Case Report
Basilar Artery Herniation into the Sphenoid Sinus Secondary to Traumatic Skull Base Fractures: Case Report and Review of the Literature Arthur Wang1, John Wainwright1, Jared Cooper1, Michael S. Tenner2, Adesh Tandon1
Key words Basilar artery - Herniation - Sphenoid sinus -
Abbreviations and Acronyms CT: Computed tomography GCS: Glasgow Coma Scale MRI: Magnetic resonance imaging PTD: Post-trauma day From the Departments of 1Neurological Surgery and 2 Radiology, New York Medical College, Westchester, New York, USA To whom correspondence should be addressed: Arthur Wang, M.D. [E-mail:
[email protected]] Citation: World Neurosurg. (2016). http://dx.doi.org/10.1016/j.wneu.2016.11.068 Journal homepage: www.WORLDNEUROSURGERY.org
- BACKGROUND:
Traumatic clival fractures occur with less than 0.6% frequency and can be associated with significant neurovascular injuries. The most serious of these injuries is to the basilar artery in which the artery is dissected or is fully occluded, resulting in infarction of the brainstem and cerebellum. Among early reports of these injuries, postmortem autopsy showed entrapment, or incarceration, of the basilar artery at the clival fracture site. A literature search revealed 11 cases of entrapment of the basilar artery within a clival fracture.
- CASE
DESCRIPTION: This report describes a 59-year-old man after a motor vehicle crash with computed tomography showing a basilar artery herniation through a sphenoid sinus fracture. The patient subsequently developed brainstem and cerebellar infarcts.
- CONCLUSIONS:
Basilar artery incarceration and herniation through the sphenoid sinus is rare. Such an injury portends a poor prognosis. We discuss the relevant clinical imaging and review the literature.
Available online: www.sciencedirect.com 1878-8750/$ - see front matter Published by Elsevier Inc.
INTRODUCTION Traumatic basilar artery injury secondary to clival fracture is a rare and often serious entity described in the literature. Such fractures can lead to basilar artery dissection with stenosis, occlusion, or pseudoaneurysm formation at the site of the fracture.1 This carries significant morbidity and mortality secondary to ischemia and infarction of the brainstem and cerebellum. We report a case of basilar artery herniation into the sphenoid sinus in a patient with multiple skull base fractures. To date, there exist only two other case reports of traumatic basilar artery herniation into the sphenoid sinus. We describe the clinical and imaging features and review the existing literature on this rare injury. CASE DESCRIPTION A previously healthy 59-year-old man was an unrestrained passenger in a motor vehicle crash. The patient had an initial Glasgow Coma Scale (GCS) score of 15 upon arrival to the emergency department
and complained only of facial pain. His vital signs were stable. The initial neurologic examination demonstrated significant periorbital ecchymosis with absent volitional extraocular movements bilaterally, restricted forced duction of right eye, and unrestricted forced duction of the left eye. He was able to move all extremities with full strength and displayed grossly intact sensation throughout. There was no evidence of cerebrospinal fluid rhinorrhea or otorrhea. He had positive corneal, cough, and gag reflexes. The patient was admitted to the trauma intensive care unit for further monitoring and management. Noncontrast computed tomography (CT) of the head, cervical spine, and maxillofacial skull revealed multiple cervical spinal fractures with C5-C6 subluxation, a right frontal epidural hematoma, extensive subarachnoid hemorrhage within the basilar cisterns and right parietal lobe, extensive craniofacial fractures including bilateral maxillary sinus fractures, a right frontal calvarial fracture, left superior orbital roof fracture, bilateral posterior sphenoid sinus fractures with extension to the clivus, and associated pneumocephalus.
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Blood was observed in the ethmoid air cells, sphenoid sinuses, and maxillary sinuses bilaterally. Further analysis using CT angiography of the head and neck demonstrated narrowing of the right cervical internal carotid artery consistent with a Denver grade 1 blunt cerebrovascular injury, and right jugular venous narrowing at the level of the jugular canal secondary to a displaced fracture fragment. In addition, herniation of a loop of the basilar artery into the left sphenoid sinus through a fracture diastasis at the level of the basisphenoid was discovered, with associated luminal narrowing (Figure 1). Reconstitution of normal vessel caliber was appreciated distal to the herniated segment. Given the extent of the patient’s intracranial hemorrhage, antithrombotic therapy was withheld. Strict instruction to withhold nose blowing and placement of nasogastric or nasotracheal intubation was recommended. Repeated CT angiography of the head and neck on post-trauma day (PTD) 1 revealed a flow void within the basilar artery, at the level of its herniation into the sphenoid sinus with good distal, and
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Figure 1. Axial and sagittal computed tomography angiography images demonstrating the basilar artery as it (A) ascends in the prepontine cistern,
proximal opacification that was believed to represent basilar artery thrombosis (Figure 2). All additional intracranial pathology was found to be stable to imaging on presentation. On PTD 2, the patient was noted to have a sharp decline in neurologic examination result, to a GCS score of 5. He exhibited decorticate posturing, failed to open his eyes to noxious stimuli, and had sluggishly reactive pupils. The patient was intubated for airway protection. Magnetic resonance imaging (MRI) of the brain was performed, revealing regions of restricted diffusion localized to the posterior circulation territories including the right occipital lobe and caudal pons, consistent with acute infarct (Figure 3). The decision was made to initiate therapy with aspirin (325 mg), given the contraindications to heparin. Noncontrast CT of the head performed on PTD 4 revealed a significant
(B) herniates into and (D) exits from (C) the sphenoid sinus.
