprasad Burjonrappa ⁎ Division of Pediatric Surgery, Department of Surgery, New York Medical College, Valhalla, NY 10595, USA Received 10 August 2010; accepted 30 August 2010
Key words: Blunt cerebrovascular injuries; Carotid dissection; Congenital spine deformity; Cervical trauma
Abstract Blunt cerebrovascular injuries (BCVI) carry significant morbidity if not diagnosed and treated early. A high index of clinical suspicion is needed to recognize the injury patterns associated with this condition and to order the requisite imaging studies needed to diagnose it accurately. We report of BCVI associated with a congenital cervical spine malformation after blunt trauma. We recommend inclusion of cervical spine malformations to the current Eastern Association for the Surgery of Trauma screening criteria for BCVI and explain our rationale for the same. © 2010 Elsevier Inc. All rights reserved.
Blunt cerebrovascular injuries (BCVI) have historically been considered a rare group of injuries causing substantial morbidity and mortality if unrecognized and untreated [1]. Although liberal screening and advanced imaging have aided in increased recognition of BCVI, early diagnosis remains difficult. Clinical symptoms are often absent at an early stage and defining the patient population who should be screened in asymptomatic blunt neck trauma is controversial. We encountered a patient with an unusual presentation leading up to his diagnosis of BCVI. The case is presented with a brief review of the relevant literature.
1. Case report A 12-year-old boy presented to the emergency department at our pediatric trauma center after he was kicked on the neck/back of the head while swimming. There was no loss of ⁎ Corresponding author. Tel.: +1 914 419 8681. E-mail address: [email protected] (S. Burjonrappa). 0022-3468/$ – see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1016/j.jpedsurg.2010.08.065
consciousness, and the Glasgow Coma Scale was equal to 15. At the scene, although awake and oriented, the patient was reportedly not moving his extremities. On arrival, initial physical examination showed decreased sensation in the lower extremities and weakness (3/5) throughout his extremities. These observed neurologic deficits completely resolved over the next few hours. A left internal carotid artery dissection was noted on imaging after the history coupled with the initial physical examination prompted further radiographic evaluation. The computed tomographic scan of the cervical spine showed that the posterior arch and lateral masses of the atlas were hypoplastic/dysplastic and partially fused with the base of the skull. There were partial segmentation anomalies at the C2-C3 levels and C3-C4 levels. Chronic degenerative disk changes and acute disk herniation at C3-C4 were also noted (Fig. 1). Findings were confirmed on subsequent cervical magnetic resonance imaging. Left internal carotid artery dissection was noted on computed tomographic angiography of the neck (Fig. 2) and further evaluated with a carotid Doppler ultrasound. Ultrasound and Doppler images showed velocities in the region of the proximal, and mid left internal
Blunt cerebrovascular injuries
2445
Fig. 1 Computed tomographic scan of the cervical spine: coronal and sagittal sections. Extensive congenital dysmorphology is noted within the cervical spine with multiple segmentation abnormalities and an error in spinal fusion (arrows). There is no evidence of acute fracture.
carotid artery were 262 cm/s corresponding to 50% to 69% stenosis. No dissection flap was identified. As treatment for the dissection, the patient was started on a heparin drip and monitored with periodic neurologic checks in the intensive care unit. Over the next few days, the patient was switched to aspirin and long-acting heparin for anticoagulation as the left carotid dissection was stable with no residual or new neurologic deficits. Vascular surgical intervention was not indicated. Initially, surgical management for the C3-C4 disk herniation was to be discussed on an elective outpatient basis. However, as the patient increasingly ambulated, an episode of neck pain associated with lower extremity paresthesia and gait disturbance was observed. The deficits resolved with rest, and no motor or sensory deficits were noted on repeat examination. Repeat Doppler ultrasound of the carotids was unchanged. The onset of new neurologic symptoms coupled with the known radiographic abnormalities precipitated in-patient surgical management with an
Fig. 2 Computed tomographic angiography of the neck. Focal stenosis in the left internal carotid artery distal to the left internal carotid artery bulb with stenosis of approximately 60%.
anterior cervical decompression and fusion of C3-C4. Anticoagulation was held before surgery. The patient tolerated the operation well, there were no complications, and the postoperative period was uneventful. There were no neurologic deficits, and the patient ambulated well. The patient was discharged in a stable condition on aspirin 81 mg once a day. A total duration of 6 months of antiplatelet therapy was recommended.
