Basilar Artery Occlusion Following C1 Lateral Mass ... - Springer Link

Neurocrit Care (2009) 11:255–260 DOI 10.1007/s12028-008-9159-7

PRACTICAL PEARL

Basilar Artery Occlusion Following C1 Lateral Mass Fracture Managed by Mechanical and Pharmacological Thrombolysis Patrick A. Sugrue Æ Ziad A. Hage Æ Daniel L. Surdell Æ Mina Foroohar Æ John Liu Æ Bernard R. Bendok

Published online: 28 October 2008 Ó Humana Press Inc. 2008

Abstract Background Vertebral artery injury following cervical spine trauma can be associated with stroke. We present a case of a C1 fracture resulting in vertebral artery dissection and neurological decline as a result of basilar artery occlusion treated with chemical and mechanical thrombolysis resulting in basilar artery patency and clinical improvement. Case description The patient is a 43-year-old female who was involved in a motor vehicle collision where she sustained multiple cervical spine injuries including a comminuted fracture of the left lateral mass of C1 resulting in vertebral artery dissection which eventually led to a basilar artery embolus and occlusion. A total of 15 mg of intraarterial tissue plasminogen activator was infused throughout the clot, followed by mechanical clot embolectomy using an FDA-approved device. Her neurological exam improved post-procedurally and she was discharged with a left hemiparesis to a rehabilitation facility 3 weeks after admission. At 15 month follow up, she is neurologically intact with the exception of some subtle difficulty with fine motor movement in the right upper extremity and mild dysmetria on the right. Conclusions With this case, we report a rare and potentially devastating complication of C1 fracture. To our knowledge

P. A. Sugrue Z. A. Hage D. L. Surdell J. Liu B. R. Bendok (&) Department of Neurological Surgery, Northwestern University, Feinberg School of Medicine, 676 N. St. Clair, Suite 2210, Chicago, IL 60611, USA e-mail: [email protected] M. Foroohar Department of Neurosurgery, Northwest Community Hospital, Arlington Heights, IL, USA

there are only two previously reported cases where a C1 fracture has been associated with basilar artery occlusion resulting in death and locked-in syndrome respectively. In this case, chemical thrombolysis and mechanical thrombectomy resulted in recanalization of the basilar artery with excellent long-term neurological outcome. Keywords Cervical spine trauma Vertebral artery injury Basilar artery occlusion Mechanical thrombolysis Dissection Chemical thrombolysis

Introduction Arterial dissections can be complicated by an embolic stroke and the majority of such strokes involve distal branches. However, basilar artery occlusion in the setting of cervical spine trauma is rare and to our knowledge reported in only five cases [1–5]. Basilar artery occlusion is associated with high morbidity and mortality [6, 7]. Intraarterial (IA) thrombolysis has emerged as a potential treatment for acute basilar artery occlusion with promising results [8–10]. Moreover, mechanical thrombolysis/ thrombectomy can be performed in patients for whom intravenous (IV) thrombolytics are contraindicated or as an adjunct to IA chemical thrombolysis [4, 8, 11, 12]. We present a rare case of basilar artery occlusion in the setting of cervical spine trauma treated successfully with IA chemical thrombolysis and mechanical thrombectomy.

Case Description The patient is a 43-year-old female who was involved in a motor vehicle collision where she sustained multiple

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cervical spine injuries including a comminuted fracture of the left lateral mass of C1 (Fig. 1). The posterior fracture fragment was slightly compressing the left vertebral artery. There was an additional fracture involving the inferior facet of C6 and superior facet of C7 on the left. The patient also had a complex ankle fracture and was on oral contraceptives. On the morning after admission, approximately 15 h after the accident, the patient’s neurologic condition deteriorated. While initially neurologically intact, she then was noted to have dysarthria, right-sided ptosis, and dysconjugate gaze due to right third nerve palsy. At that time computed tomography angiography (CTA) at the outside hospital revealed basilar artery occlusion. She was started on a heparin infusion and transferred to our institution for further management. On physical exam she had a right third nerve palsy and was unable to look to the left on command with her right eye, and was no longer able to move her left upper extremity to command. Voluntary muscle movement in her right upper extremity remained unimpaired. Repeat imaging revealed acute ischemia in the pons, posterior right occipital lobe, and left cerebellum (Fig. 2). Angiography revealed occlusion of the basilar artery (Fig. 3). Approximately 24 h after injury and approximately 10 h after onset of basilar occlusion symptoms at the outside hospital, the patient was in the angiography suite and underwent catheterization of the right vertebral artery then of the left P1 with the L5 compatible Concentric microcatheter (Concentric Medical, Inc., Mountain View, CA) over an Agility soft wire (Cordis Neurovascular, Miami, FL) with a J tip followed by

Fig. 1 CT scan of the cervical spine showing a comminuted fracture of the left lateral mass of C1

Neurocrit Care (2009) 11:255–260

Fig. 2 Diffusion weighted image (DWI) demonstrating the extent of diffusion restriction consistent with infarction prior to thrombectomy

removal of the Agility 14 soft wire and placement of an exchange length Mirage (Micro Therapeutics Incorporated, Irvine, CA) wire into the left posterior cerebral artery (PCA). The clot was then irrigated with an injection of 15 mg of tissue plasminogen activator (t-PA) via a pulsing technique up and down the clot without losing wire access. Nonetheless, an angiogram post infusion of thrombolytic

Fig. 3 Cerebral angiogram demonstrating occlusion of the basilar artery (arrow) prior to thrombectomy


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post-stroke), the patient was neurologically intact with the exception of some minor difficulty with fine motor movement in the right upper extremity and some difficulty with finger to nose testing on the right.