increase in the posterior circulation infarct volume, including the pons and bilateral posterior cerebral artery and left anterior inferior cerebellar artery territories (Figure 4). Subsequent neurologic examination results continued to demonstrate declining function, and the patient ultimately progressed to a locked-in state. DISCUSSION Traumatic clival fractures occur with less than 0.6% frequency, and they can be associated with significant neurovascular injuries.2 They are classified as longitudinal, transverse, or oblique. Longitudinal fractures are associated with a 67%e80% mortality rate.2,3 The most serious of these injuries is to the basilar artery in which the artery is dissected or is fully occluded resulting in infarction of
Figure 2. (A) Three-dimensional reconstruction of computed tomography (CT) angiography images performed at initial presentation, showing a patent basilar artery with focal stenosis at the level of the fracture defect. (B) Three-dimensional reconstruction of CT angiography images performed after an interval of 24-hours, showing an occlusion of the basilar artery at the level of the fracture defect. Resumption of flow is seen as the basilar artery exits the herniation site.
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the brainstem and cerebellum.4,5 Among early reports of these injuries, postmortem autopsy showed entrapment, or incarceration, of the basilar artery at the clival fracture site.6-8 A literature search revealed 11 cases of entrapment of the basilar artery within a clival fracture. The mechanism proposed for basilar artery incarceration was initially proposed by Sights in 1967 and includes two components.6 The first involves an axial load injury leading to a linear longitudinal fracture in the coronal plane of the clivus. Second, the momentum and subsequent inertia of the basilar artery in the forward direction leads to entrapment of the artery in the fracture site. The artery is “pinched off” at the diastatic fracture site and subsequent infarction of the brainstem and cerebellum develops. Our patient sustained significant maxillofacial and skull base fractures, including comminuted sphenoid sinus fractures and focal herniation of the basilar artery into the sphenoid sinus. To our knowledge, only two cases of posttraumatic basilar artery herniation through the sphenoid sinus have been reported in the literature.9,10 In both cases, a small loop of the basilar artery extended into and then out of the sphenoid sinus with marked focal constriction of the basilar artery at the sphenoid sinus defect. There was normal diameter of the basilar artery proximal and distal to the stenotic site. Despite patency of the basilar artery, both patients subsequently developed pontine and cerebellar infarcts demonstrated on MRI, presumably from occlusive changes in the paramedian pontine perforators and anterior inferior cerebellar artery branches of the basilar artery. In our case, 3D reconstructions of the CTA images demonstrate interval changes
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Figure 3. Axial diffusion-weighted (b ¼ 1000) magnetic resonance images confirming regions of acute infarction in the (A) caudal pons and (B) right occipital lobe.
in the caliber of the basilar artery from focal stenosis to complete occlusion at the fracture site over the course of 24 hours (Figure 2). Despite these changes, our patient surprisingly did not show any new neurologic deficits until 24 hours after the second CTA was performed. At that time, MRI of the brain demonstrated infarction changes in the left midbrain, pons, and right occipital lobe corresponding to thromboembolic changes in the posterior circulation (Figure 3). A repeated CT scan of the head performed 48 hours after occlusion of the basilar artery demonstrated the full extent of the infarction changes in the distribution of the basilar pontine perforators, bilateral posterior cerebral arteries, and left anterior inferior cerebellar artery (Figure 4).
Our patient, and the previously described two cases in the literature highlight a few important points. First, what is the optimal imaging modality for diagnosis of vascular injuries associated with clival fractures? We believe that CTA will be adequate for diagnosis as it is rapid and affordable, and it can be performed on noncompliant patients who would otherwise require anesthesia for magnetic resonance imaging/angiography. We believe that cerebral angiography would be necessary only if endovascular intervention is planned, despite it being the gold standard for vascular imaging. Second, what is optimal treatment strategy for basilar artery injuries associated with clival fractures? There are currently no reports of endovascular treatment of such injuries.