2. Discussion Blunt cerebrovascular injuries can be described as any pseudoaneurysm formation, dissection, or occlusion of the carotid or vertebral arteries. Blunt cerebrovascular injuries is diagnosed in 0.1% to 0.67% of patients hospitalized for severe trauma with associated head and neck injuries or in patients hospitalized for trauma presenting with symptoms of central nervous system ischemia [1-3]. The incidence of BCVI rises to about 1% when asymptomatic patients are screened, suggesting BCVI occur in the absence of classically described risk factors and screening criteria [4]. We encountered a patient with carotid artery dissection after trauma unassociated with the classically described risk factors. During his workup, he was found to have congenital dysmorphology in the cervical spine that we believe independently increased his risk for a BCVI. Anatomical injuries sustained during a trauma and classically associated with BCVI include severe facial fractures, skull base fractures, cervical spine fractures, spinal cord injury, major thoracic injury, and traumatic brain injury [5]. Central nervous system symptoms associated with trauma are also associated with an increased risk of BCVI [6]. Of BCVI, injury to the carotid artery is more likely to be associated with severe facial fractures, skull base fractures, and major thoracic injuries, whereas injury to the vertebral artery is more likely to be associated with cervical spine
2446 Table 1 Eastern Association for the Surgery of Trauma screening criteria for BCVI [4] Anatomical injuries Diffuse axonal injury Basilar skull fracture Petrous bone fracture Fracture through the foramen transversum Cervical vertebral body fracture Displaced midface or complex mandibular fracture (Le Fort II or III) Physical signs Neurologic abnormalities unexplained by diagnosed injury Glasgow Coma Scale ≤ 8 Epistaxis from suspected arterial source post trauma Seat belt abrasion or soft tissue injury of the anterior neck resulting in swelling or altered mental status
fractures and spinal cord injuries [7]. These correlations have been used as indicators to screen for BCVI. Recently, the Eastern Association for the Surgery of Trauma evaluated evidence behind using the correlations as screening indicators and developed new practice management guidelines from their analysis. Their recommended indications for screening of BCVI are listed in Table 1 [4]. Several mechanisms leading to BCVI, particularly in patients with associated injuries, have been described and include cervical hyperextension and rotation, hyperflexion, or direct force [4]. These mechanisms are known to cause either a stretching or a compression of an artery beyond its natural compliance curve and are described in both spontaneous and traumatic vascular dissections. During natural head rotation, the carotid artery straightens along and in compliance with the axis of motion, ultimately distributing potentially damaging stress forces throughout the artery. As the limit to head rotation is reached, the carotid artery is less compliant and straightens at a lesser rate. This causes localized stress development on the posterior side of the vessel at the internal lumen wall and can ultimately lead to spontaneous intimal tears and arterial dissections in patients with less compliant arteries [8]. Medical conditions causing underlying vasculopathy such as fibromuscular dysplasia, cystic medical necrosis, oral contraceptive use, and recent history of infections change arterial compliance and can predispose patients to spontaneous dissections when minor traumatic force is applied to a less compliant artery [9]. In trauma, rapid deceleration forces can overwhelm the natural compliance of the artery stretching the internal carotid over the lateral portion of C3 and C4 vertebrae and initiating an intimal tear/arterial dissection. Similarly, hyperflexion forces during trauma compress and deform the artery against its natural compliance curve. Hyperflexion
C. Capone, S. Burjonrappa forces, particularly in the upper cervical spine, can lead to BCVI through either localized stress development from deformation or direct compression of the artery between the mandible and cervical spine [10]. The association between BCVI and cervical spine fractures is well documented, with recent studies detailing the specific fracture patterns associated with increased risk of BCVI. These patterns include subluxation, fracture extension to the foramen transversum, or any C1-C3 fractures. These patterns are caused by an abnormal loading of flexionextension forces and high-speed transfer of energy involved in arterial dissections [11]. The congenital cervical spine abnormalities in our patient likely predisposed him to developing BCVI. We suspect that the increased motion around the upper cervical vertebrae in cervical spinal dysmorphism could increase the amount and duration of focal stress applied to the artery during head rotation, deceleration, or hyperextension forces and/or lead to its positional compression. We propose that cervical spinal deformities be added to the selection criteria for screening of BCVI after major trauma.
