The devastating potential of blunt vertebral arterial injuries.

OBJECTIVE: To formulate management guidelines for blunt vertebral arterial injury (BVI). SUMMARY BACKGROUND DATA: Compared with carotid arterial injuries, BVIs have been considered innocuous. Although screening for BVI has been advocated, particularly in patients with cervical spine injuries, the appropriate therapy of lesions is controversial. METHODS: In 1996 an aggressive arteriographic screening protocol for blunt cerebrovascular injuries was initiated. A prospective database of all screened patients has been maintained. Analysis of injury mechanisms and patterns, BVI grades, treatment, and outcomes was performed. RESULTS: Thirty-eight patients (0.53% of blunt trauma admissions) were diagnosed with 47 BVIs during a 3.5-year period. Motor vehicle crash was the most common mechanism, and associated injuries were common. Cervical spine injuries were present in 71% of patients, but there was no predilection for cervical vertebral level or fracture pattern. The incidence of posterior circulation stroke was 24%, and the BVI-attributable death rate was 8%. Stroke incidence and neurologic outcome were independent of BVI injury grade. In patients treated with systemic heparin, fewer overall had a poor neurologic outcome, and fewer had a poor outcome after stroke. Trends associated with heparin therapy included fewer injuries progressing to a higher injury grade, fewer patients in whom stroke developed, and fewer patients deteriorating neurologically from diagnosis to discharge. CONCLUSIONS: Blunt vertebral arterial injuries are more common than previously reported. Screening patients based on injury mechanisms and patterns will diagnose asymptomatic injuries, allowing the institution of therapy before stroke. Systemic anticoagulation appears to be effective therapy: it is associated with improved neurologic outcome in patients with and without stroke, and it appears to prevent progression to a higher injury grade, stroke, and deterioration in neurologic status.

Treatment of posttraumatic internal carotid arterial pseudoaneurysms with endovascular stents.

BACKGROUND: The sequelae of blunt injury to the carotid arteries are unusual, but pseudoaneurysms causing subsequent strokes are devastating. The utility of treatment of these pseudoaneurysms was examined. METHODS: All patients at a Level I trauma center with previously documented traumatic risk factors were assessed for blunt injury to the carotid arteries and, when a pseudoaneurysm was present, a self-expanding metallic stent was placed across the lesion and the patient placed on anticoagulation. Follow-up arteriograms were obtained in 2 months and every 6 months thereafter. RESULTS: Fourteen patients (7 men, 7 women) with an average age of 27 years, an Injury Severity Score of 38, had formed pseudoaneurysms in 16 extracranial internal carotid arteries. These were stented with metallic endoprostheses. No strokes occurred after the placement of the stents. Mean follow-up period has been 2.5 years. CONCLUSIONS: Use of metallic endoprostheses is an effective method to treat this potentially devastating injury. However, longer follow-up and more patients studied are needed to further examine this promising treatment.

Selective infusion of urokinase and thrombectomy in the treatment of acute cerebral sinus thrombosis.

Acute cerebral sinus thrombosis caused a patient to decompensate rapidly and required immediate relief of her venous thrombosis as a life-saving procedure. The thrombus was laced with urokinase and removed from the sinuses with thrombectomy catheters. This reinstituted flow and she recovered full neurologic function within 4 hours.

Blunt carotid arterial injuries: implications of a new grading scale.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Blunt cerebrovascular injuries.

On the basis of our experience and the available literature, we submit that aggressive screening for BCI based on injury patterns is warranted. However, several important clinical issues remain unresolved. The precise injury patterns and relative cerebrovascular risks remain to be defined. Furthermore, the optimal diagnostic screening test remains to be identified, with consideration of the relative risk-benefit profile. Finally, we must determine the best methods for the treatment of BCI. Although the definitive study has yet to be completed, the use of heparin was associated with a trend toward improved outcomes in symptomatic patients. In addition, no asymptomatic patient experienced the development of new neurologic deficits during heparin therapy. Therefore we believe that the early institution of heparin therapy is indicated. The role of endovascular stenting, however, remains unclear.

