- Email: [email protected]
Bilateral internal carotid and vertebral artery dissection after a horse-riding injury
Bilateral internal carotid and vertebral artery dissection after a horse-riding injury Zeid M. Keilani, MD,a John D. Berne, MD,b and Mouchammed Agko, MD,c New Orleans, La; Tyler, Tex; and Toledo, Ohio Blunt cerebrovascular injuries, defined as blunt injuries to the internal carotid or vertebral arteries, are uncommon and usually occur in victims of high-speed deceleration motor vehicle crashes. A blunt cerebrovascular injury after an equestrian accident is an extremely unusual presentation. In recent years, advances in screening and treatment with pharmacologic anticoagulation before the onset of neurologic symptoms have improved outcomes for these patients. Endovascular stenting and embolization, although unproven, offer a new potential approach for these complex injuries. We present a unique case of four-vessel blunt cerebrovascular injuries after a horse-riding injury that required multidisciplinary management. ( J Vasc Surg 2010;52:1052-7.)
Early recognition and treatment of blunt cerebrovascular injuries (BCVIs) has been shown to prevent strokerelated morbidity and mortality. Early screening of asymptomatic patients based on injury-related mechanism and associated injuries has been proposed to identify the at-risk population that may benefit from screening. Equestrianrelated injuries have only rarely been associated with blunt injuries to the internal carotid or vertebral arteries.1 We report an unusual case of bilateral internal carotid (ICA) and vertebral artery (VA) dissection after a horse-related crush chest injury. The patient was treated with systemic anticoagulation and subsequent endovascular stenting of the bilateral ICAs. CASE REPORT A 52-year-old woman sustained multiple injuries after she fell off a horse. After throwing her to the ground, the horse jumped up and landed on her chest, causing a severe crush injury to the thoracic cavity. She initially lost consciousness, but on arrival to our facility, she had a Glasgow Coma Score of 15, with no focal neurologic deficits, was in severe respiratory distress, with flail chest requiring immediate intubation. She was also in shock. Bilateral thoracostomy tubes were placed, and an infusion of packed red blood cells was begun. After some improvement in her vital signs and a bedside abdominal ultrasound examination showed no clear free fluid in the abdomen, a computed tomography (CT) scan of the chest was performed that demonstrated multiple bilateral displaced rib fractures with bilateral hemopneumothoraces, mediastinal shift to the From the Department of Surgery, Ochsner Clinic Foundation, New Orleansa; East Texas Medical Center, Tylerb; and the Department of Surgery, University of Toledo Medical Center, Toledoc. Competition of interest: none. Reprint requests: Zeid M. Keilani, MD, Department of Surgery, Ochsner Clinic Foundation, 1514 Jefferson Hwy, New Orleans, LA 70121 (email: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Copyright © 2010 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. doi:10.1016/j.jvs.2010.05.065
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right, and hemopneumopericardium. A CT of the abdomen demonstrated extensive pneumoperitoneum with no evidence of solid organ injury, and multiple thoracic and lumbar spinal vertebral fractures with no involvement of the spinal cord. Results of head and cervical spine CT were negative. Screening CT angiography (CTA) of the neck demonstrated left ICA dissection just above the bifurcation and extending toward the base of the neck, along with proximal dissection of the proximal left VA, with no involvement of her right side (Fig 1). The patient underwent an exploratory laparotomy, clamshell thoracotomy with wedge resection of the left lower lobe and lingula, release of hemopneumopericardium, and temporary negative pressure vacuum-assisted dressing closure (VAC; Kinetic Concepts Inc, San Antonio, Tex) of the abdominal and thoracic cavities. She was further stabilized in the intensive care unit, where an unfractionated heparin drip was started on postoperative day 1. She was taken back to the operating room on postoperative day 3 for closure of her abdominal and thoracic cavities. Heparin was held intraoperatively but was restarted postoperatively. The next morning she was unresponsive, prompting a magnetic resonance imaging of the brain, which revealed multiple areas of ischemic strokes in her left frontal and occipital lobes as well as the left cerebellar hemisphere (Fig 2). She continued to improve gradually, but had persistent right-sided hemiplegia. Aspirin and clopidogrel were started, and heparin was discontinued in anticipation of possible stent placement. Because of the well-documented progression of these lesions over the first 7 to 10 days, a routine follow-up arteriogram was performed 9 days later.2 This demonstrated a long segment spiral dissection and pseudoaneurysm of the left ICA, small pseudoaneurysm with minimal areas of narrowing of the proximal left VA, a 6-cm dissection of the right ICA, and a small pseudoaneurysm of the proximal right VA (Fig 3). Bilateral stent placement with 7 ⫻ 30-mm and 7 ⫻ 20-mm nitinol uncovered metal stents in the right ICA, and 7 ⫻ 30-mm and 8 ⫻ 30-mm nitinol uncovered metal stents in the left ICA over a 0.035-inch Bentson wire (Cook Inc, Bloomington, Ind) was performed (Fig 4 and 5). She continued to improve with physical therapy. A follow-up angiogram before discharge demonstrated good patency of bilateral stents, without flow restrictions. She was discharged to a rehabilitation facility on clopidogrel (75-mg daily). A follow-up
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Fig 1. A computed tomography angiography (CTA) of the neck demonstrates (a) a small dissection of the proximal left vertebral artery (close-up in inset) and (b) dissection of the left internal carotid artery just above the bifurcation extending toward the base of the neck (close-up in inset).
