Treatment-Related Outcomes From Blunt Cerebrovascular Injuries

Abstract

Objective

To assess the impact of routine follow-up arteriography on the management and outcome of patients with acute blunt cerebrovascular injuries (BCVI).

Summary Background Data

During the past 5 years there has been increasing recognition of BCVI, but the management of these lesions remains controversial. The authors previously proposed a grading system for BCVI, with grade-specific management guidelines. The authors have noted that a significant number of injuries evolve within 7 to 10 days, warranting alterations in therapy.

Methods

A prospective database of a regional trauma center’s experience with BCVI has been maintained since 1990. A policy of arteriographic screening for BCVI based on injury mechanism (e.g., cervical hyperextension) and injury patterns (e.g., cervical and facial fractures) was instituted in 1996. A grading system was devised to develop management protocols: I = intimal irregularity; II = dissection/flap/thrombus; III = pseudoaneurysm; IV = occlusion; V = transection.

Results

From June 1990 to October 2001, 171 patients (115 male, age 36 ± 1 years) were diagnosed with BCVI. Mean injury severity score was 28 ± 1; associated injuries included brain (57%), spine (44%), chest (43%), and face (34%). Mechanism was motor vehicle crash in 50%, fall in 11%, pedestrian struck in 11%, and other in 29%. One hundred fourteen patients had 157 carotid artery injuries (43 bilateral), and 79 patients had 97 vertebral artery injuries (18 bilateral). The breakdown of injury grades was 137 grade I, 52 grade II, 32 grade III, 25 grade IV, and 8 grade V. One hundred fourteen (73%) carotid and 65 (67%) vertebral arteries were restudied with arteriography 7 to 10 days after the injury. Eight-two percent of grade IV and 93% of grade III injuries were unchanged. However, grade I and II lesions changed frequently. Fifty-seven percent of grade I and 8% of grade II injuries healed, allowing cessation of therapy, whereas 8% of grade I and 43% of grade II lesions progressed to pseudoaneurysm formation, prompting interventional treatment. There was no significant difference in healing or in progression of injuries whether treated with heparin or antiplatelet therapy or untreated. However, heparin may improve the neurologic outcome in patients with ischemic deficits and may prevent stroke in asymptomatic patients.

Conclusions

Routine follow-up arteriography is warranted in patients with grade I and II BCVIs because most of these patients (61% in this series) will require a change in management. A prospective randomized trial will be necessary to identify the optimal treatment of BCVI.

Blunt cerebrovascular injuries (BCVIs) have the potential for devastating consequences. Increasing awareness of the presence and the varied presentations of these injuries ^1–3 and the adoption of screening protocols ^4–14 have led to a dramatic rise in reported BCVIs during the past 5 years. Many aspects of the management of these injuries remain controversial, including the most appropriate screening criteria, ^4–16 the ideal diagnostic modality, 4,5,9–11,17,18 and the optimal treatment for various lesions. ^2,19–21

One management issue that has not received much attention in the literature is the angiographic follow-up of patients once an injury is diagnosed. The pathophysiology of BCVI typically involves an initial intimal tear. This exposes the thrombogenic subendothelial collagen, initiating platelet aggregation with subsequent thrombus formation that can embolize or occlude the artery. Alternatively, the tear may offer a portal of egress for a dissecting column of blood, which may narrow or occlude the vessel, or a pseudoaneurysm may form. Because this is a dynamic process, there may be substantial change in the injury over time. Since we began our screening protocol, we have attempted to routinely reimage patients with BCVI with arteriography at 7 to 10 days after the injury. This allows an assessment of the arterial lesion and the adequacy of therapy—specifically, the need for continued treatment or a modification of treatment. The purpose of this study was to determine whether routine follow-up arteriography is justified after the diagnosis of BCVI.

METHODS

Patients

Denver Health Medical Center (DHMC) is a state-certified and American College of Surgeons-verified urban level 1 trauma center with pediatric commitment and serves as the Rocky Mountain Regional Trauma Center for Colorado and adjoining states. Since 1990, patients diagnosed with BCVI have been identified and entered into a prospectively maintained database. Detailed analysis of these patients’ records was performed in accordance with the standards set forth by the Colorado Multi-Institutional Review Board.

