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Management of Extracranial Blunt Cerebrovascular Injuries: Experience with an Aspirin-Based Approach
Journal Pre-proof Management of extracranial blunt cerebrovascular injuries: experience with an aspirin-based approach Joshua S. Catapano, MD, Sharjeel Israr, MD, Alexander C. Whiting, MD, Omar M. Hussain, BS, Laura A. Snyder, MD, Felipe C. Albuquerque, MD, Andrew F. Ducruet, MD, Peter Nakaji, MD, Michael T. Lawton, MD, Jordan A. Weinberg, MD, Joseph M. Zabramski, MD PII:
S1878-8750(19)32443-X
DOI:
https://doi.org/10.1016/j.wneu.2019.09.013
Reference:
WNEU 13312
To appear in:
World Neurosurgery
Received Date: 14 May 2019 Revised Date:
4 September 2019
Accepted Date: 5 September 2019
Please cite this article as: Catapano JS, Israr S, Whiting AC, Hussain OM, Snyder LA, Albuquerque FC, Ducruet AF, Nakaji P, Lawton MT, Weinberg JA, Zabramski JM, Management of extracranial blunt cerebrovascular injuries: experience with an aspirin-based approach, World Neurosurgery (2019), doi: https://doi.org/10.1016/j.wneu.2019.09.013. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Elsevier Inc. All rights reserved.
Catapano JS et al. 1
Management of extracranial blunt cerebrovascular injuries: experience with an aspirinbased approach
Joshua S. Catapano, MD Sharjeel Israr, MD Alexander C. Whiting, MD Omar M. Hussain, BS Laura A. Snyder, MD Felipe C. Albuquerque, MD Andrew F. Ducruet, MD Peter Nakaji, MD Michael T. Lawton, MD Jordan A. Weinberg, MD Joseph M. Zabramski, MD
Department of Neurosurgery Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona
Correspondence: Joseph M. Zabramski, MD c/o Neuroscience Publications; Barrow Neurological Institute
Catapano JS et al. 2 St. Joseph’s Hospital and Medical Center 350 W. Thomas Rd.; Phoenix, AZ 85013 Tel: 602.406.3593; Fax: 602.406.4104 E-mail: [email protected]
DISCLOSURES: None FINANCIAL SUPPORT: None ACKNOWLEDGMENTS: The authors thank the staff of Neuroscience Publications at Barrow Neurological Institute for assistance with manuscript preparation.
SUBMISSION CATEGORY: Original Article
Catapano JS et al. 3 ABSTRACT Background: Optimal management of patients with extracranial blunt cerebrovascular injury (BCVI) remains controversial, with both anticoagulation and antiplatelet therapy being recommended. The purpose of this study was to evaluate the efficacy and safety of using acetylsalicylic acid (ASA) in the management of BCVI. Methods: Patients with BCVI were identified from the registry of a Level 1 trauma center between 2010 and 2017. Digital imaging and electronic medical records were reviewed for patient information including demographic characteristics, injury type, therapy, outcomes, and follow-up. Results: Over the study period, 13,578 patients were admitted following blunt trauma, with 94 (0.7%) having confirmed BCVI (mean age, 42 years; 72% male). Mean Injury Severity Score and Glasgow Coma Score were 27 and 10, respectively. BCVI was identified in 130 vessels with Biffl grade I (38%) and grade II injury (29%) being most common. Twelve (13%) patients experienced an ischemic event, but only 3 events occurred after diagnosis. ASA was primary treatment for 56 (60%) patients. Thirty patients (32%) received no treatment; 21 patients died within 24 hours of primary injury. Only 4 patients had ASA contraindications. Four patients (7%) had ASA-related complications; there were 2 cases of intracranial hemorrhage progression and 2 cases of gastrointestinal bleeding. Follow-up vascular imaging at a mean of 36 days demonstrated stable or improved levels of BCVI in 94% of patients. Conclusion: An ASA-based management strategy for BCVI was efficacious and relatively safe in this study. This approach may be the preferred treatment for BCVI, but confirmation is needed.
Catapano JS et al. 4 RUNNING TITLE: Management of BCVI with ASA KEYWORDS: ASA; extracranial blunt cerebral vascular injury; stroke
ABBREVIATIONS: ASA = acetylsalicylic acid; BCVI = blunt cerebrovascular injury; CTA = computed tomographic angiography; ICH = intracerebral hemorrhage
Catapano JS et al. 5 INTRODUCTION Extracranial blunt cerebrovascular injury (BCVI) is defined as nonpenetrating damage to one or more of the extracranial cerebrovascular arteries, including the internal carotid and/or vertebral vessels. BCVIs are rare and occur in approximately 0.1% to 3% of trauma patients.1-4 When present, however, these injuries are associated with significant morbidity and mortality from ischemic disease, especially if undiagnosed or left untreated. The incidence of stroke among patients with BCVI is between 10% and 13%.2, 4 Isolated injury to the carotid arteries or vertebral arteries is associated with mortality rates ranging from 17% to 38%.1, 5, 6 Thus, timely treatment is essential for reducing the burden of neurologic deficits in these patients. The introduction of effective screening protocols and advanced imaging techniques, including digital subtraction angiography and computed tomographic angiography (CTA), combined with prophylactic treatment to reduce thrombotic complications, has greatly reduced the burden of BCVI-related ischemia among trauma patients.5, 7 While screening protocols have largely become standardized, treatment remains controversial. Initial reports advocated that anticoagulant therapy with heparin be administered only following the onset of ischemia after a BCVI8, 9; however, more recent observational studies have demonstrated better outcomes among patients who are treated prophylactically.1, 10-12 Most centers currently treat with either a prophylactic anticoagulant or antiplatelet therapy, whereas endovascular therapy is reserved for a select few.1, 10 Furthermore, the prophylactic treatment of asymptomatic BCVI patients with aspirin has been associated with increased risk of transfusion with pack red blood cells.13 In 2011, the ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease found Level
Catapano JS et al. 6 B evidence for the treatment of symptomatic (either stroke or transient ischemic attack) BCVI patients for 3-6 months with either an anticoagulant (low-molecular-weight heparin, heparin, or warfarin) or an antiplatelet (either aspirin with or without extended release dipyridamole, or clopidogrel exclusively).14 In addition, U.S. physicians are divided on the appropriate treatment, with greater than 40% favoring anticoagulation and greater than 30% ASA (~17% favor both).15 Hence, optimal management of patients with BCVI greatly differs among institutions, with the optimal antithrombotic regimen and agent yet to be determined, while the role of endovascular treatment remains largely unknown. Further investigations regarding management of these devastating injuries are warranted. In this study, we analyzed an acetylsalicylic acid (ASA)– based model with aggressive endovascular therapy in select patients with high-grade injuries, with a primary outcome of an ischemic stroke. We hypothesized that our rate of cerebrovascular accident would be lower than or equivalent to those reported in the literature.
METHODS This was a retrospective cohort study of adult trauma patients at least 18 years of age admitted to a Level 1 trauma center from January 1, 2010, through August 31, 2017. This study was approved by the institutional review board of St. Joseph’s Hospital and Medical Center (Phoenix, AZ), which waived the need for informed consent. The trauma registry was queried for all adult patients with an extracranial BCVI, and patient characteristics and other data were abstracted from review of the prospectively collected data. Additional clinical data were collected from the electronic medical record. A 64-slice computed tomography scanner was used to perform all CTA examinations. Modified Denver criteria were used at admission to screen patients and determine when CTA was appropriate. Scans with positive findings were graded
Catapano JS et al. 7 using the Biffl scale (Table 1). Appropriate treatment was determined by the on-call endovascular neurosurgeon, with ASA (325 mg daily) administered to all patients without contraindications (large/enlarging acute hemorrhage—either intracranial or in another organ, history of allergy to aspirin, severe thrombocytopenia, or history of recent gastrointestinal bleed) who were treated medically. Data collected included age, sex, race, comorbidities, baseline antithrombotic medications, days to stroke diagnosis, in-hospital procedures, complications, reoperations, discharge antithrombotic medications, hospital disposition, injury seen on imaging with Biffl scale grading, hospital days, intensive care unit days, ventilator days, and hospital readmissions. IBM SPSS Statistics 25 (IBM Corporation, Armonk, NY) was used for data analysis.