Fig 2. Magnetic resonance imaging of the brain shows multiple areas of ischemic stroke in the left (a) frontal and (b) occipital lobes, and in the left (c) cerebellar hemisphere.
arteriogram at 3 months after discharge demonstrated patency of bilateral ICA without stenosis or residual pseudoaneurysm. The left vertebral artery showed complete healing. The right vertebral artery showed a persistent and slightly enlarged pseudoaneurysm. Coil embolization with Matrix 2 detachable coils (Boston Scientific, Natick, Mass) of the entire lumen at its origin was accomplished without any complications. She has since discontinued taking the clopidogrel but continued low-dose aspirin. She has regained full cognition but has a persistent mild right-sided weakness.
DISCUSSION Collective incidence of BCVIs in the literature have been reported to range between 0.1% to 1.6%, with overall reported mortality rates of 13% to 23% for blunt carotid artery injury and 6.8% to 8% for blunt VA injury, and overall stroke rate of 14% to 50% for blunt carotid artery injury and
9% to 25% for blunt VA injury.3-11 BCVI are usually associated with closed head and cervical trauma, basilar skull and facial fractures, thoracic, and seat belt injuries. Therefore, screening has been advocated in such clinical scenarios to identify these injuries in asymptomatic patients and to initiate treatment before the appearance of neurologic sequelae (Table I).4 Delgado-Almandoz et al12 recently published a proposed scoring system for the prediction of a patient’s risk of arterial injury from acute blunt craniocervical trauma that could be used to select patients for multidetector CTA screening. This scoring system is based on three independent predictors of a higher risk of arterial injury demonstrated from a multivariate logistic regression analysis: cervical interfacetal subluxations/dislocations, fracture lines reaching an arterial structure, and high-impact mechanism of injury. Patients with scores of 2 and 3 are at highest risk
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Fig 5. Four-vessel neck arteriogram demonstrates (a) a long segment dissection of the right internal carotid artery and (b) stenting of the right internal carotid artery with good flow.
Table I. Denver screening criteria for blunt cerebrovascular injuries4 Fig 3. A four-vessel neck arteriogram demonstrates (a) a small pseudoaneurysm of the proximal right vertebral artery and (b) a small pseudoaneurysm with minimal areas of narrowing of the proximal left vertebral artery.
Fig 4. A four-vessel neck arteriogram demonstrates (a) a long segment of spiral dissection and pseudoaneurysm of the left internal carotid artery and (b) stenting of the left internal carotid artery with good flow.
of arterial injury (21.9% and 52.2%, respectively; P ⬍ .0001), whereas patients with a score of 1 carry a risk of 10.1% (P ⬍ .0001). This study is still a retrospective, single-patient cohort study that relies heavily on radiographic findings and requires further future validation (Table II).12 Based on our own risk factor study, we have liberalized screening at our institution to include patients with several “soft” risk factors, with low GCS and high injury severity score (ISS) being the most important, which pan out on a
Signs/symptoms of blunt cerebrovascular injury ● Arterial hemorrhage ● Cervical bruit ● Expanding cervical hematoma ● Focal neurologic deficit ● Findings from neurologic examination incongruous with head CT scan findings ● Stroke on secondary CT scan ● Neurologic deficit inconsistent with head CT Risk factors for blunt cerebrovascular injury ● High-energy transfer mechanism with Le Forte II or III fracture ● Cervical spine fracture patterns: subluxation, fractures extending into the transverse foramen, fractures of C1-C3 vertebrae ● Basilar skull fracture with carotid canal involvement ● Diffuse axonal injury with GCS ⬍6 ● Near hanging with anoxic brain injury CT, Computed tomography; GCS, Glasgow Coma Score. Source: Reprinted from Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg. 2009;144:685-90. © 2009. With permission from American Medical Association. All rights reserved.
multivariate logistic regression analysis. Some of the patients with BCVIs in our series, including this patient, would have been missed if only the Denver criteria had been used (Table III).13 Screening can be performed with duplex ultrasound imaging, four-vessel cerebral arteriography, CT angiography, or magnetic resonance angiography. Duplex ultrasound imaging and magnetic resonance angiography are no longer considered as a standard screening test for BCVIs due to documented poor sensitivity and specificity in the literature. Angiogram has been considered the gold standard for diagnosis of BCVI, but is invasive and associated
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Table II. Calculation of proposed acute craniocervical trauma scoring system12
Table IV. Denver grading scale for blunt cerebrovascular injury4
Parameter points Mechanism of injury Low impacta High impactb Cervical interfacetal subluxation/dislocation No Yes Fracture line reaching an arterial structure No Yes
Grade 0 1
II 0 1 0 1
a Includes hanging or strangulation, low-speed motor vehicle accident, fall from standing, and other blunt trauma to the head or neck. b Includes high-speed motor vehicle accident, including motorcycle accidents, struck pedestrian or bicyclist, fall from height greater than standing, fall down stairs, and high-force blows to the head or neck, including assault. The score is calculated by adding the total number of points. Source: Reprinted from Delgado-Almandoz JE, Schaefer PW, Kelly HR, Lev MH, Gonzalez RG, Romero JM. Multidetector CT Angiography in the evaluation of acute blunt head and neck trauma: a proposed acute craniocervical trauma scoring system. Radiology 2010;254:236-244. With permission from the Radiological Society of North America.