Discussion

Fig. 4 Cerebral angiogram demonstrating recanalization of basilar artery following chemical and mechanical thrombectomy

showed persistent occlusion of the basilar artery. A MERCI L5 device (Concentric, Mountain View, CA) was then deployed into the upper basilar artery. The device was slowly pulled back while the guide catheter was aspirated. This resulted in recanalization of the basilar artery (Fig. 4). Left vertebral artery angiography revealed a dissection of the vertebral artery at the level of C1 with associated intraluminal clot which was the likely culprit of the basilar artery thromboembolus. A total of 5 mg of ReoPro (abciximab) was then infused proximal to this clot. All devices were then removed and a closure device was used to seal the access site. Her neurological exam demonstrated reactive pupils, no spontaneous movement, extensor movement to painful stimuli on the right greater than the left, and decreased tone throughout. Post-procedurally, the patient’s systolic blood pressure was kept between 100 and 130 mmHg in order to balance the risk of post-traumatic contusion/hemorrhage with the need to maximally maintain cerebral perfusion. Likewise, the patient was started on a heparin infusion at the time of transfer from the outside hospital and maintained on that infusion post-procedurally with a modest partial thromboplastin time (PTT) goal of 50–70 s, given the need to balance the risk of hemorrhage versus the need for anticoagulation in the setting of basilar occlusion and dissection. Follow-up CTA 1 week after intervention revealed a patent basilar artery and no sign of flow limiting stenosis in the left vertebral artery at the site of prior dissection. At the time of transfer to a rehabilitation facility, she had a left hemiparesis and was able to blink to command. On her most recent exam (15 months

The incidence of a vertebral artery injury in the setting of cervical spine trauma has been described extensively in the literature. A recent prospective study of 64 patients who sustained cervical spine injuries over a 2-year period found the rate of traumatically induced vertebral artery occlusion detected by magnetic resonance angiography (MRA) to be 17.2% [13]. Moreover, other studies have shown that the overall stroke rate following traumatic vertebral artery injury ranges from 5 to 24% [14–19]. Such injury has significant sequelae and should be considered in the evaluation of a patient who has sustained cervical spine trauma and in particular if he or she has any neurological findings such as altered consciousness, dysarthria, blurred vision, nystagmus, ataxia, or dysphagia [20]. Likewise, radiographic findings particularly suggestive of vertebral artery injury include subluxation, extension of the fracture line into the transverse foramen, facet dislocation, and upper cervical spine fracture [19, 21–23]. Veras et al., in a series of 399 patients over the course of 5 years, found six patients who had evidence of vertebral artery injury following cervical spine trauma. All six had unilateral vertebral artery injury in the V2 segment between C2 and C6 and the occlusion was adjacent to the fracture [22]. The mechanism of injury in such patients is thought to be due to stretching and/or tearing of the media and intima or compression of the vertebral vessel. Intimal tear can trigger platelet aggregation and clot formation with the potential for embolization [20, 24, 25]. Basilar artery occlusion accounts for 6–10% of large vessel strokes [12, 26]. Kubik and Adams [27] were among the first to describe the clinical symptomatology associated with basilar artery occlusion. This subject was later tackled by Ferbert et al. [28]. They found that patients with basilar artery occlusion could present with a variety of neurological findings including cranial nerve palsies, seizures, altered level of consciousness, and even long tract signs. It was also determined that ischemic damage to the pontine pyramidal tracts can lead to quadriplegia, anarthria, and preserved consciousness, a collection of symptoms known as locked-in syndrome [29]. The natural history of basilar artery occlusion reported in the literature is based on isolated case reports and small studies [26, 30, 31] and is associated with high morbidity and mortality. In their series, Hacke et al. [7] found an 86.4% mortality rate among 22 patients with basilar artery