RESULTS During the 7-year study period, a total of 13,578 patients with blunt trauma were admitted to the hospital, with 94 patients (0.7 %) found to have an extracranial BCVI. The demographic and clinical characteristics of patients with BCVI are presented in Table 2. The mean age was 41.8 (range 16-92; standard deviation [SD] 17.7) years, and 68 (72%) of the patients were male. The most common mechanism of injury was a motor vehicle collision (41 patients; 44%). The mean (SD) Glasgow Coma Score and Injury Severity Score on arrival in the trauma bay were 9.6 (5) and 26.9 (17), respectively. Cervical fractures were present in 61 (65%) of the patients, and 37 (39%) sustained an intracerebral hemorrhage (ICH). Three (3%) patients died in the trauma bay, and 71 (76%) patients were intubated with a mean (SD) of 8.4 (7.8) days of ventilator support. The mean (SD) length of hospital stay was 11.6 (11.2) days, with 9 (7.8) days in the intensive care unit. The in-hospital mortality rate was 28% (26 of 94 patients died).
Catapano JS et al. 8 Nine patients presented with ischemic events in the trauma bay. An additional 3 (3%) patients developed delayed ischemic events. In Table 3, the Biffl grades of the vessels that were injured are shown. There were 130 injured vessels identified in 94 patients, including 52 internal carotid artery and 78 vertebral artery injuries. Grade I (40.8%) and grade II (29.2%) were the most common Biffl grades, followed by grade IV (19.2%), grade III (7.7%), and finally grade V (3.1%). Treatment and outcomes are presented in Table 4. ASA was the primary treatment in 56 patients (60%), and 1 patient who was already being treated with oral anticoagulants for atrial fibrillation continued to receive warfarin. There were also 7 patients (7%) who were treated primarily via endovascular means (5 treated with coil embolization and 2 treated with stent placements). Another 30 patients (32%) did not receive any treatment for BCVI, including 21 (70%) who died during the acute period, 4 (13%) in whom treatment was contraindicated, and 5 (17%) in whom the degree of vessel injury was considered to be minor. Treatment was contraindicated for 3 patients because of large ICHs and for 1 patient because of injury to another organ. Of the 56 patients who received primary treatment with ASA, 2 had progression of an ICH (neither required surgery) and 2 experienced severe gastrointestinal bleeding. The majority of patients with a BCVI (39 patients; 30%) were discharged to either a rehabilitation center or skilled nursing facility, 29 (22%) were discharged home, and 26 (20%) died. Follow-up imaging was performed for 33 of 68 surviving patients at a mean (SD) of 35.5 (52.3) days. CTA was the most common follow-up imaging (27 patients; 82%), followed by magnetic resonance angiography (6 patients; 18%). Of the 33 patients with follow-up imaging, 16 (49%) were found to have stability of their BCVI, 15 (46%) had improvement, and 2 (6%) had progression of their
Catapano JS et al. 9 initial injury. There were no delayed strokes or deaths among the 33 patients with follow-up imaging. Table 5 shows the treatment provided for the various injury grades. Endovascular therapy was reserved for patients with higher-grade injuries (2 grade III, 4 grade IV, and 2 grade V injuries), and ASA was used to treat injuries ranging from grade I to grade IV. Table 6 examines the outcomes for the 68 patients who survived their hospital stay on the basis of their primary treatment. The mean admission Glasgow Coma Score of patients who received ASA (n=49) was 12, compared with 11.4 for the endovascular treated group (n=7) and 8.6 for those not receiving treatment (n=11). The mean Glasgow Coma Score at discharge from the hospital was 14.3 in the ASA group, 13 in the endovascular group, and 13.7 in the untreated group. Five patients in the ASA group experienced a stroke (3 before and 2 after ASA treatment initiation), 2 patients in the endovascular group experienced a stroke (1 before and 1 after endovascular treatment), and 1 patient in the untreated group experienced a stroke.
DISCUSSION BCVIs are rare injuries that are often associated with high-impact blunt trauma with multiple injuries.4, 15 These injuries place patients at high risk of ischemic complications and are associated with stroke rates ranging from 10% to 64%, with lower rates reported in more recent studies.1-4, 7, 15-21 In this study, the risk of stroke was relatively low (10%) among patients with BCVI (Table 2). It is thought that most strokes occur during the acute period, within 72 hours after injury prior to a screening CTA, with 44% to 82% of strokes associated with BCVI detected on initial imaging and with the majority of such injuries being embolic in nature.15, 18, 19 Likewise, in this study, 9 of 12 BCVI-related strokes were identified at the time of diagnostic
Catapano JS et al. 10 imaging, all within the first 24 hours after presentation. There were no strokes during follow-up in our study at a mean of 35.5 days. Antithrombotic therapy remains the mainstay for the majority of patients with BCVI without contraindications.9, 10, 15, 16 However, the type of agent used remains controversial, with unfractionated heparin being recommended in recent guidelines from trauma societies.1, 10 Although no randomized controlled trials have been performed for treatment of BCVI, several retrospective studies have indicated that antiplatelet therapy may be at least as efficacious as heparin and equivalent in terms of neurologic outcomes.16, 18, 22-26 At our institution, patients with blunt trauma are screened for BCVI with use of the modified Denver criteria1, 10 and are administered a regimen of ASA if there are no contraindications (e.g., gastrointestinal bleeding, large ICH, or progression of ICH). We found a relatively low stroke rate among the 56 patients treated with ASA, with only 1 stroke (2%) after the initiation of treatment. Comparably, in a large retrospective study of 301 patients with BCVIs, Cothren et al.22 found 1 stroke among 192 patients treated with heparin and no strokes among 67 patients treated with ASA. In the same study, follow-up imaging demonstrated improvement of the BCVI in 39% of patients treated with heparin and 43% of patients treated with ASA; there was progression of the BCVI in 12% of patients treated with heparin versus 10% of patients treated with ASA. In the present report, follow-up imaging demonstrated stable (46%) or improved (50%) BCVI in patients treated with ASA and progression of injury in only 1 patient (4%); however, 26 (52%) of the ASA-treated patients had no follow-up imaging. In our study, ASA was chosen as the first-line therapy for patients with BCVI because of the large number of patients with contraindications to full-dose heparin therapy, with rates as high as 32% reported in earlier literature.26 Contrary to the rate of heparin contraindications, only
Catapano JS et al. 11 4 patients (7%) in the present series had a contraindication to ASA therapy (3 patients with enlarging ICH and 1 patient with injury to another organ). Furthermore, among patients treated with ASA, only 4 (7%) had a complication due to the treatment, including 2 patients with progression of ICH (among 22 total patients with ICH who were treated with ASA) and 2 patients with gastrointestinal bleeding, which is much lower than the rates reported in the literature; in a prospective study, Wahl et al.26 found that 57% of patients who were treated with heparin experienced a bleeding complication. Endovascular therapy is typically reserved for select high-risk lesions in patients with BCVI. However, with no randomized controlled trials and some controversy in the literature regarding the benefits of treatment, there has been no consensus regarding indications for the use of endovascular therapy.1, 7, 10, 16, 23, 27-36 At our institution, endovascular therapy is reserved for a highly selected group of patients in whom the benefit of the procedure is judged to outweigh the risks. Of 94 patients with a BCVI, only 7 patients (7%) underwent endovascular treatment. Two patients with grade III internal carotid artery injuries underwent stenting, and 3 patients with grade IV vertebral artery injuries and 2 patients with grade V vertebral artery injuries underwent coil embolization. Both patients with grade V injury survived the BCVI and had a transected vertebral artery sacrificed. The 3 patients with grade IV injury had the artery sacrificed to reduce the risk of future emboli. Only 1 patient (with grade V injury) had a stroke after endovascular therapy. The literature has reported stroke rates among patients with vertebral artery grade IV injuries of approximately 28%; however, none of the 3 patients with grade IV vertebral artery injuries in this series experienced a stroke.16 Follow-up imaging was available for 4 of the 7 patients with endovascular therapy; 1 patient with grade III injury had improvement of the BCVI, whereas the other 3 patients had stable dissections.
Catapano JS et al. 12 This study has the usual limitations inherent to retrospective evaluations. Three patients died before any imaging could be obtained, and another 23 patients died during the hospital stay. However, the mean Injury Severity Score of patients in this group was 39, and they likely died due to severe polytrauma rather than due to a cerebrovascular accident. Similar to other studies that have examined trauma patients, our study found that a large percentage of surviving patients (52%) were lost to follow-up. This may have resulted in lower rates of delayed stroke and progression of BCVI and lower overall mortality. Another limitation of our study was that the BCVIs in this series were classified using the results of CTA, and the Biffl grading system was developed using digital subtraction angiography. When evaluating CTA, it is more difficult to identify low-grade injuries (grade I and II injuries). However, CTA has become the standard of care at most trauma centers for the initial evaluation of BCVI.
CONCLUSION Our results imply that an ASA-based approached for the treatment of BCVI is as efficacious, has fewer contraindications, and is possibly safer than full-dose heparin anticoagulation. Furthermore, in a highly selected group of patients, aggressive endovascular therapy may be safe and potentially reduce the risk of stroke. However, because of the retrospective nature of this study, no definitive conclusions can be made. A future randomized controlled trial investigating the proper treatment of patients with BCVI, in which anticoagulation therapy is compared with antiplatelet therapy, is warranted. Additionally, further studies on outcomes among patients with BCVI treated with endovascular therapy are needed to develop clear indications for such treatments.