Table III. Multivariate logistic regression model for blunt cerebrovascular injuries13 Variable Cervical spine injury Mandible Fx Basilar skull Fx Thoracic or lumbar spine Fx Any facial injury Injury severity score Le Fort Fx ED GCS
I
OR (95% CI)
P
7.46 (4.87-11.44) 2.59 (1.30-5.15) 1.76 (1.02-3.01) 1.29 (0.82-2.03) 1.16 (0.73-1.86) 1.05 (1.04-1.07) 0.97 (0.50-1.86) 0.93 (0.89-0.97)
⬍ .001 .007 .041 .28 .53 ⬍ .001 .92 .001
CI, Confidence interval; ED GCS, emergency department Glasgow Coma Score; Fx, fracture; OR, odds ratio. Source: Reprinted from Berne JD, Cook AP, Rowe SA, and Norwood SH. A Multivariate logistic regression analysis of risk factors for blunt cerebrovascular injury. J Vasc Surg 2010;51:57-64. © 2010 With permission from Elsevier.
with potential risks and complications, including hematoma, arterial pseudoaneurysm, and renal dysfunction.2,3 Accuracy of CTA has improved with multidetector-row CTA, with the 16-slice CTA emerging as a reliable method for detecting clinically significant BCVI (100% sensitivity for carotid and 96% for vertebral artery injuries).13-17 CTA has also been reported to be oversensitive, with reported false-positive rates of 43%, but these results could be largely attributed to the radiologists’ inexperience.18,19 If CTA is not available or in the setting of high clinical suspicion and a normal CTA, a four-vessel angiogram is considered the gold standard.3 Management of a BCVI includes observation, surgery, antithrombotic therapy, or endovascular therapy. Management is largely determined by symptoms, location, and grade of the injury, although this has not been standardized, and recommendations are made based on retrospec-
III IV V
Description Irregularity of the vessel wall or a dissection/intramural hematoma with less than 25% luminal stenosis Intraluminal thrombus or raised intimal flap is visualized or dissection/intramural hematoma with 25% or more luminal narrowing Pseudoaneurysm Vessel occlusion Vessel transaction
Source: Reprinted from Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg 2009;144:685-90. © 2009. With permission from American Medical Association. All rights reserved.
tive analyses of patients managed per institutional protocols (Table IV).4 Observation is chosen if other treatment modalities are contraindicated. Surgery is warranted in highergrade (grade 2-5) surgically accessible injuries, but most BCVIs occur in surgically challenging or inaccessible areas, such as at base of the skull or within the foramen transversarium.3,20 Early antithrombotic therapy, either anticoagulation or antiplatelet agents, in asymptomatic patients reduces or nearly eliminates BCVI-related strokes, down to 6.8% for blunt carotid artery injury and 2.6% for BVAI.20 Early antithrombotic therapy has also been demonstrated to improve neurologic outcomes among symptomatic patients. Early reports from Denver suggest that systemic heparinization may be superior to antiplatelet therapy in stroke prevention and in neurologic improvement after ischemic insult, although results were statistically insignificant,2,20-24 and heparin should be considered for grade 1 through 4 vertebral injuries and grade 1 through 3 carotid injuries. To date, several nonrandomized studies with relatively small numbers of patients suggest equivalence for anticoagulation and antiplatelet agents with regard to stroke rate, although the exact regimen (aspirin or clopidogrel) has not been well studied.2,21-24 With modern endovascular techniques, stenting has been increasingly advocated for flow-limiting grade 2 injuries and all grade 3 injuries, but results of safety and patency vary between reports. Earlier series, however, may have had higher reported stroke rates because antiplatelet therapy was not used as a pharmacologic adjunct.2,24-27 Stents use is not preferred within the first several days after injury because of the bleeding risk in multitrauma patients. Once the patient is cleared as being safe for stenting, the initiation of poststent antithrombotic therapy is critical.3 Long-term antithrombotic therapy has been recommended, especially if the lesion persists, as stroke has been reported as long as 14 years after injury, but the optimal drug and duration have not been studied. Long-term antiplatelet therapy is preferable to warfarin for its safety and
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cost profile. Clopidogrel is indicated for both stented and nonstented patients until healing can be documented. Healing occurs in most patients by 3 months and should be documented with angiography. Aspirin is recommended for life-long therapy to reduce intimal hyperplasia, but long-term data showing benefit are currently lacking.3 Four-vessel BCVI is an extremely rare occurrence, with only five reported cases in the literature resulting from chiropractic cervical manipulation,28-30 neck hyperextension, and thoracic trauma after motor vehicle and motorcycle crashes.31,32 Two cases have also been reported from equine injuries involving either or both ICAs and/or VAs.33,34 We report this as the first case of equine-related injury of bilateral internal carotid and vertebral arteries after a crush injury to the chest, with no associated head, facial, or cervical trauma, that was managed with medical and endovascular therapy. Our patient suffered from a right-sided hemiplegia, due to an embolic stroke, that was probably attributed to holding heparin intraoperatively in the second operation. CONCLUSIONS Complications from BCVI, including death, are potentially preventable by screening in the appropriate clinical setting and early treatment. Screening guidelines may need to be broadened to include equine injuries, particularly when associated with a high-force mechanism to the neck and torso. Our case gives a good example of how screening may have helped prevent serious complications or even death. More research is needed to define the risk of BCVI in large-animal–related injuries. REFERENCES 1. Loder RT. The demographics of equestrian-related injuries in the united states: injury patterns, orthopedic specific injuries, and avenues for injury prevention. J Trauma 2008;65:447-60. 2. Biffl WL, Ray CE Jr, Moore EE, Franciose RJ, Aly S, Heyrosa MG, et al. Treatment-related outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography. Ann Surg 2002;5:699707. 3. Biffl WL, Cothren CC, Moore EE, Kozar R, Cocanour C, Davis JW, et al. Western Trauma Association critical decisions in trauma: screening for and treatment of blunt cerebrovascular injuries. J Trauma 2009;67: 1150-3. 4. Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg 2009;144:685-90. 5. Davis JW, Holbrook TL, Hoyt DB, Mackersie RC, Field TO Jr, Shackford SR. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma 1990;30:1514-17. 6. Martin RF, Eldrup-Jorgensen J, Clark DE, Bredenberg CE. Blunt Trauma to the Carotid Arteries. J Vasc Surg 1991;14:789-95. 7. Cogbill TH, Moore EE, Meissner M, Fischer RP, Hoyt DB, Morris JA, et al. The spectrum of blunt injury to the carotid artery: a multicenter perspective. J Trauma 1994;37:473-9. 8. Ramadan F, Rutledge R, Oller D, Howell P, Baker C, Keagy B. Carotid artery trauma: a review of contemporary trauma center experiences. J Vasc Surg 1995;21:46-54. 9. Fabian TC, Patton JH Jr, Croce MA, Minard G, Kudsk KA, Pritchard FE. Blunt carotid injury: importance of early diagnosis and anticoagulant therapy. Ann Surg 1996;223:513-25.