References [1] Cogbill TH, Moore EE, Meissner M, et al. The spectrum of blunt injury to the carotid artery: a multicenter perspective. J Trauma 1994; 37:473-9. [2] Berne JD, Norwood SC, McAuley CE, et al. The high morbidity of blunt cerebrovascular injury in an unscreened population: more evidence of the need for mandatory screening protocols. J Am Coll Surg 2001;192:314-21. [3] Stein DM, Boswell S, Sliker CW, et al. Blunt cerebrovascular injuries: does treatment always matter? J Trauma 2009;66:132-44. [4] Bromberg WJ, Collier BC, Diebel LN, et al. Blunt cerebrovascular injury practice management guidelines: the Eastern Association for the Surgery of Trauma. J Trauma 2010 Feb;68(2):471-7. [5] Davis JW, Holbrook TL, Hoyt DB, et al. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma 1990;30:1514-7. [6] Cothren CC, Moore EE, Biffl WL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg 2004;139:540-5 discussion 545-546. [7] Biffl WL, Moore EE, Offner PJ, et al. Optimizing screening for blunt cerebrovascular injuries. Am J Surg 1999;178:517-22. [8] Callaghan FM, Soellinger M, Baumgartner RW, et al. The role of the carotid sinus in the reduction of arterial wall stresses due to head movements—potential implications for cervical artery dissection. J Biomech 2009;42(6):755-61 Epub 2009 Mar 17. [9] Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurol 2009;8(7):668-78. [10] Biffl WL, Moore EE, Ryu RK, et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg 1998;228:462-70. [11] Cothren CC, Moore EE, Ray Jr CE, et al. Screening for blunt cerebrovascular injuries is cost effective. Am J Surg 2005;190:845-9.
www.elsevier.com/locate/jpedsurg
Congenital spine deformities: a new screening indication for blunt cerebrovascular injuries after cervical trauma? Christine Capone, Sathyaprasad Burjonrappa ⁎ Division of Pediatric Surgery, Department of Surgery, New York Medical College, Valhalla, NY 10595, USA Received 10 August 2010; accepted 30 August 2010
Key words: Blunt cerebrovascular injuries; Carotid dissection; Congenital spine deformity; Cervical trauma
Abstract Blunt cerebrovascular injuries (BCVI) carry significant morbidity if not diagnosed and treated early. A high index of clinical suspicion is needed to recognize the injury patterns associated with this condition and to order the requisite imaging studies needed to diagnose it accurately. We report of BCVI associated with a congenital cervical spine malformation after blunt trauma. We recommend inclusion of cervical spine malformations to the current Eastern Association for the Surgery of Trauma screening criteria for BCVI and explain our rationale for the same. © 2010 Elsevier Inc. All rights reserved.
Blunt cerebrovascular injuries (BCVI) have historically been considered a rare group of injuries causing substantial morbidity and mortality if unrecognized and untreated [1]. Although liberal screening and advanced imaging have aided in increased recognition of BCVI, early diagnosis remains difficult. Clinical symptoms are often absent at an early stage and defining the patient population who should be screened in asymptomatic blunt neck trauma is controversial. We encountered a patient with an unusual presentation leading up to his diagnosis of BCVI. The case is presented with a brief review of the relevant literature.