Catapano JS et al. 13 REFERENCES 1. Bromberg WJ, Collier BC, Diebel LN, Dwyer KM, Holevar MR, Jacobs DG, Kurek SJ, Schreiber MA, Shapiro ML, Vogel TR. Blunt cerebrovascular injury practice management guidelines: the Eastern Association for the Surgery of Trauma. J Trauma. Feb 2010;68(2):471-477. 2. DiCocco JM, Fabian TC, Emmett KP, Magnotti LJ, Zarzaur BL, Bate BG, Muhlbauer MS, Khan N, Kelly JM, Williams JS, Croce MA. Optimal outcomes for patients with blunt cerebrovascular injury (BCVI): tailoring treatment to the lesion. J Am Coll Surg. Apr 2011;212(4):549-557; discussion 557-549. 3. Franz RW, Willette PA, Wood MJ, Wright ML, Hartman JF. A systematic review and metaanalysis of diagnostic screening criteria for blunt cerebrovascular injuries. J Am Coll Surg. Mar 2012;214(3):313-327. 4. Geddes AE, Burlew CC, Wagenaar AE, Biffl WL, Johnson JL, Pieracci FM, Campion EM, Moore EE. Expanded screening criteria for blunt cerebrovascular injury: a bigger impact than anticipated. Am J Surg. Dec 2016;212(6):1167-1174. 5. Nagpal P, Policeni BA, Bathla G, Khandelwal A, Derdeyn C, Skeete D. Blunt cerebrovascular injuries: advances in screening, imaging, and management trends. AJNR Am J Neuroradiol. Oct 12 2017. 6. Sliker CW. Blunt cerebrovascular injuries: imaging with multidetector CT angiography. Radiographics. Oct 2008;28(6):1689-1708; discussion 1709-1610. 7. Cothren CC, Moore EE, Ray CE, Jr., Ciesla DJ, Johnson JL, Moore JB, Burch JM. Screening for blunt cerebrovascular injuries is cost-effective. Am J Surg. Dec 2005;190(6):845-849.
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Catapano JS et al. 15 Prevention, Society for Cardiovascular A, Interventions, Society of Interventional R, Society of NeuroInterventional S, Society for Vascular M, Society for Vascular S, American Academy of N, Society of Cardiovascular Computed T. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease. Stroke. Aug 2011;42(8):e464-540. 15. Foreman PM, Harrigan MR. Blunt traumatic extracranial cerebrovascular injury and ischemic stroke. Cerebrovasc Dis Extra. 2017;7(1):72-83. 16. Biffl WL, Ray CE, Jr., Moore EE, Franciose RJ, Aly S, Heyrosa MG, Johnson JL, Burch JM. Treatment-related outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography. Ann Surg. May 2002;235(5):699-706; discussion 706-697. 17. Crawford JD, Allan KM, Patel KU, Hart KD, Schreiber MA, Azarbal AF, Liem TK, Mitchell EL, Moneta GL, Landry GJ. The natural history of indeterminate blunt cerebrovascular injury. JAMA Surg. Sep 2015;150(9):841-847. 18. Stein DM, Boswell S, Sliker CW, Lui FY, Scalea TM. Blunt cerebrovascular injuries: does treatment always matter? J Trauma. Jan 2009;66(1):132-143; discussion 143-134. 19. Griessenauer CJ, Fleming JB, Richards BF, Cava LP, Cure JK, Younan DS, Zhao L, Alexandrov AV, Barlinn K, Taylor T, Harrigan MR. Timing and mechanism of ischemic stroke due to extracranial blunt traumatic cerebrovascular injury. J Neurosurg. Feb 2013;118(2):397-404. 20. Scott WW, Sharp S, Figueroa SA, Eastman AL, Hatchette CV, Madden CJ, Rickert KL. Clinical and radiographic outcomes following traumatic grade 1 and 2 carotid artery
Catapano JS et al. 16 injuries: a 10-year retrospective analysis from a level I trauma center. Parkland Carotid and Vertebral Artery Injury Survey. J Neurosurg. May 2015;122(5):1196-1201. 21. Scott WW, Sharp S, Figueroa SA, Eastman AL, Hatchette CV, Madden CJ, Rickert KL. Clinical and radiographic outcomes following traumatic grade 3 and 4 carotid artery injuries: a 10-year retrospective analysis from a level 1 trauma center. Parkland Carotid and Vertebral Artery Injury Survey. J Neurosurg. Mar 2015;122(3):610-615. 22. Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg. Jul 2009;144(7):685-690. 23. 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 longterm followup. J Am Coll Surg. May 2007;204(5):1007-1013; discussion 1014-1005. 24. Colella JJ, Diamond DL. Blunt carotid injury: reassessing the role of anticoagulation. Am Surg. Mar 1996;62(3):212-217. 25. Eachempati SR, Vaslef SN, Sebastian MW, Reed RL, 2nd. Blunt vascular injuries of the head and neck: is heparinization necessary? J Trauma. Dec 1998;45(6):997-1004. 26. Wahl WL, Brandt MM, Thompson BG, Taheri PA, Greenfield LJ. Antiplatelet therapy: an alternative to heparin for blunt carotid injury. J Trauma. May 2002;52(5):896-901. 27. Biffl WL, Moore EE, Offner PJ, Brega KE, Franciose RJ, Burch JM. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma. Nov 1999;47(5):845-853.
Catapano JS et al. 17 28. Jindal G, Fortes M, Miller T, Scalea T, Gandhi D. Endovascular stent repair of traumatic cervical internal carotid artery injuries. J Trauma Acute Care Surg. Nov 2013;75(5):896903. 29. Nanda A, Vannemreddy PS, Willis BK, Baskaya MK, Jawahar A. Management of carotid artery injuries: Louisiana State University Shreveport experience. Surg Neurol. Mar 2003;59(3):184-190; discussion 190. 30. Duke BJ, Ryu RK, Coldwell DM, Brega KE. Treatment of blunt injury to the carotid artery by using endovascular stents: an early experience. J Neurosurg. Dec 1997;87(6):825-829. 31. Li W, D'Ayala M, Hirshberg A, Briggs W, Wise L, Tortolani A. Comparison of conservative and operative treatment for blunt carotid injuries: analysis of the National Trauma Data Bank. J Vasc Surg. Mar 2010;51(3):593-599, 599 e591-592. 32. Moulakakis KG, Mylonas S, Avgerinos E, Kotsis T, Liapis CD. An update of the role of endovascular repair in blunt carotid artery trauma. Eur J Vasc Endovasc Surg. Sep 2010;40(3):312-319. 33. Berne JD, Reuland KR, Villarreal DH, McGovern TM, Rowe SA, Norwood SH. Internal carotid artery stenting for blunt carotid artery injuries with an associated pseudoaneurysm. J Trauma. Feb 2008;64(2):398-405. 34. Cohen JE, Gomori JM, Itshayek E, Spektor S, Shoshan Y, Rosenthal G, Moscovici S. Singlecenter experience on endovascular reconstruction of traumatic internal carotid artery dissections. J Trauma Acute Care Surg. Jan 2012;72(1):216-221. 35. Burlew CC, Biffl WL, Moore EE, Pieracci FM, Beauchamp KM, Stovall R, Wagenaar AE, Jurkovich GJ. Endovascular stenting is rarely necessary for the management of blunt cerebrovascular injuries. J Am Coll Surg. May 2014;218(5):1012-1017.
Catapano JS et al. 18 36. Stager V, Gandhi R, Stroman D, Timaran C, Broker H. Traumatic internal carotid artery injury treated with overlapping bare metal stents under intravascular ultrasound guidance. J Vasc Surg. Feb 2011;53(2):483-486.