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10. Parikh AA, Luchette FA, Valente JF, Johnson RC, Anderson GL, Blebea J, et al. Blunt carotid artery injuries. J Am Coll Surg 1997;185: 80-6. 11. Berne JD, Norwood SH, McAuley CE, Vallina VL, Creath RG, McLarty J. 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. 12. Delgado-Almandoz JE, Schaefer PW, Kelly HR, Lev MH, Gonzalez RG, Romero JM. Multidetector CT angiography in the evaluation of acute blunt head and neck trauma: a proposed acute craniocervical trauma scoring system. Radiology 2010;254:236-44. 13. Berne JD, Cook AP, Rowe SA, Norwood SH. A multivariate logistic regression analysis of risk factors for blunt cerebrovascular injury. J Vasc Surg 2010;51:57-64. 14. Utter GH, Hollingworth W, Hallam DK, Jarvik JG, Jurkovich GJ. Sixteen-slice CT angiography in patients with suspected blunt carotid and vertebral artery injuries. J Am Coll Surg 2006;203:838-48. 15. Bub LD, Hollingworth W, Jarvik JG, Hallam DK. Screening for blunt cerebrovascular injury: evaluating the accuracy of multidetector computed tomographic angiography. J Trauma 2005;59:691-7. 16. Berne JD, Reuland KS, Villarreal DH, McGovern TM, Rowe SA, Norwood SH. Sixteen-slice multi-detector computed tomographic angiography improves the accuracy of screening for blunt cerebrovascular injury. J Trauma 2006;60:1204-9. 17. Biffl WL, Egglin T, Benedetto B, Gibbs F, Cioffi WG. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma 2006;60:745-51. 18. Eastman AL, Chason DP, Perez CL, McAnulty AL, Minei JP. Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime? J Trauma 2006;60:925-9. 19. Malhotra AK, Camacho M, Ivatury RR, Davis IC, Komorowski DJ, Leung DA, et al. Computed tomographic angiography for the diagnosis of blunt carotid/vertebral artery injury: a note of caution. Ann Surg 2007;246:632-43. 20. Utter GH, Hollingworth W, Hallam DK, Jarvik JG, Jurkovich GJ. Sixteen-slice CT angiography in patients with suspected blunt carotid and vertebral artery injuries. J Am Coll Surg 2006;203:838-48. 21. Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg 2009;144:685-9. 22. Miller PR, Fabian TC, Croce MA, Cagiannos C, Williams JS, Vang M, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg 2002;236:386-95. 23. Cothren CC, Moore EE, Biffl WL, Ciesla DJ, Ray CE Jr, Johnson JL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg 2004;139:540-6. 24. Cothren CC, Moore EE, Ray CE Jr, Ciesla DJ, Johnson JL, Moore JB, et al. Screening for blunt cerebrovascular injuries is cost effective. Am J Surg 2005;190:845-9. 25. Edwards NM, Fabian TC, Claridge JA, Timmons SD, Fischer PE, Croce MA. Antithrombotic therapy and endovascular stents are effective treatment for blunt carotid injuries: results from long-term followup. J Am Coll Surg 2007;204:1007-15. 26. Biffl WL, Moore EE, Offner PJ, Brega KE, Franciose RJ, Burch JM. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma 1999;47:845-53. 27. Cothren CC, Moore EE, Ray CE Jr, Ciesla DJ, Johnson JL, Moore JB, et al. Carotid artery stents for blunt cerebrovascular injury: risks exceed benefits. Arch Surg 2005;140:480-6. 28. Nadgir RN, Loevner LA, Ahmed T, Moonis G, Chalela J, Slawek K, et al. Simultaneous bilateral internal carotid and vertebral artery dissection following chiropractic manipulation: case report and review of the literature. Neuroradiology 2003;45:311-4. 29. Yong RL, Heran NS. Traumatic carotid cavernous fistula with bilateral carotid artery and vertebral artery dissections. Acta Neurochir (Wien) 2005;147:1109-13. 30. Chakrapani AL, Zink W, Zimmerman R, Riina H, Benitez R. Bilateral carotid and bilateral vertebral artery dissection following facial massage. Angiology 2009;59:761-4.
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31. Kutlu NO, Sarac K, Yakinci C. Dissection of bilateral internal carotid arteries and occlusion of both vertebral arteries in a child patient. Comput Med Imaging Graph 2002;26:205-9. 32. Fukuda I, Meguro K, Matsusita S, Shigeta O, Oohashi N, Nakata Y. Traumatic disruption of bilateral vertebral arteries and internal carotid arteries: case report. J Trauma 1989;29:263-6. 33. Nunnink L, Abu-Zidan F. Accidental carotid artery injury caused by a horse rope. Br J Sports Med 2003;37:460-1.