The literature on basilar artery reconstruction via stenting have been reported on dissections and dissecting aneurysms of the vertebrobasilar system.11,12 All treated patients required postoperative dual antiplatelet agents. Our patient did not qualify for such intervention given his right frontal epidural hematoma and bifrontal contusions. Reports of medical therapy for basilar artery dissections using aspirin, argatroban, and warfarin have also been reported with some success, depending on the clot burden on the basilar artery.1,5 Our treatment options were more limited given the intracranial hemorrhage that the patient suffered initially. We initiated aspirin (325 mg) daily with limited success in our patient, as he ultimately progressed to locked-in syndrome.4 Third, the natural history of vertebrobasilar arterial injuries can be poor. In our patient, distal thromboembolization and the sensitivity of the small pontine perforators to decreased blood flow through a stenotic basilar artery most likely led to his infarcts.9 Given the high morbidity and mortality associated with vertebrobasilar arterial injuries, treatment modalities should be investigated in the future to prevent progressive ischemic events. CONCLUSIONS This case report adds to the growing literature of posttraumatic basilar artery herniation into the sphenoid sinus. This rare injury can be seen in association with clival fractures, and it has a poor prognosis despite medical therapy. Clinical and radiologic findings are described. Salient points regarding optimal imaging and management strategies are also discussed. REFERENCES 1. Taguchi Y, Matsuzawa M, Morishima H, Ono H, Oshima K, Hayakawa M. Incarceration of the basilar artery in a longitudinal fracture of the clivus: case report and literature review. J Trauma. 2000;48:1148-1152. 2. Corradino G, Wolf AL, Mirvis S, Joslyn J. Fractures of the clivus; classification and clinical fractures. Neurosurgery. 1990;27:592-596.
Figure 4. Axial computed tomography images revealing extensive low-attenuation changes in the distribution of the pontine branches of the basilar artery, bilateral posterior cerebral arteries, and left anterior inferior cerebellar artery, representing territories of infarction.
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3. Joslyn JN, Mirvis SE, Markowitz B. Complex fractures of the clivus: diagnosis with CT and clinical outcome in 11 patients. Radiology. 1988; 166:817-821.
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4. Sen-Gupta I, Daiga DA, Alberts MJ. Teaching NeuroImages: locked-in syndrome resulting from traumatic basilar artery occlusion following clivus fracture. Neurology. 2012;78:e148-149. 5. Sato S, Lida H, Hirayama H, Endo M, Ohwada T, Fujii K. Traumatic basilar artery occlusion caused by a fracture of the clivus—case report. Neurol Med Chir. 2001;41:541-544. 6. Sights WP Jr. Incarceration of the basilar artery in a fracture of the clivus. Case report. J Neurosurg. 1968;28:588-591. 7. Anthony DC, Atwater SK, Rozear MP, Burger PC. Occlusion of the basilar artery within a fracture of the clivus. J Neurosurg. 1987;66:929-931. 8. Bala A, Knuckey N, Wong G, Lee GY. Longitudinal clivus fracture associated with trapped
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basilar artery: unusual survival with good neurological recovery. J Clin Neurosci. 2004;11:660-663. 9. Kaakaji R, Russell EJ. Basilar artery herniation into the sphenoid sinus resulting in pontine and cerebellar infarction: demonstration by three-dimensional time-of-flight MRI angiography. AJNR Am J Neuroradiol. 2004;25: 1348-1350. 10. Khanna P, Bobinski M. Computed tomography and magnetic resonance imaging of a basilar artery herniation into the sphenoid sinus. Skull Base. 2010;20:269-273. 11. Hauck EF, Natarajan SK, Horvathy D, Hopkins LN, Siddiqui AH, Levy EI . Stentassisted basilar reconstruction for a traumatic vertebral dissection with a large basilar artery thrombosis. J Neurointerv Surg. 2011;3:47-49.
12. Li C, Li Y, Jian C, Wu Z, Wang Y, Yang X. Stent alone treatment for dissections and dissecting aneurysms involving the basilar artery. J Neurointerv Surg. 2015;7:50-55.
Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Received 14 October 2016; accepted 12 November 2016 Citation: World Neurosurg. (2016). http://dx.doi.org/10.1016/j.wneu.2016.11.068 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter Published by Elsevier Inc.
WORLD NEUROSURGERY, http://dx.doi.org/10.1016/j.wneu.2016.11.068