Catapano JS et al. 19 Table 1. Biffl Grading of Blunt Cerebrovascular Injury Grade I II III IV V
Description Mild intimal tear of vessel wall Dissection of vessel wall with >25% narrowing Pseudoaneurysm Occlusion and/or thrombosis of vessel wall Transection of vessel wall
Catapano JS et al. 20 Table 2. Demographic and Clinical Characteristics of Patients with Blunt Cerebrovascular Injury Variable Patients (n=94) Male sex
68 (72)
Age (years), mean (SD)
41.8 (18)
Race/ethnicity White
40 (43)
Hispanic
32 (34)
Black
9 (10)
Asian
1 (1)
American Indian
3 (3)
Other
9 (10)
Mechanism of injury Motor vehicle collision
41 (44)
Motorcycle crash
17 (18)
Auto vs pedestrian
19 (20)
Other
17 (18)
GCS on arrival, mean (SD)
9.6 (5)
ISS,a mean (SD)
26.9 (17)
Cervical fracture
61 (65)
TBI with ICHb
37 (39)
Death in trauma bay
3 (3)
Intubation
71 (76)
Ventilator days, mean (SD)
8.4 (8)
Length of stay, days, mean (SD)
11.6 (11)
ICU days, mean (SD)
9.0 (8)
Outcome Death in hospital
26 (28)
Stroke before or during diagnosisc
9 (10)
Stroke after diagnosisd
3 (3)
Data are no. (%) of patients unless otherwise indicated. Abbreviations: GCS = Glasgow Coma Score; ICH = intracerebral hemorrhage; ICU = intensive care unit; ISS = Injury Severity Score; SD = standard deviation; TBI = traumatic brain injury.
Catapano JS et al. 21 a
The mean ISS of the 26 patients who died was 39. Twenty-two patients with ICH initiated acetylsalicylic acid therapy. c No grade I vessels. d All patients had at least a grade IV dissection and multiple dissections. b
Catapano JS et al. 22 Table 3. No. of Injured Vessels by Biffl Grade and Location Grade Left ICA Right ICA Left VA
Right VA
I 10 10 15 18 II 7 8 10 13 III 3 5 1 1 IV 4 4 10 7 V 1 0 1 2 Total 25 27 37 41 Abbreviations: ICA = internal carotid artery; VA = vertebral artery.
Total no. (%) of vessels (n=130) 53 (40.8) 38 (29.2) 10 (7.7) 25 (19.2) 4 (3.1) 130 (100)
Catapano JS et al. 23 Table 4. Treatment and Outcomes of Patients with Blunt Cerebrovascular Injury Treatment or Outcome Patients Primary treatment (n=94) ASAa
56 (60)
Warfarinb
1 (1)
Endovascular
7 (7)
None
30 (32)
Reason for no treatment (n=30) Contraindication
4 (13)
Large or enlarging ICH
3 (10)
Other organ injury
1 (3)
Death
21 (70)
Not indicated
5 (17)
Complication from treatment with ASA (n=56) Overall
4 (7) c
Progression of ICH
2 (4)
Gastrointestinal bleeding
2 (4)
Other
0 (0)
Discharge disposition (n=94) Home
29 (31)
Rehabilitation or skilled nursing facility
39 (41)
Death
26 (28)
Follow-up imaging (n=68) Overall
33 (49)
CTA
27 (40)
MRA
6 (9)
Catheter-based angiography
0 (0)
Imaging results (n=33) Improved
15 (46)
Stable
16 (49)
Worse
2 (6)
Catapano JS et al. 24 Follow-up, days, mean (SD) d
Delayed adverse events (n=33)
35.5 (52.3) 0 (0)
Data are no. (%) of patients unless otherwise indicated. Abbreviations: ASA = acetylsalicylic acid; CTA = computed tomographic angiography; ICH = intracerebral hemorrhage; MRA = magnetic resonance angiography; SD = standard deviation. a Two patients initiated heparin drip, but therapy was changed to ASA therapy within 24 hours. b This patient was receiving warfarin before blunt cerebrovascular injury, and this therapy was continued when dissection was found. c A total of 2 (9%) of 23 patients with ICH who initiated ASA had progression of their bleed. d Including delayed stroke and delayed death.
Catapano JS et al. 25 Table 5. Primary Treatment by Biffl Grade of Injured Vessels No. of Vessels, by Biffl Grade Primary Treatment I II III IV None 12 16 3 11 Acetylsalicylic 40 acid therapy Anticoagulation 1 therapy Endovascular 0 therapy
V 2
22
4
10
0
0
0
0
0
0
2
4
2
Catapano JS et al. 26 Table 6. Outcomes for Patients who Survived Hospital Stay Primary Therapy Variable
ASA
Endovascular
None
Patients who survived hospital stay (n=68) GCS at admission, mean
12
11.4
8.6
GCS at discharge, mean
14.3
13
13.7
No stroke
45
5
10
Stroke at or before diagnosis
3
1
1
Stroke after diagnosisa
2
1
0
Dissection improved
12
1
2
Dissection stable
11
3
1
Dissection progressed
1
0
1
Patients with follow-up imaging (n=33)
Abbreviations: ASA = acetylsalicylic acid; GCS = Glasgow Coma Score. a All patients had at least grade IV dissections and multiple dissections. One of the patients who received ASA therapy and experienced a stroke after diagnosis had the stroke prior to initiation of ASA treatment.
Table 1. Biffl Grading of Blunt Cerebrovascular Injury Grade Description I Mild intimal tear of vessel wall II Dissection of vessel wall with >25% narrowing III Pseudoaneurysm IV Occlusion and/or thrombosis of vessel wall V Transection of vessel wall
Catapano JS et al. 1 Table 2. Demographic and Clinical Characteristics of Patients with Blunt Cerebrovascular Injury Variable Patients (n=94) Male sex
68 (72)
Age (years), mean (SD)
41.8 (18)
Race/ethnicity White
40 (43)
Hispanic
32 (34)
Black
9 (10)
Asian
1 (1)
American Indian
3 (3)
Other
9 (10)
Mechanism of injury Motor vehicle collision
41 (44)
Motorcycle crash
17 (18)
Auto vs pedestrian
19 (20)
Other
17 (18)
GCS on arrival, mean (SD)
9.6 (5)
ISS,a mean (SD)
26.9 (17)
Cervical fracture
61 (65)
TBI with ICHb
37 (39)
Death in trauma bay
3 (3)
Intubation
71 (76)
Ventilator days, mean (SD)
8.4 (8)
Length of stay, days, mean (SD)
11.6 (11)
ICU days, mean (SD)
9.0 (8)
Outcome Death in hospital
26 (28)
Stroke before or during diagnosisc
9 (10)
Stroke after diagnosisd
3 (3)
Data are no. (%) of patients unless otherwise indicated. Abbreviations: GCS = Glasgow Coma Score; ICH = intracerebral hemorrhage; ICU = intensive care unit; ISS = Injury Severity Score; SD = standard deviation; TBI = traumatic brain injury.
Catapano JS et al. 2 a
The mean ISS of the 26 patients who died was 39. Twenty-two patients with ICH initiated acetylsalicylic acid therapy. c No grade I vessels. d All patients had at least a grade IV dissection and multiple dissections. b
Catapano JS et al. 1 Table 3. No. of Injured Vessels by Biffl Grade and Location Grade Left ICA Right ICA Left VA
Right VA
I 10 10 15 18 II 7 8 10 13 III 3 5 1 1 IV 4 4 10 7 V 1 0 1 2 Total 25 27 37 41 Abbreviations: ICA = internal carotid artery; VA = vertebral artery.
Total no. (%) of vessels (n=130) 53 (40.8) 38 (29.2) 10 (7.7) 25 (19.2) 4 (3.1) 130 (100)
Catapano JS et al. 1 Table 4. Treatment and Outcomes of Patients with Blunt Cerebrovascular Injury Treatment or Outcome Patients Primary treatment (n=94) ASAa
56 (60)
Warfarinb
1 (1)
Endovascular
7 (7)
None
30 (32)
Reason for no treatment (n=30) Contraindication
4 (13)
Large or enlarging ICH
3 (10)
Other organ injury
1 (3)
Death
21 (70)
Not indicated
5 (17)
Complication from treatment with ASA (n=56) Overall
4 (7)
Progression of ICHc
2 (4)
Gastrointestinal bleeding
2 (4)
Other
0 (0)
Discharge disposition (n=94) Home
29 (31)
Rehabilitation or skilled nursing facility
39 (41)
Death
26 (28)
Follow-up imaging (n=68) Overall
33 (49)
CTA
27 (40)
MRA
6 (9)
Catheter-based angiography
0 (0)
Imaging results (n=33) Improved
15 (46)
Stable
16 (49)
Catapano JS et al. 2 Worse
2 (6)
Follow-up, days, mean (SD)
35.5 (52.3)
Delayed adverse eventsd (n=33)
0 (0)
Data are no. (%) of patients unless otherwise indicated. Abbreviations: ASA = acetylsalicylic acid; CTA = computed tomographic angiography; ICH = intracerebral hemorrhage; MRA = magnetic resonance angiography; SD = standard deviation. a Two patients initiated heparin drip, but therapy was changed to ASA therapy within 24 hours. b This patient was receiving warfarin before blunt cerebrovascular injury, and this therapy was continued when dissection was found. c A total of 2 (9%) of 23 patients with ICH who initiated ASA had progression of their bleed. d Including delayed stroke and delayed death.