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34. Fletcher J, Davies PT, Lewis T, Campbell MJ. Traumatic carotid and vertebral artery dissection in a professional jockey: a cautionary tale. Br J Sports Med 1995;29:143-4.
Submitted Feb 15, 2010; accepted May 15, 2010.
Early recognition and treatment of blunt cerebrovascular injuries (BCVIs) has been shown to prevent strokerelated morbidity and mortality. Early screening of asymptomatic patients based on injury-related mechanism and associated injuries has been proposed to identify the at-risk population that may benefit from screening. Equestrianrelated injuries have only rarely been associated with blunt injuries to the internal carotid or vertebral arteries.1 We report an unusual case of bilateral internal carotid (ICA) and vertebral artery (VA) dissection after a horse-related crush chest injury. The patient was treated with systemic anticoagulation and subsequent endovascular stenting of the bilateral ICAs. CASE REPORT A 52-year-old woman sustained multiple injuries after she fell off a horse. After throwing her to the ground, the horse jumped up and landed on her chest, causing a severe crush injury to the thoracic cavity. She initially lost consciousness, but on arrival to our facility, she had a Glasgow Coma Score of 15, with no focal neurologic deficits, was in severe respiratory distress, with flail chest requiring immediate intubation. She was also in shock. Bilateral thoracostomy tubes were placed, and an infusion of packed red blood cells was begun. After some improvement in her vital signs and a bedside abdominal ultrasound examination showed no clear free fluid in the abdomen, a computed tomography (CT) scan of the chest was performed that demonstrated multiple bilateral displaced rib fractures with bilateral hemopneumothoraces, mediastinal shift to the From the Department of Surgery, Ochsner Clinic Foundation, New Orleansa; East Texas Medical Center, Tylerb; and the Department of Surgery, University of Toledo Medical Center, Toledoc. Competition of interest: none. Reprint requests: Zeid M. Keilani, MD, Department of Surgery, Ochsner Clinic Foundation, 1514 Jefferson Hwy, New Orleans, LA 70121 (email: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Copyright © 2010 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. doi:10.1016/j.jvs.2010.05.065
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right, and hemopneumopericardium. A CT of the abdomen demonstrated extensive pneumoperitoneum with no evidence of solid organ injury, and multiple thoracic and lumbar spinal vertebral fractures with no involvement of the spinal cord. Results of head and cervical spine CT were negative. Screening CT angiography (CTA) of the neck demonstrated left ICA dissection just above the bifurcation and extending toward the base of the neck, along with proximal dissection of the proximal left VA, with no involvement of her right side (Fig 1). The patient underwent an exploratory laparotomy, clamshell thoracotomy with wedge resection of the left lower lobe and lingula, release of hemopneumopericardium, and temporary negative pressure vacuum-assisted dressing closure (VAC; Kinetic Concepts Inc, San Antonio, Tex) of the abdominal and thoracic cavities. She was further stabilized in the intensive care unit, where an unfractionated heparin drip was started on postoperative day 1. She was taken back to the operating room on postoperative day 3 for closure of her abdominal and thoracic cavities. Heparin was held intraoperatively but was restarted postoperatively. The next morning she was unresponsive, prompting a magnetic resonance imaging of the brain, which revealed multiple areas of ischemic strokes in her left frontal and occipital lobes as well as the left cerebellar hemisphere (Fig 2). She continued to improve gradually, but had persistent right-sided hemiplegia. Aspirin and clopidogrel were started, and heparin was discontinued in anticipation of possible stent placement. Because of the well-documented progression of these lesions over the first 7 to 10 days, a routine follow-up arteriogram was performed 9 days later.2 This demonstrated a long segment spiral dissection and pseudoaneurysm of the left ICA, small pseudoaneurysm with minimal areas of narrowing of the proximal left VA, a 6-cm dissection of the right ICA, and a small pseudoaneurysm of the proximal right VA (Fig 3). Bilateral stent placement with 7 ⫻ 30-mm and 7 ⫻ 20-mm nitinol uncovered metal stents in the right ICA, and 7 ⫻ 30-mm and 8 ⫻ 30-mm nitinol uncovered metal stents in the left ICA over a 0.035-inch Bentson wire (Cook Inc, Bloomington, Ind) was performed (Fig 4 and 5). She continued to improve with physical therapy. A follow-up angiogram before discharge demonstrated good patency of bilateral stents, without flow restrictions. She was discharged to a rehabilitation facility on clopidogrel (75-mg daily). A follow-up
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Fig 1. A computed tomography angiography (CTA) of the neck demonstrates (a) a small dissection of the proximal left vertebral artery (close-up in inset) and (b) dissection of the left internal carotid artery just above the bifurcation extending toward the base of the neck (close-up in inset).
Fig 2. Magnetic resonance imaging of the brain shows multiple areas of ischemic stroke in the left (a) frontal and (b) occipital lobes, and in the left (c) cerebellar hemisphere.
arteriogram at 3 months after discharge demonstrated patency of bilateral ICA without stenosis or residual pseudoaneurysm. The left vertebral artery showed complete healing. The right vertebral artery showed a persistent and slightly enlarged pseudoaneurysm. Coil embolization with Matrix 2 detachable coils (Boston Scientific, Natick, Mass) of the entire lumen at its origin was accomplished without any complications. She has since discontinued taking the clopidogrel but continued low-dose aspirin. She has regained full cognition but has a persistent mild right-sided weakness.