Diagnosis

The diagnosis of BCVI is confirmed by four-vessel cerebral arteriography. Digital subtraction techniques are used, and all studies include the aortic arch, carotid and vertebral arteries, and intracerebral vessels. Injured patients undergo emergent arteriography for any of the following signs or symptoms suggestive of cerebrovascular injury: hemorrhage (from mouth, nose, ears, or wounds) of potential arterial origin; expanding cervical hematoma; cervical bruit in a patient younger than 50 years old; evidence of cerebral infarction on computed tomography (CT) scan; or unexplained or CT incongruous central or lateralizing neurologic deficit, transient ischemic attack (TIA), or Horner syndrome. In addition, at-risk asymptomatic patients (i.e., exhibiting no suggestive signs or symptoms for BCVI) undergo prompt arteriographic evaluation. The criteria for screening arteriography include an injury mechanism compatible with severe cervical hyperextension/rotation or hyperflexion, and associated with displaced midface or complex mandibular fracture, or closed head injury consistent with diffuse axonal injury of the brain; near-hanging resulting in cerebral anoxia; seat belt abrasion or other soft tissue injury of the anterior neck resulting in significant cervical swelling or altered mental status; basilar skull fracture involving the carotid canal; and cervical vertebral body fracture or distraction injury, excluding isolated spinous process fracture. Follow-up arteriography is performed within 7 to 10 days when possible to evaluate the efficacy of the initial therapy.

Injury Grading

Cerebrovascular injuries are classified according to our grading scale. ²¹ In brief, grade I injuries are defined by the arteriographic appearance of irregularity of the vessel wall or a dissection/intramural hematoma with less than 25% luminal stenosis; grade II injuries include those in which an intraluminal thrombus or raised intimal flap is visualized, small (hemodynamically insignificant) arteriovenous fistulae, or dissection/intramural hematoma with 25% or more luminal narrowing; pseudoaneurysms are classified as grade III; vessel occlusions as grade IV, and transections or hemodynamically significant arteriovenous fistulae as grade V injuries.

Treatment

Systemic heparin is administered to patients with no contraindications. A continuous infusion of unfractionated heparin is initiated at 15 U/kg/h, without bolus dosing, and is adjusted to maintain the partial thromboplastin time (PTT) between 40 and 50 seconds. Patients with relative contraindications to systemic heparin are given an antiplatelet agent (aspirin 325 mg q.d. or clopidogrel 75 mg q.d.). Patients with absolute contraindications to anticoagulation are observed without specific treatment. Intraluminal stents are deployed for persistent pseudoaneurysms or stenoses that threaten to occlude the vessel; unless contraindicated, systemic anticoagulation is then administered to prevent stent thrombosis. Embolization or balloon occlusion is reserved for transected vessels, significant arteriovenous fistulae, or pseudoaneurysms that are not amenable to stenting.

Outcome

Neurologic deficits are classified as severe (institutionalized or requiring assistance at home with activities of daily living) or mild (independent in activities of daily living but with residual cognitive or sensorimotor deficit).

Data Analysis

Data were managed with Microsoft Excel 97 SR-2 software (Microsoft, Redmond, WA). Statistical analysis was performed on an IBM-compatible personal computer using GB-STAT v. 6.5 software (Dynamic Microsystems, Inc., Silver Spring, MD). Means of continuous data were compared using the Student t test and are expressed as mean ± the standard error of the mean. Categorical data were compared using chi-square analysis or Fisher exact test, where appropriate.

RESULTS

Patients

From January 1990 through October 2001, BCVIs were diagnosed by cerebral arteriography in 171 patients. A total of 157 blunt carotid artery injuries (BCIs) were diagnosed in 114 patients; 41 had right, 30 had left, and 43 (38%) had bilateral BCIs. A total of 97 blunt vertebral artery injuries (BVIs) were diagnosed in 79 patients; 27 had right, 34 had left, and 18 (23%) had bilateral BVIs. Of the 171 patients, 22 (13%) had both BCI and BVI. The mean age of the patients was 35.6 ± 1.1 years (range, 10–81). Male patients represented 67% of the total group (115 patients).