Table 5. Primary Treatment by Biffl Grade of Injured Vessels No. of Vessels, by Biffl Grade Primary Treatment I II III IV None 12 16 3 11 Acetylsalicylic 40 acid therapy Anticoagulation 1 therapy Endovascular 0 therapy
V 2
22
4
10
0
0
0
0
0
0
2
4
2
Catapano JS et al. 1 Table 6. Outcomes for Patients who Survived Hospital Stay Primary Therapy Variable
ASA
Endovascular
None
Patients who survived hospital stay (n=68) GCS at admission, mean
12
11.4
8.6
GCS at discharge, mean
14.3
13
13.7
No stroke
45
5
10
Stroke at or before diagnosis
3
1
1
Stroke after diagnosisa
2
1
0
Dissection improved
12
1
2
Dissection stable
11
3
1
Dissection progressed
1
0
1
Patients with follow-up imaging (n=33)
Abbreviations: ASA = acetylsalicylic acid; GCS = Glasgow Coma Score. a All patients had at least grade IV dissections and multiple dissections. One of the patients who received ASA therapy and experienced a stroke after diagnosis had the stroke prior to initiation of ASA treatment.
DISCLOSURES: None FINANCIAL SUPPORT: None
S1878-8750(19)32443-X
DOI:
https://doi.org/10.1016/j.wneu.2019.09.013
Reference:
WNEU 13312
To appear in:
World Neurosurgery
Received Date: 14 May 2019 Revised Date:
4 September 2019
Accepted Date: 5 September 2019
Please cite this article as: Catapano JS, Israr S, Whiting AC, Hussain OM, Snyder LA, Albuquerque FC, Ducruet AF, Nakaji P, Lawton MT, Weinberg JA, Zabramski JM, Management of extracranial blunt cerebrovascular injuries: experience with an aspirin-based approach, World Neurosurgery (2019), doi: https://doi.org/10.1016/j.wneu.2019.09.013. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Elsevier Inc. All rights reserved.
Catapano JS et al. 1
Management of extracranial blunt cerebrovascular injuries: experience with an aspirinbased approach
Joshua S. Catapano, MD Sharjeel Israr, MD Alexander C. Whiting, MD Omar M. Hussain, BS Laura A. Snyder, MD Felipe C. Albuquerque, MD Andrew F. Ducruet, MD Peter Nakaji, MD Michael T. Lawton, MD Jordan A. Weinberg, MD Joseph M. Zabramski, MD
Department of Neurosurgery Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona
Correspondence: Joseph M. Zabramski, MD c/o Neuroscience Publications; Barrow Neurological Institute
Catapano JS et al. 2 St. Joseph’s Hospital and Medical Center 350 W. Thomas Rd.; Phoenix, AZ 85013 Tel: 602.406.3593; Fax: 602.406.4104 E-mail: [email protected]
DISCLOSURES: None FINANCIAL SUPPORT: None ACKNOWLEDGMENTS: The authors thank the staff of Neuroscience Publications at Barrow Neurological Institute for assistance with manuscript preparation.
SUBMISSION CATEGORY: Original Article
Catapano JS et al. 3 ABSTRACT Background: Optimal management of patients with extracranial blunt cerebrovascular injury (BCVI) remains controversial, with both anticoagulation and antiplatelet therapy being recommended. The purpose of this study was to evaluate the efficacy and safety of using acetylsalicylic acid (ASA) in the management of BCVI. Methods: Patients with BCVI were identified from the registry of a Level 1 trauma center between 2010 and 2017. Digital imaging and electronic medical records were reviewed for patient information including demographic characteristics, injury type, therapy, outcomes, and follow-up. Results: Over the study period, 13,578 patients were admitted following blunt trauma, with 94 (0.7%) having confirmed BCVI (mean age, 42 years; 72% male). Mean Injury Severity Score and Glasgow Coma Score were 27 and 10, respectively. BCVI was identified in 130 vessels with Biffl grade I (38%) and grade II injury (29%) being most common. Twelve (13%) patients experienced an ischemic event, but only 3 events occurred after diagnosis. ASA was primary treatment for 56 (60%) patients. Thirty patients (32%) received no treatment; 21 patients died within 24 hours of primary injury. Only 4 patients had ASA contraindications. Four patients (7%) had ASA-related complications; there were 2 cases of intracranial hemorrhage progression and 2 cases of gastrointestinal bleeding. Follow-up vascular imaging at a mean of 36 days demonstrated stable or improved levels of BCVI in 94% of patients. Conclusion: An ASA-based management strategy for BCVI was efficacious and relatively safe in this study. This approach may be the preferred treatment for BCVI, but confirmation is needed.
Catapano JS et al. 4 RUNNING TITLE: Management of BCVI with ASA KEYWORDS: ASA; extracranial blunt cerebral vascular injury; stroke
ABBREVIATIONS: ASA = acetylsalicylic acid; BCVI = blunt cerebrovascular injury; CTA = computed tomographic angiography; ICH = intracerebral hemorrhage
Catapano JS et al. 5 INTRODUCTION Extracranial blunt cerebrovascular injury (BCVI) is defined as nonpenetrating damage to one or more of the extracranial cerebrovascular arteries, including the internal carotid and/or vertebral vessels. BCVIs are rare and occur in approximately 0.1% to 3% of trauma patients.1-4 When present, however, these injuries are associated with significant morbidity and mortality from ischemic disease, especially if undiagnosed or left untreated. The incidence of stroke among patients with BCVI is between 10% and 13%.2, 4 Isolated injury to the carotid arteries or vertebral arteries is associated with mortality rates ranging from 17% to 38%.1, 5, 6 Thus, timely treatment is essential for reducing the burden of neurologic deficits in these patients. The introduction of effective screening protocols and advanced imaging techniques, including digital subtraction angiography and computed tomographic angiography (CTA), combined with prophylactic treatment to reduce thrombotic complications, has greatly reduced the burden of BCVI-related ischemia among trauma patients.5, 7 While screening protocols have largely become standardized, treatment remains controversial. Initial reports advocated that anticoagulant therapy with heparin be administered only following the onset of ischemia after a BCVI8, 9; however, more recent observational studies have demonstrated better outcomes among patients who are treated prophylactically.1, 10-12 Most centers currently treat with either a prophylactic anticoagulant or antiplatelet therapy, whereas endovascular therapy is reserved for a select few.1, 10 Furthermore, the prophylactic treatment of asymptomatic BCVI patients with aspirin has been associated with increased risk of transfusion with pack red blood cells.13 In 2011, the ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease found Level
Catapano JS et al. 6 B evidence for the treatment of symptomatic (either stroke or transient ischemic attack) BCVI patients for 3-6 months with either an anticoagulant (low-molecular-weight heparin, heparin, or warfarin) or an antiplatelet (either aspirin with or without extended release dipyridamole, or clopidogrel exclusively).14 In addition, U.S. physicians are divided on the appropriate treatment, with greater than 40% favoring anticoagulation and greater than 30% ASA (~17% favor both).15 Hence, optimal management of patients with BCVI greatly differs among institutions, with the optimal antithrombotic regimen and agent yet to be determined, while the role of endovascular treatment remains largely unknown. Further investigations regarding management of these devastating injuries are warranted. In this study, we analyzed an acetylsalicylic acid (ASA)– based model with aggressive endovascular therapy in select patients with high-grade injuries, with a primary outcome of an ischemic stroke. We hypothesized that our rate of cerebrovascular accident would be lower than or equivalent to those reported in the literature.
METHODS This was a retrospective cohort study of adult trauma patients at least 18 years of age admitted to a Level 1 trauma center from January 1, 2010, through August 31, 2017. This study was approved by the institutional review board of St. Joseph’s Hospital and Medical Center (Phoenix, AZ), which waived the need for informed consent. The trauma registry was queried for all adult patients with an extracranial BCVI, and patient characteristics and other data were abstracted from review of the prospectively collected data. Additional clinical data were collected from the electronic medical record. A 64-slice computed tomography scanner was used to perform all CTA examinations. Modified Denver criteria were used at admission to screen patients and determine when CTA was appropriate. Scans with positive findings were graded
Catapano JS et al. 7 using the Biffl scale (Table 1). Appropriate treatment was determined by the on-call endovascular neurosurgeon, with ASA (325 mg daily) administered to all patients without contraindications (large/enlarging acute hemorrhage—either intracranial or in another organ, history of allergy to aspirin, severe thrombocytopenia, or history of recent gastrointestinal bleed) who were treated medically. Data collected included age, sex, race, comorbidities, baseline antithrombotic medications, days to stroke diagnosis, in-hospital procedures, complications, reoperations, discharge antithrombotic medications, hospital disposition, injury seen on imaging with Biffl scale grading, hospital days, intensive care unit days, ventilator days, and hospital readmissions. IBM SPSS Statistics 25 (IBM Corporation, Armonk, NY) was used for data analysis.