DISCUSSION Collective incidence of BCVIs in the literature have been reported to range between 0.1% to 1.6%, with overall reported mortality rates of 13% to 23% for blunt carotid artery injury and 6.8% to 8% for blunt VA injury, and overall stroke rate of 14% to 50% for blunt carotid artery injury and
9% to 25% for blunt VA injury.3-11 BCVI are usually associated with closed head and cervical trauma, basilar skull and facial fractures, thoracic, and seat belt injuries. Therefore, screening has been advocated in such clinical scenarios to identify these injuries in asymptomatic patients and to initiate treatment before the appearance of neurologic sequelae (Table I).4 Delgado-Almandoz et al12 recently published a proposed scoring system for the prediction of a patient’s risk of arterial injury from acute blunt craniocervical trauma that could be used to select patients for multidetector CTA screening. This scoring system is based on three independent predictors of a higher risk of arterial injury demonstrated from a multivariate logistic regression analysis: cervical interfacetal subluxations/dislocations, fracture lines reaching an arterial structure, and high-impact mechanism of injury. Patients with scores of 2 and 3 are at highest risk
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Fig 5. Four-vessel neck arteriogram demonstrates (a) a long segment dissection of the right internal carotid artery and (b) stenting of the right internal carotid artery with good flow.
Table I. Denver screening criteria for blunt cerebrovascular injuries4 Fig 3. A four-vessel neck arteriogram demonstrates (a) a small pseudoaneurysm of the proximal right vertebral artery and (b) a small pseudoaneurysm with minimal areas of narrowing of the proximal left vertebral artery.
Fig 4. A four-vessel neck arteriogram demonstrates (a) a long segment of spiral dissection and pseudoaneurysm of the left internal carotid artery and (b) stenting of the left internal carotid artery with good flow.
of arterial injury (21.9% and 52.2%, respectively; P ⬍ .0001), whereas patients with a score of 1 carry a risk of 10.1% (P ⬍ .0001). This study is still a retrospective, single-patient cohort study that relies heavily on radiographic findings and requires further future validation (Table II).12 Based on our own risk factor study, we have liberalized screening at our institution to include patients with several “soft” risk factors, with low GCS and high injury severity score (ISS) being the most important, which pan out on a
Signs/symptoms of blunt cerebrovascular injury ● Arterial hemorrhage ● Cervical bruit ● Expanding cervical hematoma ● Focal neurologic deficit ● Findings from neurologic examination incongruous with head CT scan findings ● Stroke on secondary CT scan ● Neurologic deficit inconsistent with head CT Risk factors for blunt cerebrovascular injury ● High-energy transfer mechanism with Le Forte II or III fracture ● Cervical spine fracture patterns: subluxation, fractures extending into the transverse foramen, fractures of C1-C3 vertebrae ● Basilar skull fracture with carotid canal involvement ● Diffuse axonal injury with GCS ⬍6 ● Near hanging with anoxic brain injury CT, Computed tomography; GCS, Glasgow Coma Score. Source: Reprinted from Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg. 2009;144:685-90. © 2009. With permission from American Medical Association. All rights reserved.
multivariate logistic regression analysis. Some of the patients with BCVIs in our series, including this patient, would have been missed if only the Denver criteria had been used (Table III).13 Screening can be performed with duplex ultrasound imaging, four-vessel cerebral arteriography, CT angiography, or magnetic resonance angiography. Duplex ultrasound imaging and magnetic resonance angiography are no longer considered as a standard screening test for BCVIs due to documented poor sensitivity and specificity in the literature. Angiogram has been considered the gold standard for diagnosis of BCVI, but is invasive and associated
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Table II. Calculation of proposed acute craniocervical trauma scoring system12
Table IV. Denver grading scale for blunt cerebrovascular injury4
Parameter points Mechanism of injury Low impacta High impactb Cervical interfacetal subluxation/dislocation No Yes Fracture line reaching an arterial structure No Yes
Grade 0 1
II 0 1 0 1
a Includes hanging or strangulation, low-speed motor vehicle accident, fall from standing, and other blunt trauma to the head or neck. b Includes high-speed motor vehicle accident, including motorcycle accidents, struck pedestrian or bicyclist, fall from height greater than standing, fall down stairs, and high-force blows to the head or neck, including assault. The score is calculated by adding the total number of points. Source: Reprinted from Delgado-Almandoz JE, Schaefer PW, Kelly HR, Lev MH, Gonzalez RG, Romero JM. Multidetector CT Angiography in the evaluation of acute blunt head and neck trauma: a proposed acute craniocervical trauma scoring system. Radiology 2010;254:236-244. With permission from the Radiological Society of North America.
Table III. Multivariate logistic regression model for blunt cerebrovascular injuries13 Variable Cervical spine injury Mandible Fx Basilar skull Fx Thoracic or lumbar spine Fx Any facial injury Injury severity score Le Fort Fx ED GCS
I
OR (95% CI)
P
7.46 (4.87-11.44) 2.59 (1.30-5.15) 1.76 (1.02-3.01) 1.29 (0.82-2.03) 1.16 (0.73-1.86) 1.05 (1.04-1.07) 0.97 (0.50-1.86) 0.93 (0.89-0.97)
⬍ .001 .007 .041 .28 .53 ⬍ .001 .92 .001
CI, Confidence interval; ED GCS, emergency department Glasgow Coma Score; Fx, fracture; OR, odds ratio. Source: Reprinted from Berne JD, Cook AP, Rowe SA, and Norwood SH. A Multivariate logistic regression analysis of risk factors for blunt cerebrovascular injury. J Vasc Surg 2010;51:57-64. © 2010 With permission from Elsevier.