Twelve patients were diagnosed with BCI between January 1990 and May 1996; the incidence during this time period was 1 injury per 1,000 blunt trauma admissions. Since the introduction of a screening protocol for BCVI in May 1996, 10,279 patients have been admitted to the DHMC trauma service after blunt trauma. This excludes patients seen by the trauma service but discharged from our emergency department observation unit, a subgroup that would likely be admitted to most trauma centers. During this time period, BCVIs have been diagnosed in 159 patients for an incidence of 1.55% among all patients admitted with blunt trauma. The incidence of BCI among blunt trauma admissions during this time period has been 1.11%; the incidence of BVI has been 0.77%.

Injury Mechanism and Associated Injuries

The mechanism of injury leading to BCVI was a motor vehicle crash in 86 (50%), fall in 19 (11%), pedestrian struck in 17 (10%), and motorcycle crash in 16 (9%) patients. Other mechanisms, including near-hangings; assaults; ski, snowboard, snowmobile, or bicycle crashes; falls from horseback; construction mishaps; and other bizarre occurrences (e.g., being caught in a tornado) were uncommon individually but accounted for 33 (19%) of the patients. The mean Injury Severity Score (ISS) was 27.7 ± 1.2. Associated injuries were present in 156 (91%) patients and included injury to the brain in 97 (57%), spine in 76 (44%), chest in 73 (43%), extremities in 62 (36%), face (fracture) in 58 (34%), abdomen in 44 (26%), skull base in 34 (20%), and pelvis in 26 (15%) patients. Injury mechanisms and associated injuries of patients with BCI and those with BVI are summarized and compared in Table 1. There were no significant differences between the groups in terms of age, gender distribution, or injury mechanism. Patients with BVI were more likely to have spinal injury; this was primarily due to the presence of cervical spine injury in 67% of BVI victims. Patients sustaining BCI were more likely to have brain injury, facial fracture, or basilar skull fracture; their ISS was higher, and their admission Glasgow Coma Scale (GCS) score was lower compared with patients with BVI.

Table 1. PATIENT DEMOGRAPHICS, INJURY MECHANISMS, AND ASSOCIATED INJURIES

Injury Grade and Treatment

At the time of initial diagnosis, the grade distribution of the 157 BCIs was as follows: 89 grade I, 31 grade II, 24 grade III, 5 grade IV, and 8 grade V. The initial grades of the 97 BVIs were 48 grade I, 21 grade II, 8 grade III, and 20 grade IV. Follow-up arteriograms were obtained on 83 (73%) patients with BCI and 49 (62%) patients with BVI. Failure to obtain a follow-up arteriogram was generally due to poor outcome of the patient, usually secondary to brain injury. The number of injured vessels that were reimaged was 114 (73%) carotid arteries and 65 (67%) vertebral arteries. There were no notable differences in the follow-up arteriography results between patients with BCI and BVI; thus, they have been combined for this analysis. Of 133 grade I injuries, 93 (70%) were reimaged. The artery was healed in 53 (57%), allowing cessation of therapy; however, 7 (8%) had progressed to pseudoaneurysm formation, prompting alternative intervention. The results of follow-up arteriography of grade I BCVI, according to the treatment the patient received, are stratified in Table 2. The healing rate of grade I injuries was 62% when treated with systemic heparin, compared with 50% with antiplatelet agents and 54% when untreated; these differences were not statistically significant. Similarly, rates of worsening of the injuries (9% vs. 4% vs. 13%) did not differ among the various treatment groups.

Table 2. RESULTS OF FOLLOW-UP ARTERIOGRAPHY FOR GRADE I LESIONS

Follow-up arteriograms were obtained on 37 (76%) of 49 grade II injuries (Table 3). The arteries had healed in 3 (8%) patients but progressed to pseudoaneurysm formation in 16 (43%). Overall, 8 (22%) of grade II injuries improved and 17 (46%) worsened. There were no significant differences related to treatment. Thirty (97%) of 31 pseudoaneurysms were reimaged with arteriography; only 1 (3%) had healed (Table 4). Eleven (44%) of 25 grade IV injuries were examined with follow-up arteriography, and 9 (82%) were unchanged (Table 5). No grade V injuries were reimaged because they invariably proved fatal.