RESULTS During the 7-year study period, a total of 13,578 patients with blunt trauma were admitted to the hospital, with 94 patients (0.7 %) found to have an extracranial BCVI. The demographic and clinical characteristics of patients with BCVI are presented in Table 2. The mean age was 41.8 (range 16-92; standard deviation [SD] 17.7) years, and 68 (72%) of the patients were male. The most common mechanism of injury was a motor vehicle collision (41 patients; 44%). The mean (SD) Glasgow Coma Score and Injury Severity Score on arrival in the trauma bay were 9.6 (5) and 26.9 (17), respectively. Cervical fractures were present in 61 (65%) of the patients, and 37 (39%) sustained an intracerebral hemorrhage (ICH). Three (3%) patients died in the trauma bay, and 71 (76%) patients were intubated with a mean (SD) of 8.4 (7.8) days of ventilator support. The mean (SD) length of hospital stay was 11.6 (11.2) days, with 9 (7.8) days in the intensive care unit. The in-hospital mortality rate was 28% (26 of 94 patients died).
Catapano JS et al. 8 Nine patients presented with ischemic events in the trauma bay. An additional 3 (3%) patients developed delayed ischemic events. In Table 3, the Biffl grades of the vessels that were injured are shown. There were 130 injured vessels identified in 94 patients, including 52 internal carotid artery and 78 vertebral artery injuries. Grade I (40.8%) and grade II (29.2%) were the most common Biffl grades, followed by grade IV (19.2%), grade III (7.7%), and finally grade V (3.1%). Treatment and outcomes are presented in Table 4. ASA was the primary treatment in 56 patients (60%), and 1 patient who was already being treated with oral anticoagulants for atrial fibrillation continued to receive warfarin. There were also 7 patients (7%) who were treated primarily via endovascular means (5 treated with coil embolization and 2 treated with stent placements). Another 30 patients (32%) did not receive any treatment for BCVI, including 21 (70%) who died during the acute period, 4 (13%) in whom treatment was contraindicated, and 5 (17%) in whom the degree of vessel injury was considered to be minor. Treatment was contraindicated for 3 patients because of large ICHs and for 1 patient because of injury to another organ. Of the 56 patients who received primary treatment with ASA, 2 had progression of an ICH (neither required surgery) and 2 experienced severe gastrointestinal bleeding. The majority of patients with a BCVI (39 patients; 30%) were discharged to either a rehabilitation center or skilled nursing facility, 29 (22%) were discharged home, and 26 (20%) died. Follow-up imaging was performed for 33 of 68 surviving patients at a mean (SD) of 35.5 (52.3) days. CTA was the most common follow-up imaging (27 patients; 82%), followed by magnetic resonance angiography (6 patients; 18%). Of the 33 patients with follow-up imaging, 16 (49%) were found to have stability of their BCVI, 15 (46%) had improvement, and 2 (6%) had progression of their
Catapano JS et al. 9 initial injury. There were no delayed strokes or deaths among the 33 patients with follow-up imaging. Table 5 shows the treatment provided for the various injury grades. Endovascular therapy was reserved for patients with higher-grade injuries (2 grade III, 4 grade IV, and 2 grade V injuries), and ASA was used to treat injuries ranging from grade I to grade IV. Table 6 examines the outcomes for the 68 patients who survived their hospital stay on the basis of their primary treatment. The mean admission Glasgow Coma Score of patients who received ASA (n=49) was 12, compared with 11.4 for the endovascular treated group (n=7) and 8.6 for those not receiving treatment (n=11). The mean Glasgow Coma Score at discharge from the hospital was 14.3 in the ASA group, 13 in the endovascular group, and 13.7 in the untreated group. Five patients in the ASA group experienced a stroke (3 before and 2 after ASA treatment initiation), 2 patients in the endovascular group experienced a stroke (1 before and 1 after endovascular treatment), and 1 patient in the untreated group experienced a stroke.
DISCUSSION BCVIs are rare injuries that are often associated with high-impact blunt trauma with multiple injuries.4, 15 These injuries place patients at high risk of ischemic complications and are associated with stroke rates ranging from 10% to 64%, with lower rates reported in more recent studies.1-4, 7, 15-21 In this study, the risk of stroke was relatively low (10%) among patients with BCVI (Table 2). It is thought that most strokes occur during the acute period, within 72 hours after injury prior to a screening CTA, with 44% to 82% of strokes associated with BCVI detected on initial imaging and with the majority of such injuries being embolic in nature.15, 18, 19 Likewise, in this study, 9 of 12 BCVI-related strokes were identified at the time of diagnostic
Catapano JS et al. 10 imaging, all within the first 24 hours after presentation. There were no strokes during follow-up in our study at a mean of 35.5 days. Antithrombotic therapy remains the mainstay for the majority of patients with BCVI without contraindications.9, 10, 15, 16 However, the type of agent used remains controversial, with unfractionated heparin being recommended in recent guidelines from trauma societies.1, 10 Although no randomized controlled trials have been performed for treatment of BCVI, several retrospective studies have indicated that antiplatelet therapy may be at least as efficacious as heparin and equivalent in terms of neurologic outcomes.16, 18, 22-26 At our institution, patients with blunt trauma are screened for BCVI with use of the modified Denver criteria1, 10 and are administered a regimen of ASA if there are no contraindications (e.g., gastrointestinal bleeding, large ICH, or progression of ICH). We found a relatively low stroke rate among the 56 patients treated with ASA, with only 1 stroke (2%) after the initiation of treatment. Comparably, in a large retrospective study of 301 patients with BCVIs, Cothren et al.22 found 1 stroke among 192 patients treated with heparin and no strokes among 67 patients treated with ASA. In the same study, follow-up imaging demonstrated improvement of the BCVI in 39% of patients treated with heparin and 43% of patients treated with ASA; there was progression of the BCVI in 12% of patients treated with heparin versus 10% of patients treated with ASA. In the present report, follow-up imaging demonstrated stable (46%) or improved (50%) BCVI in patients treated with ASA and progression of injury in only 1 patient (4%); however, 26 (52%) of the ASA-treated patients had no follow-up imaging. In our study, ASA was chosen as the first-line therapy for patients with BCVI because of the large number of patients with contraindications to full-dose heparin therapy, with rates as high as 32% reported in earlier literature.26 Contrary to the rate of heparin contraindications, only
Catapano JS et al. 11 4 patients (7%) in the present series had a contraindication to ASA therapy (3 patients with enlarging ICH and 1 patient with injury to another organ). Furthermore, among patients treated with ASA, only 4 (7%) had a complication due to the treatment, including 2 patients with progression of ICH (among 22 total patients with ICH who were treated with ASA) and 2 patients with gastrointestinal bleeding, which is much lower than the rates reported in the literature; in a prospective study, Wahl et al.26 found that 57% of patients who were treated with heparin experienced a bleeding complication. Endovascular therapy is typically reserved for select high-risk lesions in patients with BCVI. However, with no randomized controlled trials and some controversy in the literature regarding the benefits of treatment, there has been no consensus regarding indications for the use of endovascular therapy.1, 7, 10, 16, 23, 27-36 At our institution, endovascular therapy is reserved for a highly selected group of patients in whom the benefit of the procedure is judged to outweigh the risks. Of 94 patients with a BCVI, only 7 patients (7%) underwent endovascular treatment. Two patients with grade III internal carotid artery injuries underwent stenting, and 3 patients with grade IV vertebral artery injuries and 2 patients with grade V vertebral artery injuries underwent coil embolization. Both patients with grade V injury survived the BCVI and had a transected vertebral artery sacrificed. The 3 patients with grade IV injury had the artery sacrificed to reduce the risk of future emboli. Only 1 patient (with grade V injury) had a stroke after endovascular therapy. The literature has reported stroke rates among patients with vertebral artery grade IV injuries of approximately 28%; however, none of the 3 patients with grade IV vertebral artery injuries in this series experienced a stroke.16 Follow-up imaging was available for 4 of the 7 patients with endovascular therapy; 1 patient with grade III injury had improvement of the BCVI, whereas the other 3 patients had stable dissections.
Catapano JS et al. 12 This study has the usual limitations inherent to retrospective evaluations. Three patients died before any imaging could be obtained, and another 23 patients died during the hospital stay. However, the mean Injury Severity Score of patients in this group was 39, and they likely died due to severe polytrauma rather than due to a cerebrovascular accident. Similar to other studies that have examined trauma patients, our study found that a large percentage of surviving patients (52%) were lost to follow-up. This may have resulted in lower rates of delayed stroke and progression of BCVI and lower overall mortality. Another limitation of our study was that the BCVIs in this series were classified using the results of CTA, and the Biffl grading system was developed using digital subtraction angiography. When evaluating CTA, it is more difficult to identify low-grade injuries (grade I and II injuries). However, CTA has become the standard of care at most trauma centers for the initial evaluation of BCVI.