with potential risks and complications, including hematoma, arterial pseudoaneurysm, and renal dysfunction.2,3 Accuracy of CTA has improved with multidetector-row CTA, with the 16-slice CTA emerging as a reliable method for detecting clinically significant BCVI (100% sensitivity for carotid and 96% for vertebral artery injuries).13-17 CTA has also been reported to be oversensitive, with reported false-positive rates of 43%, but these results could be largely attributed to the radiologists’ inexperience.18,19 If CTA is not available or in the setting of high clinical suspicion and a normal CTA, a four-vessel angiogram is considered the gold standard.3 Management of a BCVI includes observation, surgery, antithrombotic therapy, or endovascular therapy. Management is largely determined by symptoms, location, and grade of the injury, although this has not been standardized, and recommendations are made based on retrospec-
III IV V
Description Irregularity of the vessel wall or a dissection/intramural hematoma with less than 25% luminal stenosis Intraluminal thrombus or raised intimal flap is visualized or dissection/intramural hematoma with 25% or more luminal narrowing Pseudoaneurysm Vessel occlusion Vessel transaction
Source: Reprinted from Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg 2009;144:685-90. © 2009. With permission from American Medical Association. All rights reserved.
tive analyses of patients managed per institutional protocols (Table IV).4 Observation is chosen if other treatment modalities are contraindicated. Surgery is warranted in highergrade (grade 2-5) surgically accessible injuries, but most BCVIs occur in surgically challenging or inaccessible areas, such as at base of the skull or within the foramen transversarium.3,20 Early antithrombotic therapy, either anticoagulation or antiplatelet agents, in asymptomatic patients reduces or nearly eliminates BCVI-related strokes, down to 6.8% for blunt carotid artery injury and 2.6% for BVAI.20 Early antithrombotic therapy has also been demonstrated to improve neurologic outcomes among symptomatic patients. Early reports from Denver suggest that systemic heparinization may be superior to antiplatelet therapy in stroke prevention and in neurologic improvement after ischemic insult, although results were statistically insignificant,2,20-24 and heparin should be considered for grade 1 through 4 vertebral injuries and grade 1 through 3 carotid injuries. To date, several nonrandomized studies with relatively small numbers of patients suggest equivalence for anticoagulation and antiplatelet agents with regard to stroke rate, although the exact regimen (aspirin or clopidogrel) has not been well studied.2,21-24 With modern endovascular techniques, stenting has been increasingly advocated for flow-limiting grade 2 injuries and all grade 3 injuries, but results of safety and patency vary between reports. Earlier series, however, may have had higher reported stroke rates because antiplatelet therapy was not used as a pharmacologic adjunct.2,24-27 Stents use is not preferred within the first several days after injury because of the bleeding risk in multitrauma patients. Once the patient is cleared as being safe for stenting, the initiation of poststent antithrombotic therapy is critical.3 Long-term antithrombotic therapy has been recommended, especially if the lesion persists, as stroke has been reported as long as 14 years after injury, but the optimal drug and duration have not been studied. Long-term antiplatelet therapy is preferable to warfarin for its safety and
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cost profile. Clopidogrel is indicated for both stented and nonstented patients until healing can be documented. Healing occurs in most patients by 3 months and should be documented with angiography. Aspirin is recommended for life-long therapy to reduce intimal hyperplasia, but long-term data showing benefit are currently lacking.3 Four-vessel BCVI is an extremely rare occurrence, with only five reported cases in the literature resulting from chiropractic cervical manipulation,28-30 neck hyperextension, and thoracic trauma after motor vehicle and motorcycle crashes.31,32 Two cases have also been reported from equine injuries involving either or both ICAs and/or VAs.33,34 We report this as the first case of equine-related injury of bilateral internal carotid and vertebral arteries after a crush injury to the chest, with no associated head, facial, or cervical trauma, that was managed with medical and endovascular therapy. Our patient suffered from a right-sided hemiplegia, due to an embolic stroke, that was probably attributed to holding heparin intraoperatively in the second operation. CONCLUSIONS Complications from BCVI, including death, are potentially preventable by screening in the appropriate clinical setting and early treatment. Screening guidelines may need to be broadened to include equine injuries, particularly when associated with a high-force mechanism to the neck and torso. Our case gives a good example of how screening may have helped prevent serious complications or even death. More research is needed to define the risk of BCVI in large-animal–related injuries. REFERENCES 1. Loder RT. The demographics of equestrian-related injuries in the united states: injury patterns, orthopedic specific injuries, and avenues for injury prevention. J Trauma 2008;65:447-60. 2. Biffl WL, Ray CE Jr, Moore EE, Franciose RJ, Aly S, Heyrosa MG, et al. Treatment-related outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography. Ann Surg 2002;5:699707. 3. Biffl WL, Cothren CC, Moore EE, Kozar R, Cocanour C, Davis JW, et al. Western Trauma Association critical decisions in trauma: screening for and treatment of blunt cerebrovascular injuries. J Trauma 2009;67: 1150-3. 4. Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg 2009;144:685-90. 5. Davis JW, Holbrook TL, Hoyt DB, Mackersie RC, Field TO Jr, Shackford SR. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma 1990;30:1514-17. 6. Martin RF, Eldrup-Jorgensen J, Clark DE, Bredenberg CE. Blunt Trauma to the Carotid Arteries. J Vasc Surg 1991;14:789-95. 7. Cogbill TH, Moore EE, Meissner M, Fischer RP, Hoyt DB, Morris JA, et al. The spectrum of blunt injury to the carotid artery: a multicenter perspective. J Trauma 1994;37:473-9. 8. Ramadan F, Rutledge R, Oller D, Howell P, Baker C, Keagy B. Carotid artery trauma: a review of contemporary trauma center experiences. J Vasc Surg 1995;21:46-54. 9. Fabian TC, Patton JH Jr, Croce MA, Minard G, Kudsk KA, Pritchard FE. Blunt carotid injury: importance of early diagnosis and anticoagulant therapy. Ann Surg 1996;223:513-25.