Table 3. RESULTS OF FOLLOW-UP ARTERIOGRAPHY FOR GRADE II LESIONS

Table 4. RESULTS OF FOLLOW-UP ARTERIOGRAPHY FOR GRADE III LESIONS

Table 5. RESULTS OF FOLLOW-UP ARTERIOGRAPHY FOR GRADE IV LESIONS

Injury Grade, Treatment, and Outcome

The neurologic outcomes for each patient with BCIand BVI are listed in Tables 6 and 7, respectively. The “worst injury grade” is the worst grade diagnosed in any vessel in a given patient. Sixteen (14%) patients with BCI died, and 37 (38%) of the survivors had severe neurologic deficits. The death rate directly attributable to BCI was 11% (13 patients), with a 10% (10 patients) attributable rate of severe neurologic complications. Eight (10%) patients with BVI died, and 21 (30%) of the survivors had severe neurologic deficits. The death and severe neurologic complication rates directly attributable to BVI were 5% (four patients) and 8% (six patients), respectively. The death rate associated with combined BCI and BVI was 27%; in contrast, the death rate in patients with isolated BCI was 11% (P = .056) and in isolated BVI 4% (P < .05). The rate of severe neurologic complications among nonsurvivors was similar whether they had isolated or combined BCI and BVI.

Table 6. NEUROLOGIC OUTCOME IN PATIENTS WITH BLUNT CAROTID ARTERY INJURIES

Table 7. NEUROLOGIC OUTCOME IN PATIENTS WITH BLUNT VERTEBRAL ARTERY INJURIES

Fifty (29%) of the 171 patients with BCVI were symptomatic, 5 with hemorrhage and 45 with ischemic neurologic deficits. All 12 of the patients diagnosed with injuries before May 1996 were symptomatic; since the institution of our screening protocol, 76% of patients have been asymptomatic. In patients who developed ischemic symptoms, the interval between the time of injury and the manifestation of cerebral ischemia was 28 ± 7 hours (range 0–190). Twenty (44%) of 45 patients with ischemic deficits first became symptomatic 18 hours or more after the injury.

Stroke occurred in 26 (23%) patients with BCI and 16 (20%) patients with BVI. The stroke incidence by injury grade for BCI and BVI is listed in Table 8. Of these 42 strokes, 38 (90%) occurred before BCVI diagnosis. Three (7%) patients were receiving aspirin, and one (2%) was receiving heparin at the time the stroke was discovered. The stroke incidence among patients treated with aspirin was 9% (3/33), and among patients treated with systemic heparin it was 1% (1/84) (P = .07). Of 43 patients with bilateral BCI, 10 (23%) had anterior circulation strokes. However, the percentage of patients with unilateral BCI having strokes was also 23%. Of 18 patients with bilateral BVI, 6 (33%) had strokes. In contrast, only 20% of patients with unilateral BVI suffered strokes (P < .05). There was no association between stroke and the presence of concomitant BCI and BVI.

Table 8. STROKE INCIDENCE BY INJURY GRADE FOR BCI AND BVI

BCI, blunt carotid artery injury; BVI, blunt vertebral artery injury.

Neurologic outcomes related to treatment are confounded by concomitant brain or spinal cord injury. Among the 45 patients who had ischemic neurologic symptoms attributable to BCVI, 31 (69%) were treated with systemic heparinization. The change in neurologic status in response to treatment is detailed in Table 9. Of those treated with systemic heparin, 71% had an improvement in their neurologic deficits by the time they were discharged; this is in contrast to those treated with aspirin (40% improved) and those not treated (55% improvement) (heparin vs. no heparin, P = .15).