Optimizing screening for blunt cerebrovascular injuries.

BACKGROUND: The recognition that early diagnosis and intervention, prior to ischemic neurologic injury, has the potential to improve outcome following blunt cerebrovascular injuries (BCVI), led to a policy of aggressive screening for these injuries. The resultant epidemic of BCVI has created a dilemma, as widespread screening is impractical. We sought to identify independent predictors of BCVI, to focus resources. METHODS: Cerebral arteriography was performed based on signs or symptoms of BCVI, or in asymptomatic patients with high-risk mechanisms (hyperextension, hyperflexion, direct blow) or injury patterns. Logistic regression analysis identified independent predictors. RESULTS: A total of 249 patients underwent arteriography; 85 (34%) had injuries. Independent predictors of carotid arterial injury were Glasgow coma score < or =6, petrous bone fracture, diffuse axonal brain injury, and LeFort II or III fracture. Having one of these factors in the setting of a high-risk mechanism was associated with 41% risk of injury. Of patients with cervical spine fracture, 39% had vertebral arterial injury. CONCLUSIONS: Patients sustaining high-risk injury mechanisms or patterns should be screened for BCVI. In the face of limited resources, screening efforts should be focused on those with high-risk predictors.

Incidence of unsuspected blunt carotid artery injury.

OBJECTIVE: This study attempts to document the incidence of unsuspected blunt carotid artery injury (BCI) in a prospective series of consecutive blunt trauma patients undergoing angiographic evaluation of the aorta. Previous studies have included mainly patients who became symptomatic from BCI, thus documenting a "detected incidence." METHODS: During a 22-month period, all patients undergoing angiographic evaluation of the aorta after blunt trauma who were not felt to be at increased risk for BCI were included in the screening protocol. All patients initially suspected of BCI were studied outside the protocol. Angiographic evaluation of the carotid arteries was performed using nonselective contrast injections after aortic injury had been ruled out. RESULTS: The incidence of BCI among those patients screened under the protocol (n = 119) was 2.5% (3 of 119). Among all patients undergoing aortic evaluation at presentation (n = 171), the detected incidence of BCI was 3.5% (6 of 171). The detected incidence of BCI among all patients during the study period was 0.32% (10 of 3174). No risk factors for BCI were identified beyond the severity of trauma that led to aortic evaluation. CONCLUSION: The incidence of BCI found in those patients screened in this study, nearly 10 times the incidence of BCI in our blunt trauma population overall, suggests that these patients represent a subgroup on which to focus screening efforts, regardless of the diagnostic tools employed. The similarity between the angiographic incidence and the detected incidence of BCI in this study argues that few BCIs remain asymptomatic. All blunt trauma patients injured sufficiently to prompt aortic evaluation at presentation should be screened in some manner for BCI.

Treatment of blunt injury to the carotid artery by using endovascular stents: an early experience.

Identification of blunt carotid injury prior to the development of ischemic symptoms requires aggressive screening of patients at risk. The treatment of these lesions has centered around long-term anticoagulation therapy. However, studies have revealed that many of these lesions persist despite medical treatment, as does the risk of distal embolization. The authors present a series of six patients who were successfully treated by means of endovascular stent placement for nonpenetrating carotid injuries. In the authors' experience this treatment requires only temporary anticoagulation therapy, results in immediate reconstruction of the injured vessel, obliterates pseudoaneurysms, and prevents distal embolization.

Traumatic bilateral jugular vein thrombosis: case report and review of the literature.