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10. Parikh AA, Luchette FA, Valente JF, Johnson RC, Anderson GL, Blebea J, et al. Blunt carotid artery injuries. J Am Coll Surg 1997;185: 80-6. 11. Berne JD, Norwood SH, McAuley CE, Vallina VL, Creath RG, McLarty J. 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. 12. Delgado-Almandoz JE, Schaefer PW, Kelly HR, Lev MH, Gonzalez RG, Romero JM. Multidetector CT angiography in the evaluation of acute blunt head and neck trauma: a proposed acute craniocervical trauma scoring system. Radiology 2010;254:236-44. 13. Berne JD, Cook AP, Rowe SA, Norwood SH. A multivariate logistic regression analysis of risk factors for blunt cerebrovascular injury. J Vasc Surg 2010;51:57-64. 14. Utter GH, Hollingworth W, Hallam DK, Jarvik JG, Jurkovich GJ. Sixteen-slice CT angiography in patients with suspected blunt carotid and vertebral artery injuries. J Am Coll Surg 2006;203:838-48. 15. Bub LD, Hollingworth W, Jarvik JG, Hallam DK. Screening for blunt cerebrovascular injury: evaluating the accuracy of multidetector computed tomographic angiography. J Trauma 2005;59:691-7. 16. Berne JD, Reuland KS, Villarreal DH, McGovern TM, Rowe SA, Norwood SH. Sixteen-slice multi-detector computed tomographic angiography improves the accuracy of screening for blunt cerebrovascular injury. J Trauma 2006;60:1204-9. 17. Biffl WL, Egglin T, Benedetto B, Gibbs F, Cioffi WG. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma 2006;60:745-51. 18. Eastman AL, Chason DP, Perez CL, McAnulty AL, Minei JP. Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime? J Trauma 2006;60:925-9. 19. Malhotra AK, Camacho M, Ivatury RR, Davis IC, Komorowski DJ, Leung DA, et al. Computed tomographic angiography for the diagnosis of blunt carotid/vertebral artery injury: a note of caution. Ann Surg 2007;246:632-43. 20. Utter GH, Hollingworth W, Hallam DK, Jarvik JG, Jurkovich GJ. Sixteen-slice CT angiography in patients with suspected blunt carotid and vertebral artery injuries. J Am Coll Surg 2006;203:838-48. 21. Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg 2009;144:685-9. 22. Miller PR, Fabian TC, Croce MA, Cagiannos C, Williams JS, Vang M, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg 2002;236:386-95. 23. Cothren CC, Moore EE, Biffl WL, Ciesla DJ, Ray CE Jr, Johnson JL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg 2004;139:540-6. 24. Cothren CC, Moore EE, Ray CE Jr, Ciesla DJ, Johnson JL, Moore JB, et al. Screening for blunt cerebrovascular injuries is cost effective. Am J Surg 2005;190:845-9. 25. Edwards NM, Fabian TC, Claridge JA, Timmons SD, Fischer PE, Croce MA. Antithrombotic therapy and endovascular stents are effective treatment for blunt carotid injuries: results from long-term followup. J Am Coll Surg 2007;204:1007-15. 26. Biffl WL, Moore EE, Offner PJ, Brega KE, Franciose RJ, Burch JM. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma 1999;47:845-53. 27. Cothren CC, Moore EE, Ray CE Jr, Ciesla DJ, Johnson JL, Moore JB, et al. Carotid artery stents for blunt cerebrovascular injury: risks exceed benefits. Arch Surg 2005;140:480-6. 28. Nadgir RN, Loevner LA, Ahmed T, Moonis G, Chalela J, Slawek K, et al. Simultaneous bilateral internal carotid and vertebral artery dissection following chiropractic manipulation: case report and review of the literature. Neuroradiology 2003;45:311-4. 29. Yong RL, Heran NS. Traumatic carotid cavernous fistula with bilateral carotid artery and vertebral artery dissections. Acta Neurochir (Wien) 2005;147:1109-13. 30. Chakrapani AL, Zink W, Zimmerman R, Riina H, Benitez R. Bilateral carotid and bilateral vertebral artery dissection following facial massage. Angiology 2009;59:761-4.
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31. Kutlu NO, Sarac K, Yakinci C. Dissection of bilateral internal carotid arteries and occlusion of both vertebral arteries in a child patient. Comput Med Imaging Graph 2002;26:205-9. 32. Fukuda I, Meguro K, Matsusita S, Shigeta O, Oohashi N, Nakata Y. Traumatic disruption of bilateral vertebral arteries and internal carotid arteries: case report. J Trauma 1989;29:263-6. 33. Nunnink L, Abu-Zidan F. Accidental carotid artery injury caused by a horse rope. Br J Sports Med 2003;37:460-1.
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34. Fletcher J, Davies PT, Lewis T, Campbell MJ. Traumatic carotid and vertebral artery dissection in a professional jockey: a cautionary tale. Br J Sports Med 1995;29:143-4.
Submitted Feb 15, 2010; accepted May 15, 2010.