Table 9. CHANGE IN NEUROLOGIC STATUS STRATIFIED BY TREATMENT

Complications of Diagnosis and Treatment

In total, 313 arteriograms were performed in the 171 patients: 171 initial, 115 primary follow-up, and 27 secondary follow-up. Four (1%) patients sustained strokes resulting from the procedure: two had catheters manipulated at the injury site, one had an intravascular ultrasound probe manipulated at the injury site, and one had coil embolization of a vertebral artery pseudoaneurysm and subsequently sustained a cerebellar stroke. In three of the instances (excluding the postembolization stroke), the procedure was done within 7 days of the injury. One patient had a TIA after the arteriogram, three had puncture site hematomas, and one suffered a small subclavian artery dissection that healed without additional treatment.

One hundred (58%) of the patients in this series were treated with heparin; 22 (22%) had bleeding complications (10 at the site of an injury, 5 intracranial, 3 gastrointestinal, and 1 retroperitoneal). Of note, 20 of the 22 bleeding complications occurred before July 1998. During the period from 1990 to July 1998, heparin was administered with an initial bolus of 70 units/kg, and the therapeutic target was a PTT of 60 to 80 seconds; 20 (43%) of 47 patients treated with systemic heparinization had bleeding complications. Subsequently, our protocol was revised, eliminating bolus dosing and lowering the therapeutic target to PTT of 40 to 50 seconds. Since that time, only 2 (4%) of 53 patients treated with systemic heparinization have had bleeding complications.

Of 33 patients who had endovascular stents placed, 1 (3%) had a TIA and 4 (12%) had stent thrombosis. None of the five was fully anticoagulated before stent thrombosis.

DISCUSSION

Increasing recognition of BCVI during the past several years has led to policies of screening in many trauma centers. ^4–14 Although there is general agreement that these injuries should be treated, there is controversy surrounding many aspects of their management. Based on the premise that different grades of BCVI should be treated differently, ^1,21 we hypothesized that routine follow-up arteriography would identify changes in the injuries, thus prompting alterations in therapy. In fact, we found that 65% of grade I and 51% of grade II injuries had evolved to a point that treatment was changed based on the follow-up arteriogram. However, there are several points worthy of discussion.

Screening for BCVI is justified because these injuries are present in more patients than had previously been recognized, 2,7,8,12 there is typically a latent period between the time of injury and the onset of symptoms, ^2,22–24 and there appears to be an effective therapy to improve neurologic outcomes and potentially prevent strokes. 2,7,14,16,21 At DHMC, an aggressive screening approach has identified BCVI in 1.55% of our blunt trauma admissions during the past 5 years, with BCI in 1.11% and BVI in 0.77%. These incidences are higher than those reported by other groups. 1–3,9,12–14 There are two potential explanations for this: first, the denominator consists of patients admitted to the DHMC trauma service and excludes those discharged from our emergency department observation unit; and second, our screening criteria are relatively liberal. Liberal screening identifies more injuries but is also resource-intensive. Several groups have proposed noninvasive tests as alternatives to arteriography. 4,5,9–11,17 Unfortunately, there is a paucity of data comparing them head-to-head with the gold standard (arteriography). We have prospectively evaluated CT angiography as well as magnetic resonance angiography in a small number of patients and found that neither modality is as sensitive as arteriography. ²⁵ Unfortunately, because we have noted that even grade I injuries (intimal irregularities without intimal flaps, luminal narrowing, dissection, or intraluminal thrombus) can cause strokes (7% incidence), it is important that the diagnostic test be as sensitive as possible. In the absence of an adequate noninvasive alternative, we continue to screen patients with four-vessel cerebral arteriography. Although there is concern that arteriography might cause more complications than would be prevented by the identification of asymptomatic injuries, this has not been borne out. In fact, the complication rate of angiography in our series is quite low (2.9% overall); all cerebral embolic events have been related to intraluminal interventions and not to the performance of angiography itself. Further, we learned that manipulation of the injury site within 7 days of the injury creates a higher-risk situation for stroke; thus, we plan follow-up arteriograms at 7 to 10 days after the injury. However, the large majority (76%) of the BCVIs we have diagnosed since May 1996 have been asymptomatic. The potential prevention of strokes in this group arguably offsets the risk of diagnostic testing.

