Dissecting Aneurysm of the Basilar Artery—A Rare Complication of Bacterial Meningitis in a Postoperative Case of CSF Rhinorrhea
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0028-3886.279691
Source of Support: None, Conflict of Interest: None
Keywords: Basilar artery, complication, dissecting aneurysm, meningitis, mycotic aneurysmKey Messages: Posterior circulation mycotic aneurysms have been reported secondary to bacterial endocarditis. Meningitis can rarely lead to development of mycotic aneurysm resulting in subarachnoid hemorrhage. It may be advisable to investigate for ruptured mycotic aneurysms or dissection in cases of bacterial meningitis leading to SAH.
Basilar artery dissection is a rare event, resulting most often in poor outcome, as the treatment options are not very well established. Of all the intracranial aneurysms, mycotic aneurysms constitute just 2.5–6.2%. There are very few cases of mycotic aneurysms reported secondary to bacterial meningitis, most of these aneurysms being in anterior circulation, involving the cavernous segment of the carotid artery.,, Even fewer patients have presented with SAH. We report a rare case of basilar artery dissecting aneurysm in a case of bacterial meningitis. This is the second case in the literature, to the best of our knowledge.
A 32-year-old gentleman met with a road traffic accident in October 2011, and had an episode of nasal bleed, seizure followed by brief loss of consciousness. A CT scan of brain revealed an undisplaced fracture of left frontal bone with tiny specks of right temporal contusion and he was managed medically. He developed CSF rhinorrhea 6 months later which was treated with bifrontal craniotomy and anterior cranial fossa base repair in another hospital, following which the leak subsided. However, he developed recurrence of CSF rhinorrhea 3 years later and presented to us in July 2015 with CSF rhinorrhea and multiple episodes of seizures. MRI brain showed a defect in the planum sphenoidale on the right side and an encephalomeningocele. Contrast MR images done at this time showed normal basilar artery caliber and course [Figure 1]a, [Figure 1]b, [Figure 1]c. He underwent endoscopic transnasal, transsphenoidal repair of the defect with fascia lata, abdominal fat and fibrin sealant glue. He had cessation of CSF leak and was on regular follow-up for 2 years.
Two years later, he presented to us once again with fever, headache, vomiting, and seizures for a week. There was no history of obvious CSF rhinorrhea before the onset of illness. The patient was conscious, obeying, irritable, and had signs of meningeal irritation. A diagnostic lumbar puncture revealed turbid CSF containing sheets of polymorphs. CSF glucose: 19 mg/dl and CSF proteins: 702 mg/dl. The patient was immediately started on antibiotics—a combination of ceftriaxone, amikacin, and metronidazole on empirical basis. A CT brain showed no evidence of hydrocephalus or meningeal enhancement [Figure 1]d. The culture of CSF grew alpha hemolytic streptococci and patient was treated according to sensitivity pattern.
The patient showed gradual improvement with intravenous antibiotics therapy. However, a week later, the patient developed a sudden deterioration in sensorium, was flexing limbs to painful response (GCS: E1V1M3). CT scan of brain revealed diffuse subarachnoid hemorrhage, more along the prepontine cisterns with hydrocephalus [Figure 1]e. He was mechanically ventilated and an external ventricular drain was placed. A possibility of post-infectious aneurysm was considered. An MRI brain with MRA was performed which showed tortuosity and dilatation of the basilar artery with adjacent thick subarachnoid hemorrhage and multiple brainstem infarcts [Figure 1]f. A CT angiography showed fusiform dilatation of basilar artery, suggesting dissecting aneurysm of basilar artery [Figure 1]g, [Figure 1]h, [Figure 1]i. A review of the CT brain images performed 2 days before the ictus had shown normal vessel anatomy and size, indicating an acute development of dissecting aneurysm in basilar artery in the background of meningitis [Figure 1]d. Cerebral angiography was not considered in view of poor sensorium of the patient. The options of management were discussed. In view of poor sensorium and the post-infectious dissecting aneurysm, it was decided to continue antibiotic therapy at anti-meningitic doses with anti-edema measures. However, the patient deteriorated further and finally succumbed to his illness, a week after the subarachnoid bleed.
Intracranial mycotic aneurysms occur usually in the background of infective endocarditis or distant septic focus and often have a tendency to involve middle cerebral artery. Meningitis has been reported to cause several cerebrovascular complications which include vasculitis, vasospasm, thrombosis, intracranial aneurysm formation, but incidence of subarachnoid hemorrhage is rare. According to Karsner's classification of mycotic aneurysms, those secondary to bacterial meningitis come under “extravascular origin,” formed as a result of extension of infection from a neighboring septic focus. These varieties of mycotic aneurysms are very rare as compared to the embolic variant which occurs due to seeding of infection from a distal focus. These are often silent until the time of rupture, when surgical treatment may be difficult or impossible. The third group that occurs in the absence of an obvious inflammatory focus elsewhere in the body has been called “primary or cryptogenic” mycotic aneurysms.
The mechanism proposed for the formation of these aneurysms is the invasion of the arterial wall by the bacteria from neighboring or contiguous inflammatory foci. Arterial thrombosis may result from diffusion of toxin or intimal involvement, which can contribute to the pathogenic process. The infection may result in disintegration and weakness of the vessel wall, causing rupture or formation of an infectious aneurysm.
Intracranial mycotic aneurysms of extravascular origin have been reported to be associated with thrombophlebitis of the cavernous sinus and with purulent or tuberculous meningitis. Some may rupture, while others may become thrombosed and decrease in size with antibiotic therapy. The frequent involvement of the cavernous segment of ICA in these cases can be attributed to location within the cavernous sinus making it vulnerable to infection from septic cavernous sinus phlebitis, resulting in varying degrees of arteritis. Post-infectious dissecting aneurysms in posterior circulation has been extremely rare. Previous reports of posterior circulation mycotic aneurysms have been secondary to bacterial endocarditis, which have been treated medically.
Zhao et al. reported a case of mycotic aneurysm of posterior cerebral artery secondary to infective endocarditis, who underwent endovascular treatment with Onyx. JR Perry et al. reported the only case in literature previously, describing development of a basilar artery dissecting aneurysm with SAH following bacterial meningitis while on antibiotic therapy for the same. The CSF culture grew Streptococcus milleri. Their patient was medically managed, initially showed improvement in sensorium, but succumbed to subarachnoid hemorrhage in 9 days. An autopsy had revealed a 10-mm fusiform aneurysm, arising from the mid portion of the basilar artery, with a clot forming one third of the outer wall. The basilar artery was involved by an angio-destructive inflammatory process in all wall layers.
The optimal treatment of acute basilar artery dissection is not defined and lack sufficient guidelines. While conservative management is opted in cases without rupture, surgical or endovascular treatment is considered in selected cases that have ruptured or revealed progressive ischemic symptoms., In cases secondary to bacterial infection however, antibiotic therapy is the mainstay of treatment which was done in our case and the previous case described in literature. Surgery or intervention was not considered owing to the poor sensorium of the patients in both instances. The utility of antiplatelet therapy in this condition is also not clear. While the dissection of basilar artery may be an indication, the setting of recent subarachnoid hemorrhage precludes its use. However, medical therapy did not result in improvement in both cases. Brain stem infarcts, possibly secondary to vasospasm or due to thrombosis of vessels secondary to dissection, or secondary to septic thrombosis marked the fatal disease course.
In conclusion, this report highlights a rare fatal complication of mycotic dissection of the basilar artery following meningitis, which developed acutely in hospital, while on treatment. Antibiotic therapy did not alter the course of disease.
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