OBJECTIVE AND IMPORTANCE: Thrombosis of the internal jugular vein (IJV) with associated elevated intracranial pressure (ICP) is a rare complication of central venous catheterization but has not been reported as a result of blunt trauma. CLINICAL PRESENTATION: An 18-year-old male patient was observed to be obtunded after an assault. The initial examination was remarkable for somnolence, bruising of the anterior neck, and diffuse, edematous swelling of the face and scalp. The results of computed tomography of the brain were normal. An angiogram obtained on the 2nd hospital day to rule out carotid injury revealed bilateral IJV thromboses to the cranial base. An ICP monitor was placed with an opening pressure of 33 mm Hg. The central venous pressure was measured to be 9 mm Hg. A catheter was passed through the left IJV thrombus and into the sigmoid sinus, where the pressure was 17 mm Hg. INTERVENTION: An intravascular stent was deployed in the left IJV. ICP rapidly normalized. A regimen of coumadin was administered to the patient for 6 weeks, at which time the stent remained patent. CONCLUSION: We conclude that traumatic jugular vein thrombosis can be associated with significant elevation in ICP and that treatment with an endovascular stent can affect the rapid correction of intracranial hypertension in patients who are candidates for anticoagulation.

Posterior circulation cerebral infarcts associated with repair of thoracic aortic disruption using partial left heart bypass.

BACKGROUND: Partial left heart bypass is widely used in the repair of traumatic aortic disruptions. We recently encountered two patients with posterior circulation infarctions after repair of traumatic aortic disruptions using heparin-less partial left heart bypass. METHODS/RESULTS: Both patients underwent interposition graft repair of thoracic aortic transections at the level of the isthmus. The first patient developed a left posterior inferior cerebellar artery infarct after a clamp time of 44 minutes. Swelling of this infarct necessitated ventriculostomy placement. The second patient developed a pontine infarct postoperatively after a cross-clamp time of 56 minutes and suffered a persistent left upper extremity paresis. CONCLUSIONS: Partial left heart bypass may have predisposed these two patients to clamp-related embolic events via the left vertebral artery. This experience warrants further surveillance to detect these infarcts which can require neurosurgical intervention. Additionally, the events suggest reconsideration of systemic anticoagulation during aortic cross-clamp times exceeding 30 minutes.

Ossification of the ligamentum flavum causing thoracic myelopathy: a case report.

Ossification of the ligamentum flavum is a well reported clinicopathologic entity causing narrowing of the spinal canal and subsequent spinal cord compression. The patient described in this case report complained of 9 mo of middle and lower back pain, difficulty with balance, progressive gait disturbance, and recent onset of bladder retention. Magnetic resonance imaging and computed tomographic scan revealed a bone density mass at the T2-3 level causing 25% cord compression and edema. A decompressive laminectomy was performed at T-2. The etiology of the compression was found to be attributable to an ossified ligamentum flavum at the T-2 level, which was confirmed by histologic examination. His neurologic signs and symptoms and functional status markedly improved after surgery and subsequent comprehensive rehabilitation. The patient was able to ambulate independently with a walker as opposed to previously being wheelchair-bound. Prompt surgical intervention and appropriate rehabilitation management play a key role in improving the functional outcome of myelopathy caused by ossified ligamentum flavum. This article acquaints rehabilitation personnel with the clinical features, proposed etiologies, association with other diseases, work-up, treatment, and rehabilitation concerns of patients with myelopathy caused by ossified ligamentum flavum.

Genotypic variations of type III collagen in patients with cerebral aneurysms.

It has been hypothesized that either qualitative or quantitative abnormalities in type III collagen may be involved in the pathogenesis of cerebral aneurysms. The current study investigated allele frequencies for the type III collagen gene in patients with cerebral aneurysms. A diallelic Ava II polymorphism defined the type III collagen gene. The smaller of the two alleles was found in 11 of 19 aneurysm patients (58%) versus two of 15 controls (13%) (p = .006). The overall frequency of this allele was 0.34 in aneurysm patients versus 0.10 in controls (p = .011). This significant difference in allele frequency suggests that genotypic variations in the type III collagen gene may be etiologically related to aneurysm formation.