Patients sustain BCVI due to a variety of injury mechanisms. Motor vehicle crashes, the most common injury mechanism, were responsible for only 50% of the injuries. Thus, BCVI must be considered after any injury mechanism. Associated injuries are very common (91% of our patients), with a slightly higher overall ISS in patients with BCI than BVI. Not surprisingly, spinal injuries are more frequently associated with BVI than BCI. Similarly, brain injury, facial fractures, and basilar skull fractures are more common, and GCS scores are lower, in patients with BCI compared with BVI. These considerations are important in formulating screening criteria for BCVI. However, it is important to recognize that 24 (14%) of our patients had no brain or spinal injury, nor any facial or basilar skull fractures, and that presumption of cervical hyperextension is sometimes enough to warrant screening.

The distribution of injury grades at the time of diagnosis was similar, but for unexplained reasons vertebral arteries were more likely to be occluded than carotid arteries (21% vs. 3%, P < .05). Follow-up arteriography changed therapy in the majority of patients with grade I and II injuries. Healing was noted in 53 (57%) of 93 grade I lesions, allowing cessation of therapy, and 7 (8%) progressed to pseudoaneurysm formation, prompting endovascular stent placement. Only 3 (8%) grade II injuries healed, but 16 (43%) worsened to pseudoaneurysms. These data support routine follow-up arteriography in patients with grade I and II injuries. Conversely, we did not find compelling data supporting reimaging grade IV injuries, because 82% were still occluded on follow-up. Grade III BCVIs infrequently heal within 7 to 10 days, but we generally deploy endovascular stents for those pseudoaneurysms that are not surgically accessible, and thus an arteriogram is routine.

There are a significant number of deaths and complications associated with BCVI. Despite diagnosing most injuries in an asymptomatic phase, the death rate and the rate of severe neurologic complications attributable to the vascular injury were 11% and 10%, respectively, for BCI and 5% and 8%, respectively, for BVI. Patients in whom ischemic neurologic deficits developed secondary to BCVI had a mean latent period of 28 ± 7 hours between the time of injury and the manifestation of symptoms; 44% first exhibited symptoms 18 or more hours after the injury.

The ability of treatment to improve neurologic outcomes is a complex issue. Fabian et al ² provided data supporting the use of systemic heparin to treat BCVI; our previous experience ^7,16,21 supported this approach, and thus systemic heparinization has been used to treat patients not having contraindications to its use. However, some groups have suggested that heparinization is not necessary and have questioned the need for any treatment. ^19,20 Further, it has been suggested that antiplatelet therapy, rather than anticoagulants, should be used preferentially to treat or prevent arterial thrombotic processes. ²⁶ This is because arterial thromboses contain relatively higher concentrations of platelets than do venous thromboses (which are, conversely, more effectively treated with anticoagulants). In the present analysis, there was no benefit of heparin in terms of injury healing, but there was a slight benefit (P = .15) of heparin to promote improvement in neurologic function in patients with lateralizing deficits. This may have been influenced by a bias toward treating symptomatic patients with heparin, even in the face of relative contraindications; and by relatively small numbers of patients. Perhaps a more important measure of the efficacy of therapy is stroke prevention. Of those patients diagnosed and treated before stroke, 9% of those treated with aspirin had a stroke, compared with 1% of those treated with heparin. Although this was not a statistically significant difference (P = .07), it may well have clinical significance. We are conducting a prospective, randomized trial to evaluate the efficacy of systemic heparin compared with antiplatelet therapy in treating grade I BCVI. However, it is likely that a multicenter trial will be required to answer the question.

The stroke incidence did not differ between BCI (23%) and BVI (20%). However, whereas the incidence of stroke increased with BCI injury grade, this did not hold true for BVI. The stroke rate was higher for grade II and lower for grade IV BVI compared with BCI. It may be that nonocclusive BVIs (grade I–III) are potentially more dangerous than grade IV injuries. This is presumably because in general collateral circulation (i.e., the contralateral vertebral artery) is sufficient to compensate for an interruption in vertebral artery flow, whereas a nonocclusive intimal injury may promote platelet thromboembolization and consequent infarction. However, in the case of BCI, the stroke rate is higher in occlusive than nonocclusive injuries, presumably because the internal carotid artery circulation is less able to compensate for an acute interruption in flow.

