Evaluation and management of blunt cerebrovascular injury: A practice management guideline from the Eastern Association for the Surgery of Trauma

Blunt carotid arterial injuries (BCI) have the potential for devastating outcomes. A paucity of literature and the absence of a formal BCI grading scale have been major impediments to the formulation of sound practice guidelines. We reviewed our experience with 109 BCI and developed a grading scale with prognostic and therapeutic implications. Patients admitted to a Level I trauma center were evaluated with cerebral arteriography if they exhibited signs or symptoms of BCI or met criteria for screening. Patients with BCI were treated with heparin unless they had contraindications, and follow-up arteriography was performed at 7 to 10 days. Endovascular stents were deployed selectively. A prospective database was used to track the patients. A total of 76 patients were diagnosed with 109 BCI. Two-thirds of mild intimal injuries (grade I) healed, regardless of therapy. Dissections or hematomas with luminal stenosis (grade II) progressed, despite heparin therapy in 70% of cases. Only 8% of pseudoaneurysms (grade III) healed with heparin, but 89% resolved after endovascular stent placement. Occlusions (grade IV) did not recanalize in the early postinjury period. Grade V injuries (transections) were lethal and refractory to intervention. Stroke risk increased with injury grade. Severe head injuries (Glasgow Coma Scale score < or =6) were found in 46% of patients and confounded evaluation of neurologic outcomes. This BCI grading scale has prognostic and therapeutic implications. Nonoperative treatment options for grade I BCI should be evaluated in prospective, randomized trials. Accessible grade II, III, IV, and V lesions should be surgically repaired. Inaccessible grade II, III, and IV injuries should be treated with systemic anticoagulation. Endovascular techniques may be the only recourse in high grade V injuries and warrant controlled evaluation in the treatment of grade III BCI.

We hypothesize that the 2 antithrombotic treatment regimens, systemic heparin sodium vs antiplatelet agents, are equivalent for the treatment of blunt cerebrovascular injuries (BCVIs) to prevent devastating injury-related strokes. Retrospective review of a prospective database. Level I trauma center. Patients with BCVIs from January 1, 1997, to January 1, 2007. Incidence of cerebrovascular accident (CVA), stratified by treatment. During the study period, 422 BCVIs were identified in 301 patients (64.8% men; mean [SEM] age, 37.0 [0.8] years; mean [SEM] injury severity score, 27.0 [0.9]). A total of 22 patients presented with neurologic ischemia, and 5 patients sustained CVAs after embolization and/or stenting of an injury. Treatment was initiated for 282 asymptomatic BCVIs (heparin, 192; aspirin, 67; aspirin and/or clopidogrel, 23); 1 patient had a CVA (0.5%). Of 107 patients with untreated, asymptomatic BCVIs, 23 (21.5%) had a CVA. For untreated patients sustaining BCVI-related CVAs, the mean (SEM) time to diagnosis was 58 (10) hours. For those who did not exhibit symptoms within 2 hours of injury, mean time to diagnosis of CVA was 75 (11) hours. Injury healing rates (heparin, 39%; aspirin, 43%; aspirin/clopidogrel, 46%) and injury progression rates (12%; 10%; 15%) were equivalent between therapeutic regimens. With an overall CVA risk of 21% and a documented latent period, comprehensive screening, early diagnosis, and institution of antithrombotic therapy for BCVI are clearly warranted. The type of treatment, heparin vs antiplatelet agents, does not appear to affect either stroke risk or injury healing rates.

Aggressive screening, early angiographic diagnosis, and prompt anticoagulation for blunt carotid artery injuries (CAIs) improves neurologic outcome. From January 1, 1996, through December 31, 2002, there were 13 280 blunt trauma admissions to our level I center, of which 643 underwent screening angiography for blunt CAI on the basis of a protocol including injury patterns and symptoms. Patients without contraindications underwent anticoagulation immediately for documented lesions. A state-designated, level I urban trauma center. Of the 643 patients undergoing screening angiography, 114 (18%) had confirmed CAI. Early angiographic diagnosis and prompt anticoagulation. Diagnosis, stroke rate, and complications stratified by method of intervention. A CAI was identified in 114 patients during the 7-year study period; the majority were men (71%), with a mean +/- SD age of 34 +/- 1.3 years and a mean +/- SD Injury Severity Score of 29 +/- 1.5. Seventy-three patients underwent anticoagulation after diagnosis (heparin in 54, low-molecular-weight heparin in 2, antiplatelet agents in 17); none had a stroke. Of the 41 patients who did not receive anticoagulation (because of a contraindication in 27, symptoms before diagnosis in 9, and carotid coil or stent in 5), 19 patients (46%) developed neurologic ischemia. Ischemic neurologic events occurred in 100% of patients who presented with symptoms before angiographic diagnosis and those receiving a carotid coil or stent without anticoagulation. Our prospective evaluation of blunt CAIs suggests that early diagnosis and prompt anticoagulation reduce ischemic neurologic events and their disability. The optimal anticoagulation regimen, however, remains to be established.