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LETTER TO EDITOR
Year : 2017  |  Volume : 65  |  Issue : 5  |  Page : 1157-1159

Unusual presentation and temporal events in a patient with cavernous carotid aneurysm


1 Department of Neurointerventions, Medanta Hospital, Indore, Madhya Pradesh, India
2 Department of Neurology, Medanta Hospital, Indore, Madhya Pradesh, India
3 Department of Neurosurgery, Medanta Hospital, Indore, Madhya Pradesh, India

Date of Web Publication6-Sep-2017

Correspondence Address:
Swati D Chinchure
Department of Neurointerventions, Medanta Hospital, Indore - 152 001, Madhya Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/neuroindia.NI_118_17

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How to cite this article:
Chinchure SD, Kataria V, Lekhara OP, Awashi R, Mathur A, Kachhara R. Unusual presentation and temporal events in a patient with cavernous carotid aneurysm. Neurol India 2017;65:1157-9

How to cite this URL:
Chinchure SD, Kataria V, Lekhara OP, Awashi R, Mathur A, Kachhara R. Unusual presentation and temporal events in a patient with cavernous carotid aneurysm. Neurol India [serial online] 2017 [cited 2019 Sep 16];65:1157-9. Available from: http://www.neurologyindia.com/text.asp?2017/65/5/1157/214032


Sir,

A 48-year old lady presented after 10 hours of acute-onset left hemiparesis; computed tomography (CT) of the brain showed an acute right middle cerebral artery (MCA) territory infarct. It also showed a hyperdense lesion in the right cavernous sinus causing adjoining bony erosions suggestive of a cavernous carotid aneurysm (CCA). The patient was managed conservatively for stroke. On postictal day 3, she showed neurological deterioration and an increase in mass effect for which an urgent decompressive craniectomy was performed [Figure 1]a and [Figure 1]b. On postoperative day 2, the patient developed an acute-onset, right retrorbital pain, chemosis, and proptosis. The ophthalmic symptoms were rapidly progressing. She also had an audible pulsatile bruit. With a clinical diagnosis of a carotid cavernous fistula (CCF), a cerebral catheter angiography was performed, which confirmed the diagnosis. There was a high-flow carotid cavernous arteriovenous fistulous communication from the right CCA and complete occlusion of the distal internal carotid artery (ICA). There was suggestion of a partial thrombus within the aneurysm (filling defects in [Figure 1]c. After a detailed counselling, the patient underwent coil embolization for the CCF and ICA trapping [Figure 1]d and [Figure 1]e. Selective injection of the left ICA showed a good cross circulation across the anterior communicating artery with filling of the right anterior cerebral artery (ACA). There was a complete and persistent occlusion of the right middle cerebral artery (MCA) [Figure 1]f. The procedure was uneventful. The patient showed good and rapid ophthalmological recovery in the next 2 days with complete reversal of symptoms of orbital chemosis and proptosis, and resolution of the retro-orbital pain.
Figure 1: CT scan of the brain (a and b) shows a large right MCA infarct with evidence of a frontoparietal decompressive craniectomy. A focal hyperdense lesion is also seen in the right cavernous sinus with bony erosion (b). Cerebral catheter angiography (c) shows a high flow carotid cavernous fistula with a cavernous ICA aneurysm. No antegrade flow is seen in the right supraclinoid ICA. A microcatheter is visualized entering the cavernous sinus through the rent (d). Complete occlusion of the fistula and a right ICA trapping was done (e). Selective injection of the left ICA showed flow through the anterior communicating artery into the right ACA with complete and persistent occlusion of the right MCA (f). Diagrammatic representation of the chronology of symptoms (g-j)

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The natural history and clinical presentation in a case of CCA are largely different from other intracranial aneurysms, ranging from spontaneous remission to gradual progressive symptoms, to a sudden rupture. The most common presentation of a CCA is diplopia (due to cranial nerve palsies either of an isolated or a combined type) followed by pain.[1] Other rare presentations of a CCF include progressive visual loss, cerebral embolic infarcts, epistaxis, and subarachnoid hemorrhage (the latter occurs if the aneurysm extends intradurally).[1],[2] A CCA may also be discovered incidentally. Our patient presented with an unusual chronology of symptoms – an acute stroke followed by aneurysmal rupture leading to CCF.