Discussion

Dr. Timothy C. Fabian (Memphis, TN): The authors have executed another excellent study in a series of studies of blunt cerebrovascular injuries from their institution. We have had a similar interest in these injuries in Memphis, and many of the findings related to incidence, pathology, and treatment are quite similar between the two programs. However, there are a few differences which I will mention and query Dr. Biffl on his interpretations.

The incidence of blunt injuries in this report is 1.55% of all blunt trauma admissions, while our incidence is 1.11% in what I believe are very similar patient populations. Are we missing some injuries due to less aggressive screening than in Denver? I suspect that is indeed part of the answer.

Walter, could you tell me how many screening four-vessel arteriographic studies are performed on an annual basis in your institution? I note in your paper from 1998 (Annals of Surgery, Vol. 228), the carotid incidence was 0.86%. In the current study it is 1.11%. So I assume you are indeed doing substantially more aggressive screening in the past 3 years.

A second possible explanation for an increase in incidence is that some of the grade I, which constitute 50% of your cases, may have been in fact contrast injection artifacts, a phenomenon we have noted on occasion in young people with otherwise healthy vessels, especially internal carotids. What gives some support to that critique is that 57% of your grade I lesions were healed on follow-up angiogram in 7 to 10 days. While some minimal lesions may heal that rapidly, 57% seems a little high.

Forty-three percent progressed to pseudoaneurysm formation, a number very similar to our findings. Thirty-three of those patients had stents placed. Were they inserted at the time of the second angiogram? That is the first question. Also, what is your protocol for short-term and long-term anticoagulation and antiplatelet therapy in that group that had stents placed?

Finally, you noted in the manuscript poor results with CTAs and MRAs for diagnostic screening. We recently completed a prospective evaluation of those techniques and found similarly poor results, with sensitivities of approximately 50%. Since you are screening a sizable cohort, do you have any suggestions regarding any other techniques that are less aggressive than angiography, such as duplex Doppler? Or what about advancing CT technologies?

I thoroughly enjoyed the presentation and the exceptional manuscript, which I recommend certainly to everyone interested in this topic. The data are analyzed in a very scholarly fashion. And I thank the Association for the privilege of the floor.

Dr. Ali f. Aburahma (Charleston, WV): A couple questions for the authors. My understanding is you have a significant number of strokes related to vertebral artery injury. Did you look to the other vertebral artery, and how do you explain these strokes if the other vertebral artery was intact? Second, I am still confused about using a stenting for the pseudoaneurysm. Do you mean a stent-graft?

Dr. Dale W. Oller (Raleigh, NC): What is the role of duplex follow-up on initial diagnosis? If you are going to be aggressive in placing stents, what is the mechanism to prevent embolization during the stent placement? If you believe in the treatment of embolic disease to the brain, which has caused recent neurological deficit, have you tried or are you willing to try TPA or urokinase for these brand-new emboli?

Dr. David V. Feliciano (Atlanta, GA): Can you clarify what your management is in the patient with a severe intracranial injury and either a blunt carotid or vertebral injury? Second, when you presented at this meeting before, you mentioned in the previous paper that 11 patients had stenting of the internal carotid artery. There is enough data in the elective vascular literature to suggest that probably 5% to 7% of patients being stented above the common carotid artery level will eventually thrombose over time. Since these are primarily young patients without atherosclerosis, can you give us any long-term data from the Denver center on what has happened to your patients with stents at the base of the skull?

Dr. Ian Hamilton (Chattanooga, TN): My question relates to the timing of follow-up arteriography. Also, another question about duplex, might there be a role for screening duplex and then using the results of duplex to determine those patients requiring subsequent arteriography?

Dr. Mellick T. Sykes (San Antonio, TX): Is there any role currently for open repair, either acutely or after follow-up arteriogram, in blunt carotid or vertebral trauma?

Dr. Walter L. Biffl (Denver, CO): I appreciate the comments of all the discussants. First I will address Dr. Fabian’s questions.