CONCLUSION Our results imply that an ASA-based approached for the treatment of BCVI is as efficacious, has fewer contraindications, and is possibly safer than full-dose heparin anticoagulation. Furthermore, in a highly selected group of patients, aggressive endovascular therapy may be safe and potentially reduce the risk of stroke. However, because of the retrospective nature of this study, no definitive conclusions can be made. A future randomized controlled trial investigating the proper treatment of patients with BCVI, in which anticoagulation therapy is compared with antiplatelet therapy, is warranted. Additionally, further studies on outcomes among patients with BCVI treated with endovascular therapy are needed to develop clear indications for such treatments.
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Catapano JS et al. 15 Prevention, Society for Cardiovascular A, Interventions, Society of Interventional R, Society of NeuroInterventional S, Society for Vascular M, Society for Vascular S, American Academy of N, Society of Cardiovascular Computed T. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease. Stroke. Aug 2011;42(8):e464-540. 15. Foreman PM, Harrigan MR. Blunt traumatic extracranial cerebrovascular injury and ischemic stroke. Cerebrovasc Dis Extra. 2017;7(1):72-83. 16. Biffl WL, Ray CE, Jr., Moore EE, Franciose RJ, Aly S, Heyrosa MG, Johnson JL, Burch JM. Treatment-related outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography. Ann Surg. May 2002;235(5):699-706; discussion 706-697. 17. Crawford JD, Allan KM, Patel KU, Hart KD, Schreiber MA, Azarbal AF, Liem TK, Mitchell EL, Moneta GL, Landry GJ. The natural history of indeterminate blunt cerebrovascular injury. JAMA Surg. Sep 2015;150(9):841-847. 18. Stein DM, Boswell S, Sliker CW, Lui FY, Scalea TM. Blunt cerebrovascular injuries: does treatment always matter? J Trauma. Jan 2009;66(1):132-143; discussion 143-134. 19. Griessenauer CJ, Fleming JB, Richards BF, Cava LP, Cure JK, Younan DS, Zhao L, Alexandrov AV, Barlinn K, Taylor T, Harrigan MR. Timing and mechanism of ischemic stroke due to extracranial blunt traumatic cerebrovascular injury. J Neurosurg. Feb 2013;118(2):397-404. 20. Scott WW, Sharp S, Figueroa SA, Eastman AL, Hatchette CV, Madden CJ, Rickert KL. Clinical and radiographic outcomes following traumatic grade 1 and 2 carotid artery
Catapano JS et al. 16 injuries: a 10-year retrospective analysis from a level I trauma center. Parkland Carotid and Vertebral Artery Injury Survey. J Neurosurg. May 2015;122(5):1196-1201. 21. Scott WW, Sharp S, Figueroa SA, Eastman AL, Hatchette CV, Madden CJ, Rickert KL. Clinical and radiographic outcomes following traumatic grade 3 and 4 carotid artery injuries: a 10-year retrospective analysis from a level 1 trauma center. Parkland Carotid and Vertebral Artery Injury Survey. J Neurosurg. Mar 2015;122(3):610-615. 22. Cothren CC, Biffl WL, Moore EE, Kashuk JL, Johnson JL. Treatment for blunt cerebrovascular injuries: equivalence of anticoagulation and antiplatelet agents. Arch Surg. Jul 2009;144(7):685-690. 23. 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 longterm followup. J Am Coll Surg. May 2007;204(5):1007-1013; discussion 1014-1005. 24. Colella JJ, Diamond DL. Blunt carotid injury: reassessing the role of anticoagulation. Am Surg. Mar 1996;62(3):212-217. 25. Eachempati SR, Vaslef SN, Sebastian MW, Reed RL, 2nd. Blunt vascular injuries of the head and neck: is heparinization necessary? J Trauma. Dec 1998;45(6):997-1004. 26. Wahl WL, Brandt MM, Thompson BG, Taheri PA, Greenfield LJ. Antiplatelet therapy: an alternative to heparin for blunt carotid injury. J Trauma. May 2002;52(5):896-901. 27. Biffl WL, Moore EE, Offner PJ, Brega KE, Franciose RJ, Burch JM. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma. Nov 1999;47(5):845-853.
Catapano JS et al. 17 28. Jindal G, Fortes M, Miller T, Scalea T, Gandhi D. Endovascular stent repair of traumatic cervical internal carotid artery injuries. J Trauma Acute Care Surg. Nov 2013;75(5):896903. 29. Nanda A, Vannemreddy PS, Willis BK, Baskaya MK, Jawahar A. Management of carotid artery injuries: Louisiana State University Shreveport experience. Surg Neurol. Mar 2003;59(3):184-190; discussion 190. 30. Duke BJ, Ryu RK, Coldwell DM, Brega KE. Treatment of blunt injury to the carotid artery by using endovascular stents: an early experience. J Neurosurg. Dec 1997;87(6):825-829. 31. Li W, D'Ayala M, Hirshberg A, Briggs W, Wise L, Tortolani A. Comparison of conservative and operative treatment for blunt carotid injuries: analysis of the National Trauma Data Bank. J Vasc Surg. Mar 2010;51(3):593-599, 599 e591-592. 32. Moulakakis KG, Mylonas S, Avgerinos E, Kotsis T, Liapis CD. An update of the role of endovascular repair in blunt carotid artery trauma. Eur J Vasc Endovasc Surg. Sep 2010;40(3):312-319. 33. Berne JD, Reuland KR, Villarreal DH, McGovern TM, Rowe SA, Norwood SH. Internal carotid artery stenting for blunt carotid artery injuries with an associated pseudoaneurysm. J Trauma. Feb 2008;64(2):398-405. 34. Cohen JE, Gomori JM, Itshayek E, Spektor S, Shoshan Y, Rosenthal G, Moscovici S. Singlecenter experience on endovascular reconstruction of traumatic internal carotid artery dissections. J Trauma Acute Care Surg. Jan 2012;72(1):216-221. 35. Burlew CC, Biffl WL, Moore EE, Pieracci FM, Beauchamp KM, Stovall R, Wagenaar AE, Jurkovich GJ. Endovascular stenting is rarely necessary for the management of blunt cerebrovascular injuries. J Am Coll Surg. May 2014;218(5):1012-1017.
Catapano JS et al. 18 36. Stager V, Gandhi R, Stroman D, Timaran C, Broker H. Traumatic internal carotid artery injury treated with overlapping bare metal stents under intravascular ultrasound guidance. J Vasc Surg. Feb 2011;53(2):483-486.
Catapano JS et al. 19 Table 1. Biffl Grading of Blunt Cerebrovascular Injury Grade I II III IV V
Description Mild intimal tear of vessel wall Dissection of vessel wall with >25% narrowing Pseudoaneurysm Occlusion and/or thrombosis of vessel wall Transection of vessel wall
Catapano JS et al. 20 Table 2. Demographic and Clinical Characteristics of Patients with Blunt Cerebrovascular Injury Variable Patients (n=94) Male sex
68 (72)
Age (years), mean (SD)
41.8 (18)
Race/ethnicity White
40 (43)
Hispanic
32 (34)
Black
9 (10)
Asian
1 (1)
American Indian
3 (3)
Other
9 (10)
Mechanism of injury Motor vehicle collision
41 (44)
Motorcycle crash
17 (18)
Auto vs pedestrian
19 (20)
Other
17 (18)
GCS on arrival, mean (SD)
9.6 (5)
ISS,a mean (SD)
26.9 (17)
Cervical fracture
61 (65)
TBI with ICHb
37 (39)
Death in trauma bay
3 (3)
Intubation
71 (76)
Ventilator days, mean (SD)
8.4 (8)
Length of stay, days, mean (SD)
11.6 (11)
ICU days, mean (SD)
9.0 (8)
Outcome Death in hospital
26 (28)
Stroke before or during diagnosisc
9 (10)
Stroke after diagnosisd
3 (3)
Data are no. (%) of patients unless otherwise indicated. Abbreviations: GCS = Glasgow Coma Score; ICH = intracerebral hemorrhage; ICU = intensive care unit; ISS = Injury Severity Score; SD = standard deviation; TBI = traumatic brain injury.