Thromboembolic events from a developing thrombus and an acute thrombosis within a CCA have been reported in up to 2% of asymptomatic and untreated CCAs.[1] In a series by Rosi et al.,[3] cerebral infarcts were identified in 13% patients as an initial presentation. Among the 48 CCAs reported by Bawinzski et al.,[4] 2 patients presented with CCF and two had transient ischemic attacks. The incidence of ruptured cavernous sinus aneurysms resulting in a CCF is reported to be around 1.5%.[5] Stiebel-Kalish et al.,[1] reported a review of 206 CCAs, discussing their presentations and endovascular management. In their study, the first presentation in 12 patients was a spontaneous CCF and 2 patients presented with stroke as the initial symptom. None of these 12 patients having a CCF experienced symptoms before the rupture of the cavernous aneurysm. In a series by Rooji et al.,[5] the occurrence of a CCF was the presenting feature in 24.4% of the treated symptomatic cavernous sinus aneurysms. None of these 10 patients of CCF experienced symptoms before the rupture of the cavernous sinus aneurysm.

Our case is unique and first to be reported in the literature in its presentation as stroke followed by aneurysmal rupture, leading to the development of a CCF. We propose that there was a spontaneous new thrombosis/previous thrombus within the cavernous aneurysm that migrated distally causing complete occlusion of the right supraclinoid ICA and the right MCA [Figure 1]g and [Figure 1]h clinically presenting as stroke. Due to the complete distal ICA occlusion, outflow from the aneurysm was blocked. This led to progressive increase in the intra-aneurysmal pressure [Figure 1]i, which resulted in aneurysmal rupture in the adjoining cavernous sinus, causing the CCF formation [Figure 1]j. Distal ICA was completely thrombosed whereas the cavernous aneurysm and its inflow were still patent, which led to the formation of CCF in our case.

The present indications for treating a cavernous ICA aneurysm are worsening of ophthalmoplegia, intractable pain, radiological evidence of adjoining bony erosions, extension of hemorrhage into the subarachnoid space, and acute thrombosis.[3] Based on this case, we insist that consideration should also be given to the presence of an intra-aneurysmal thrombus as one of the indications for treating these aneurysms.

The treatment options for a direct CCF include coil embolization either via the transarterial route through the ICA, via the transvenous coiling, by embolization using detachable balloons, and by stent graft placement.[6],[7],[8] In our case, as the supraclinoid ICA was already completely occluded by the thrombus, we did not worry about the ICA patency and, therefore, the proximal ICA was trapped using coils. If the distal ICA had not been occluded and there had not been a good cross circulation across the anterior communicating artery, then a reconstructive approach (such as stent-assisted coiling) to preserve the ICA would have been the treatment of choice. Early diagnosis and treatment resulted in complete and prompt ophthalmological recovery; however, the patient had persistent hemiparesis secondary to the MCA infarct.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Stiebel-Kalish H, Kalish Y, Bar-On RH, Setton A, Niimi Y, Berenstein A, et al. Presentation, natural history, and management of carotid cavernous aneurysms. Neurosurgery 2005;57:850-7.  Back to cited text no. 1
[PUBMED]    
2.
Linskey M, Shekhar L, Hirsch W, Yonas H, Horton J. Aneurysms of the intracavernous carotid artery: Natural history and indications for treatment. Neurosurgery 1990;26:933-8.  Back to cited text no. 2
    
3.
Rosi Junior J, Welling LC, Yeng LT, Caldas JG, Schafranski M, Teixeira MJ, et al. Cavernous carotid artery aneurysms: Epidemiology, natural history, diagnostic and treatment. An experience of a single institution. Clin Neurol Neurosurg 2014;125:32-5.  Back to cited text no. 3
[PUBMED]    
4.
Bavinzski G, Killer M, Ferraz-Leite H, Gruber A, Gross CE, Richling B. Endovascular therapy of idiopathic cavernous aneurysms over 11 years. AJNR Am J Neuroradiol 1998;19:559-65.  Back to cited text no. 4
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5.
Van Rooij WJ, Sluzewski M, Beute GN. Ruptured cavernous sinus aneurysms causing carotid cavernous fistula: Incidence, clinical presentation, treatment, and outcome. AJNR Am J Neuroradiol 2006;27:185-9.  Back to cited text no. 5
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6.
Kalyanpur TM, Narsinghpura K, Yadav M, Mehta P, Paul K, Cherian M. Covered coronary stent grafts as a treatment option for carotid-cavernous fistulas: Our initial experience. Neurol India 2011;59:895-8.  Back to cited text no. 6
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7.
Li L, Cui JG, Liang ZH, Xu SB, Li J, Tian HQ, et al. Brief report: Transvenous treatment of complex cavernous dural arteriovenous fistulae with Onyx and coils. Neurol India 2011;59:92-6.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Chen Z, Zhu G, Feng H, Liu Z. Worsening of cavernous sinus dural arteriovenous fistula with incomplete superior ophthalmic thrombosis after palliative transarterial embolization. Neurol India 2007;55:390-2.  Back to cited text no. 8
[PUBMED]  [Full text]  


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