The incidence of injuries in our study, 1.55% of the overall population, is very high, and it relates probably to two factors: one, the liberal screening criteria that we have, and two, the denominator of patients. We exclude those who are seen by the trauma service but discharged from our emergency department observation unit. This accounts for 25% to 30% of our trauma service encounters, and these patients might be admitted to other institutions. On the other hand, a recent paper from Tyler, TX, reported a 1.8% incidence of BCVI in their trauma patients in the first quarter of the year 2000. So they are being seen with increasing frequency, and it is difficult to say exactly why. I think it is a combination of suspicion and liberal screening criteria.

Are grade I injuries artifacts? That has been difficult to sort out. They do have a high healing rate, but Dr. Fabian’s group reported about an 80% healing rate of lesions on follow-up arteriography (although they were done at a later period in time). We do work with the radiologist to look at injury patterns. For example, a vertebral artery irregularity at the site of the cervical spine fracture is generally called an injury. We probably overcall some so that we can treat them and avoid the stroke risk (7% in the grade I injuries). They are not as dangerous as other lesions but not totally innocuous.

Stents are a popular topic for discussion. Early on in our series, follow-up arteriograms were done relatively early, particularly in patients with pseudoaneurysms identified. After three patients had complications related to the follow-up procedure, we stepped back and evaluated our practice. It appears that manipulation of catheters or stents at the injury site is a very dangerous maneuver in the early postinjury period. All three of our angiography-related strokes occurred with manipulation of catheters, not just with shooting dye, and they all occurred in the first 6 postinjury days. Thus, now we do the follow-up arteriogram at day 7 to 10. If a pseudoaneurysm is unchanged or enlarging or if a grade II injury is progressing toward occlusion of the artery, a stent will be placed. These are stents, not stent-grafts. Stent-grafts need to be custom-made, and the stent serves its purpose to push down the intimal flap and seal off the injury. We have had healing in all the stented injuries.

Regarding the long-term anticoagulation regimen, patients with stents are kept on full anticoagulation with warfarin for 3 months. They are reimaged at that time and then kept on aspirin lifelong.

Follow-up data goes out to a couple of years in some patients, but the median is only 3 to 6 months. We have had stent thrombosis in 3 of 22 patients, 1 of whom had an extracranial-intracranial bypass.

A couple of discussants asked about noninvasive testing. First, with regard to duplex scanning, in a Western Trauma Association multicenter study on carotid injuries published in 1994, the sensitivity of duplex was 86% in symptomatic lesions. We have not used duplex as a screening tool because we recognize its limitations at the skull base, with the intracranial carotid artery and with the vertebral artery. I don’t know of any group that has had a lot of success with this modality. And because it is likely to miss lesions that are not flow-limiting or that are not creating a pseudoaneurysm, we will miss a lot of the lower-grade lesions that we know can cause problems. As far as its role in follow-up, it may be useful, but again it won’t tell you if the artery has completely healed.

The Vermont Group has reported a series in which they identified a number of injuries with CTA. We looked at it head-to-head with arteriography and it had about 85% sensitivity. We believe it will miss the low-grade injuries, and so we have not promoted it. On the other hand, as Dr. Fabian pointed out, CT technology is improving, and CTA should be a more useful modality, particularly in centers that don’t have the resources to use arteriography routinely. The same thing goes with MRA. Our data, which we are going to report at the Western Trauma Association, indicate that MRA does not match the sensitivity arteriography either.

Strokes related to vertebral artery injuries are not related to bilaterality of the lesions. The stroke rate does not change with injury grade, probably because a nonocclusive lesion could be even more dangerous than an occlusive lesion in the vertebral artery. An occlusion would allow the other vertebral artery to carry the flow, but a nonocclusive lesion could allow thromboembolization.

Regarding patients with severe brain injury, we work with the neurosurgeons to identify a window of time where we might start anticoagulation safely. If we don’t have that window, the patients are either not treated or they are given one aspirin a day.

The location of these injuries has precluded open repair in the vast majority of patients. Only one patient in our series in the last 10 years has had surgery. The primary reason for that is these injuries will typically extend into the skull base in a very difficult-to-access area, so they are all managed nonoperatively.