1. Case report A 12-year-old boy presented to the emergency department at our pediatric trauma center after he was kicked on the neck/back of the head while swimming. There was no loss of ⁎ Corresponding author. Tel.: +1 914 419 8681. E-mail address: [email protected] (S. Burjonrappa). 0022-3468/$ – see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1016/j.jpedsurg.2010.08.065
consciousness, and the Glasgow Coma Scale was equal to 15. At the scene, although awake and oriented, the patient was reportedly not moving his extremities. On arrival, initial physical examination showed decreased sensation in the lower extremities and weakness (3/5) throughout his extremities. These observed neurologic deficits completely resolved over the next few hours. A left internal carotid artery dissection was noted on imaging after the history coupled with the initial physical examination prompted further radiographic evaluation. The computed tomographic scan of the cervical spine showed that the posterior arch and lateral masses of the atlas were hypoplastic/dysplastic and partially fused with the base of the skull. There were partial segmentation anomalies at the C2-C3 levels and C3-C4 levels. Chronic degenerative disk changes and acute disk herniation at C3-C4 were also noted (Fig. 1). Findings were confirmed on subsequent cervical magnetic resonance imaging. Left internal carotid artery dissection was noted on computed tomographic angiography of the neck (Fig. 2) and further evaluated with a carotid Doppler ultrasound. Ultrasound and Doppler images showed velocities in the region of the proximal, and mid left internal
Blunt cerebrovascular injuries
2445
Fig. 1 Computed tomographic scan of the cervical spine: coronal and sagittal sections. Extensive congenital dysmorphology is noted within the cervical spine with multiple segmentation abnormalities and an error in spinal fusion (arrows). There is no evidence of acute fracture.
carotid artery were 262 cm/s corresponding to 50% to 69% stenosis. No dissection flap was identified. As treatment for the dissection, the patient was started on a heparin drip and monitored with periodic neurologic checks in the intensive care unit. Over the next few days, the patient was switched to aspirin and long-acting heparin for anticoagulation as the left carotid dissection was stable with no residual or new neurologic deficits. Vascular surgical intervention was not indicated. Initially, surgical management for the C3-C4 disk herniation was to be discussed on an elective outpatient basis. However, as the patient increasingly ambulated, an episode of neck pain associated with lower extremity paresthesia and gait disturbance was observed. The deficits resolved with rest, and no motor or sensory deficits were noted on repeat examination. Repeat Doppler ultrasound of the carotids was unchanged. The onset of new neurologic symptoms coupled with the known radiographic abnormalities precipitated in-patient surgical management with an
Fig. 2 Computed tomographic angiography of the neck. Focal stenosis in the left internal carotid artery distal to the left internal carotid artery bulb with stenosis of approximately 60%.
anterior cervical decompression and fusion of C3-C4. Anticoagulation was held before surgery. The patient tolerated the operation well, there were no complications, and the postoperative period was uneventful. There were no neurologic deficits, and the patient ambulated well. The patient was discharged in a stable condition on aspirin 81 mg once a day. A total duration of 6 months of antiplatelet therapy was recommended.
2. Discussion Blunt cerebrovascular injuries can be described as any pseudoaneurysm formation, dissection, or occlusion of the carotid or vertebral arteries. Blunt cerebrovascular injuries is diagnosed in 0.1% to 0.67% of patients hospitalized for severe trauma with associated head and neck injuries or in patients hospitalized for trauma presenting with symptoms of central nervous system ischemia [1-3]. The incidence of BCVI rises to about 1% when asymptomatic patients are screened, suggesting BCVI occur in the absence of classically described risk factors and screening criteria [4]. We encountered a patient with carotid artery dissection after trauma unassociated with the classically described risk factors. During his workup, he was found to have congenital dysmorphology in the cervical spine that we believe independently increased his risk for a BCVI. Anatomical injuries sustained during a trauma and classically associated with BCVI include severe facial fractures, skull base fractures, cervical spine fractures, spinal cord injury, major thoracic injury, and traumatic brain injury [5]. Central nervous system symptoms associated with trauma are also associated with an increased risk of BCVI [6]. Of BCVI, injury to the carotid artery is more likely to be associated with severe facial fractures, skull base fractures, and major thoracic injuries, whereas injury to the vertebral artery is more likely to be associated with cervical spine