Catapano JS et al. 21 a
The mean ISS of the 26 patients who died was 39. Twenty-two patients with ICH initiated acetylsalicylic acid therapy. c No grade I vessels. d All patients had at least a grade IV dissection and multiple dissections. b
Catapano JS et al. 22 Table 3. No. of Injured Vessels by Biffl Grade and Location Grade Left ICA Right ICA Left VA
Right VA
I 10 10 15 18 II 7 8 10 13 III 3 5 1 1 IV 4 4 10 7 V 1 0 1 2 Total 25 27 37 41 Abbreviations: ICA = internal carotid artery; VA = vertebral artery.
Total no. (%) of vessels (n=130) 53 (40.8) 38 (29.2) 10 (7.7) 25 (19.2) 4 (3.1) 130 (100)
Catapano JS et al. 23 Table 4. Treatment and Outcomes of Patients with Blunt Cerebrovascular Injury Treatment or Outcome Patients Primary treatment (n=94) ASAa
56 (60)
Warfarinb
1 (1)
Endovascular
7 (7)
None
30 (32)
Reason for no treatment (n=30) Contraindication
4 (13)
Large or enlarging ICH
3 (10)
Other organ injury
1 (3)
Death
21 (70)
Not indicated
5 (17)
Complication from treatment with ASA (n=56) Overall
4 (7) c
Progression of ICH
2 (4)
Gastrointestinal bleeding
2 (4)
Other
0 (0)
Discharge disposition (n=94) Home
29 (31)
Rehabilitation or skilled nursing facility
39 (41)
Death
26 (28)
Follow-up imaging (n=68) Overall
33 (49)
CTA
27 (40)
MRA
6 (9)
Catheter-based angiography
0 (0)
Imaging results (n=33) Improved
15 (46)
Stable
16 (49)
Worse
2 (6)
Catapano JS et al. 24 Follow-up, days, mean (SD) d
Delayed adverse events (n=33)
35.5 (52.3) 0 (0)
Data are no. (%) of patients unless otherwise indicated. Abbreviations: ASA = acetylsalicylic acid; CTA = computed tomographic angiography; ICH = intracerebral hemorrhage; MRA = magnetic resonance angiography; SD = standard deviation. a Two patients initiated heparin drip, but therapy was changed to ASA therapy within 24 hours. b This patient was receiving warfarin before blunt cerebrovascular injury, and this therapy was continued when dissection was found. c A total of 2 (9%) of 23 patients with ICH who initiated ASA had progression of their bleed. d Including delayed stroke and delayed death.
Catapano JS et al. 25 Table 5. Primary Treatment by Biffl Grade of Injured Vessels No. of Vessels, by Biffl Grade Primary Treatment I II III IV None 12 16 3 11 Acetylsalicylic 40 acid therapy Anticoagulation 1 therapy Endovascular 0 therapy
V 2
22
4
10
0
0
0
0
0
0
2
4
2
Catapano JS et al. 26 Table 6. Outcomes for Patients who Survived Hospital Stay Primary Therapy Variable
ASA
Endovascular
None
Patients who survived hospital stay (n=68) GCS at admission, mean
12
11.4
8.6
GCS at discharge, mean
14.3
13
13.7
No stroke
45
5
10
Stroke at or before diagnosis
3
1
1
Stroke after diagnosisa
2
1
0
Dissection improved
12
1
2
Dissection stable
11
3
1
Dissection progressed
1
0
1
Patients with follow-up imaging (n=33)
Abbreviations: ASA = acetylsalicylic acid; GCS = Glasgow Coma Score. a All patients had at least grade IV dissections and multiple dissections. One of the patients who received ASA therapy and experienced a stroke after diagnosis had the stroke prior to initiation of ASA treatment.
Table 1. Biffl Grading of Blunt Cerebrovascular Injury Grade Description I Mild intimal tear of vessel wall II Dissection of vessel wall with >25% narrowing III Pseudoaneurysm IV Occlusion and/or thrombosis of vessel wall V Transection of vessel wall
Catapano JS et al. 1 Table 2. Demographic and Clinical Characteristics of Patients with Blunt Cerebrovascular Injury Variable Patients (n=94) Male sex
68 (72)
Age (years), mean (SD)
41.8 (18)
Race/ethnicity White
40 (43)
Hispanic
32 (34)
Black
9 (10)
Asian
1 (1)
American Indian
3 (3)
Other
9 (10)
Mechanism of injury Motor vehicle collision
41 (44)
Motorcycle crash
17 (18)
Auto vs pedestrian
19 (20)
Other
17 (18)
GCS on arrival, mean (SD)
9.6 (5)
ISS,a mean (SD)
26.9 (17)
Cervical fracture
61 (65)
TBI with ICHb
37 (39)
Death in trauma bay
3 (3)
Intubation
71 (76)
Ventilator days, mean (SD)
8.4 (8)
Length of stay, days, mean (SD)
11.6 (11)
ICU days, mean (SD)
9.0 (8)
Outcome Death in hospital
26 (28)
Stroke before or during diagnosisc
9 (10)
Stroke after diagnosisd
3 (3)
Data are no. (%) of patients unless otherwise indicated. Abbreviations: GCS = Glasgow Coma Score; ICH = intracerebral hemorrhage; ICU = intensive care unit; ISS = Injury Severity Score; SD = standard deviation; TBI = traumatic brain injury.
Catapano JS et al. 2 a
The mean ISS of the 26 patients who died was 39. Twenty-two patients with ICH initiated acetylsalicylic acid therapy. c No grade I vessels. d All patients had at least a grade IV dissection and multiple dissections. b
Catapano JS et al. 1 Table 3. No. of Injured Vessels by Biffl Grade and Location Grade Left ICA Right ICA Left VA
Right VA
I 10 10 15 18 II 7 8 10 13 III 3 5 1 1 IV 4 4 10 7 V 1 0 1 2 Total 25 27 37 41 Abbreviations: ICA = internal carotid artery; VA = vertebral artery.
Total no. (%) of vessels (n=130) 53 (40.8) 38 (29.2) 10 (7.7) 25 (19.2) 4 (3.1) 130 (100)
Catapano JS et al. 1 Table 4. Treatment and Outcomes of Patients with Blunt Cerebrovascular Injury Treatment or Outcome Patients Primary treatment (n=94) ASAa
56 (60)
Warfarinb
1 (1)
Endovascular
7 (7)
None
30 (32)
Reason for no treatment (n=30) Contraindication
4 (13)
Large or enlarging ICH
3 (10)
Other organ injury
1 (3)
Death
21 (70)
Not indicated
5 (17)
Complication from treatment with ASA (n=56) Overall
4 (7)
Progression of ICHc
2 (4)
Gastrointestinal bleeding
2 (4)
Other
0 (0)
Discharge disposition (n=94) Home
29 (31)
Rehabilitation or skilled nursing facility
39 (41)
Death
26 (28)
Follow-up imaging (n=68) Overall
33 (49)
CTA
27 (40)
MRA
6 (9)
Catheter-based angiography
0 (0)
Imaging results (n=33) Improved
15 (46)
Stable
16 (49)
Catapano JS et al. 2 Worse
2 (6)
Follow-up, days, mean (SD)
35.5 (52.3)
Delayed adverse eventsd (n=33)
0 (0)
Data are no. (%) of patients unless otherwise indicated. Abbreviations: ASA = acetylsalicylic acid; CTA = computed tomographic angiography; ICH = intracerebral hemorrhage; MRA = magnetic resonance angiography; SD = standard deviation. a Two patients initiated heparin drip, but therapy was changed to ASA therapy within 24 hours. b This patient was receiving warfarin before blunt cerebrovascular injury, and this therapy was continued when dissection was found. c A total of 2 (9%) of 23 patients with ICH who initiated ASA had progression of their bleed. d Including delayed stroke and delayed death.
Table 5. Primary Treatment by Biffl Grade of Injured Vessels No. of Vessels, by Biffl Grade Primary Treatment I II III IV None 12 16 3 11 Acetylsalicylic 40 acid therapy Anticoagulation 1 therapy Endovascular 0 therapy
V 2
22
4
10
0
0
0
0
0
0
2
4
2
Catapano JS et al. 1 Table 6. Outcomes for Patients who Survived Hospital Stay Primary Therapy Variable
ASA
Endovascular
None
Patients who survived hospital stay (n=68) GCS at admission, mean
12
11.4
8.6
GCS at discharge, mean
14.3
13
13.7
No stroke
45
5
10
Stroke at or before diagnosis
3
1
1
Stroke after diagnosisa
2
1
0
Dissection improved
12
1
2
Dissection stable
11
3
1
Dissection progressed
1
0
1
Patients with follow-up imaging (n=33)
Abbreviations: ASA = acetylsalicylic acid; GCS = Glasgow Coma Score. a All patients had at least grade IV dissections and multiple dissections. One of the patients who received ASA therapy and experienced a stroke after diagnosis had the stroke prior to initiation of ASA treatment.
DISCLOSURES: None FINANCIAL SUPPORT: None