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occlusion treated medically. More recently, Schonewille et al. [31] reported a mortality of 40% in 82 patients with basilar artery occlusion treated medically; however, they also found that 79.3% of cases had a poor outcome (Rankin score 4–6). The etiology of basilar artery occlusion is most commonly embolic (from a cardiac or other arterial source). However, other etiologies include atherothrombosis and vertebral artery dissection. In our patient, oral contraceptives might have increased her risk of arterial thrombosis [32]. Basilar artery occlusion related to a vertebral artery dissection is rare. However, reports have shown that approximately one-third of extracranial cerebral vasculature, including both carotid and vertebral artery injuries, will have some delayed or progressive symptoms, which have been attributed to vascular occlusion or distal thromboembolism [10]. Therefore, basilar artery occlusion as a result of an injured vertebral artery is highly plausible and may be underestimated. Our literature review suggested only two previous reports of C1 fracture and basilar artery occlusion where one patient suffered from locked-in syndrome while the other died [3, 33]. In the case of our patient, it is likely that the C1 lateral mass fracture led to the vertebral artery dissection seen on angiography. The clot at that location likely either propagated or dislodged and caused the basilar artery thrombosis. The time course of the events suggests that the dissection was indeed the source of the eventual basilar artery occlusion and the patient’s neurological decline. Of note, the patient’s C1 fracture did not require any surgical intervention and was treated with a cervical brace as supported by the literature [34]. The essential component in restoring neurological function to these patients is the ability to recanalize the occluded vessel. Spontaneous recanalization of the basilar artery may occur; however, it has been estimated to be lower than 20% [26]. Interventions aimed at achieving recanalization include both IV and IA thrombolysis and appear to improve these outcomes [7, 35]. IA thrombolytics and mechanical thrombolysis/thrombectomy can be effective when IV thrombolytics are contraindicated. The time window for basilar thrombolysis remains poorly defined but is thought to be wider than for anterior circulation occlusion. The rationale for a wider time window centers on the poor prognosis without treatment and the results of encouraging case reports of delayed treatments [9, 36, 37]. Because IV t-PA is only safe and effective within 3 h of acute ischemic stroke, interventional approaches have been developed with promising results. The safety and efficacy of IA thrombolysis was initially supported by the PROACT II trial which compared IA-rpro-Urokinase (UK) + heparin in middle cerebral artery (MCA) occlusion to heparin alone [38]. One hundred


and eighty patients with no hemorrhage and no early infarction by CT were randomized. Treatment with rpro-UK was initiated at a median of 5.3 h. The recanalization rate was 66% with IA-rpro-UK versus 18% with heparin alone. Slight or no neurological disability at 90 days occurred in 40% with IA-rpro-UK versus 25% with heparin alone. Intracerebral hemorrhage (ICH) and neurological deterioration occurred in 10% with IA-rpro-UK versus 2% with heparin alone. Mortality at 120 days was similar in both, with 25% in IA-rpro-UK versus 27% with heparin alone. The authors concluded that despite increased frequency of ICH, rpro-UK significantly improved clinical outcome. Favorable outcomes with IA thrombolysis were also observed when treating basilar artery occlusions. As stated previously, wider time windows are typically allowed when compared to anterior circulation occlusions. Egan et al. [39] published their experience on a series of 15 patients treated with IA UK at a mean of 12 h for basilar artery occlusion. A recanalization rate of 80% was achieved. Of those recanalized, 16.7% died. The authors concluded that IA thrombolysis could decrease mortality and improve outcome in patients with basilar artery occlusion even when administered after 6 h of symptom onset. In another series by Arnold et al. [40], 40 patients presenting with basilar artery occlusion and treated with IA thrombolysis at a mean of 5.5 h were analyzed. The recanalization rate was 80% and favorable outcome could be achieved in 35%. In an effort to reduce the need for thrombolytics and perhaps expand time windows, thrombectomy devices including the Merci device have been introduced. The Multi MERCI trial, which tested the safety and efficacy of the newer generation thrombectomy catheter (L5) in acute large vessel stroke, suggested that mechanical thrombectomy following IV t-PA is safe and the use of Merci devices is an effective treatment for acute ischemic stroke for those who are either ineligible for IV t-PA or who have ‘‘failed’’ such therapy [41, 42]. Of patients enrolled in the study, 164 were treated with the L5 retriever. Overall successful recanalization was achieved in 57.3% with the retriever alone and in 69.5% when adjunctive therapy (other mechanical thrombectomy or IA t-PA) was added. Overall favorable clinical outcome (mRS 0-2) was noted in 36% and mortality was 34%. Both these results were significantly associated with vessel recanalization. Symptomatic ICH was observed in 9.8%. Clinically significant procedural complications happened in 5.5%. When considering posterior circulation outcomes, Multi MERCI data showed that the overall vertebrobasilar final recanalization rate was 86% and vertebrobasilar recanalization with the L5 device was 100%. Overall favorable clinical outcome (mRS 0-2) was noted in 29% and mortality was 43%. Symptomatic ICH was observed in 29% [41, 42].


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Conclusions Vertebral artery dissection is a potentially morbid complication of cervical spine trauma. This injury can lead to thromboembolism and occasionally occlusion of large intracranial arterial branches. Basilar artery occlusion via this mechanism has only been rarely reported. Basilar artery occlusion carries significant morbidity and mortality but the natural history appears to be amenable to favorable modification by chemical and mechanical thrombolysis and/or thrombectomy. Prompt diagnosis is hence necessary to institute therapy in a timely fashion.

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