2446 Table 1 Eastern Association for the Surgery of Trauma screening criteria for BCVI [4] Anatomical injuries Diffuse axonal injury Basilar skull fracture Petrous bone fracture Fracture through the foramen transversum Cervical vertebral body fracture Displaced midface or complex mandibular fracture (Le Fort II or III) Physical signs Neurologic abnormalities unexplained by diagnosed injury Glasgow Coma Scale ≤ 8 Epistaxis from suspected arterial source post trauma Seat belt abrasion or soft tissue injury of the anterior neck resulting in swelling or altered mental status
fractures and spinal cord injuries [7]. These correlations have been used as indicators to screen for BCVI. Recently, the Eastern Association for the Surgery of Trauma evaluated evidence behind using the correlations as screening indicators and developed new practice management guidelines from their analysis. Their recommended indications for screening of BCVI are listed in Table 1 [4]. Several mechanisms leading to BCVI, particularly in patients with associated injuries, have been described and include cervical hyperextension and rotation, hyperflexion, or direct force [4]. These mechanisms are known to cause either a stretching or a compression of an artery beyond its natural compliance curve and are described in both spontaneous and traumatic vascular dissections. During natural head rotation, the carotid artery straightens along and in compliance with the axis of motion, ultimately distributing potentially damaging stress forces throughout the artery. As the limit to head rotation is reached, the carotid artery is less compliant and straightens at a lesser rate. This causes localized stress development on the posterior side of the vessel at the internal lumen wall and can ultimately lead to spontaneous intimal tears and arterial dissections in patients with less compliant arteries [8]. Medical conditions causing underlying vasculopathy such as fibromuscular dysplasia, cystic medical necrosis, oral contraceptive use, and recent history of infections change arterial compliance and can predispose patients to spontaneous dissections when minor traumatic force is applied to a less compliant artery [9]. In trauma, rapid deceleration forces can overwhelm the natural compliance of the artery stretching the internal carotid over the lateral portion of C3 and C4 vertebrae and initiating an intimal tear/arterial dissection. Similarly, hyperflexion forces during trauma compress and deform the artery against its natural compliance curve. Hyperflexion
C. Capone, S. Burjonrappa forces, particularly in the upper cervical spine, can lead to BCVI through either localized stress development from deformation or direct compression of the artery between the mandible and cervical spine [10]. The association between BCVI and cervical spine fractures is well documented, with recent studies detailing the specific fracture patterns associated with increased risk of BCVI. These patterns include subluxation, fracture extension to the foramen transversum, or any C1-C3 fractures. These patterns are caused by an abnormal loading of flexionextension forces and high-speed transfer of energy involved in arterial dissections [11]. The congenital cervical spine abnormalities in our patient likely predisposed him to developing BCVI. We suspect that the increased motion around the upper cervical vertebrae in cervical spinal dysmorphism could increase the amount and duration of focal stress applied to the artery during head rotation, deceleration, or hyperextension forces and/or lead to its positional compression. We propose that cervical spinal deformities be added to the selection criteria for screening of BCVI after major trauma.
References [1] Cogbill TH, Moore EE, Meissner M, et al. The spectrum of blunt injury to the carotid artery: a multicenter perspective. J Trauma 1994; 37:473-9. [2] Berne JD, Norwood SC, McAuley CE, et al. The high morbidity of blunt cerebrovascular injury in an unscreened population: more evidence of the need for mandatory screening protocols. J Am Coll Surg 2001;192:314-21. [3] Stein DM, Boswell S, Sliker CW, et al. Blunt cerebrovascular injuries: does treatment always matter? J Trauma 2009;66:132-44. [4] Bromberg WJ, Collier BC, Diebel LN, et al. Blunt cerebrovascular injury practice management guidelines: the Eastern Association for the Surgery of Trauma. J Trauma 2010 Feb;68(2):471-7. [5] Davis JW, Holbrook TL, Hoyt DB, et al. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma 1990;30:1514-7. [6] Cothren CC, Moore EE, Biffl WL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg 2004;139:540-5 discussion 545-546. [7] Biffl WL, Moore EE, Offner PJ, et al. Optimizing screening for blunt cerebrovascular injuries. Am J Surg 1999;178:517-22. [8] Callaghan FM, Soellinger M, Baumgartner RW, et al. The role of the carotid sinus in the reduction of arterial wall stresses due to head movements—potential implications for cervical artery dissection. J Biomech 2009;42(6):755-61 Epub 2009 Mar 17. [9] Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome. Lancet Neurol 2009;8(7):668-78. [10] Biffl WL, Moore EE, Ryu RK, et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg 1998;228:462-70. [11] Cothren CC, Moore EE, Ray Jr CE, et al. Screening for blunt cerebrovascular injuries is cost effective. Am J Surg 2005;190:845-9.