Spontaneous Occlusion of a Bilateral Post Traumatic Carotid Cavernous Fistula

Churojana, Anchalee; Chawalaparit, O.; Chiewwit, P.; Suthipongchai, Suthisak

doi:10.1177/159101990100700311

Cited by 11 publications

(17 citation statements)

References 12 publications

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“…In rare instances, treatment requires direct endovascular access of the superior ophthalmic vein, using an upper eyelid cut-down technique. Few documented cases of spontaneous resolution of type A fistulas are reported in the literature, varying anywhere from a few days to 6 months [9,10,11,12,13,14,15,16]. The exact mechanism of this process is not known.…”

Section: Discussionmentioning

confidence: 99%

Spontaneous Resolution of Post-Traumatic Direct Carotid-Cavernous Fistula

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Spontaneous Resolution of Post-Traumatic Direct Carotid-Cavernous Fistula

et al. 2017

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“…The cause of superior petrosal sinus occlusion in TCCF remains unclear. Since spontaneous occlusion of a bilateral TCCF and spontaneous thrombosis of CCF following failed transarterial balloon occlusion have been reported (17,18), we speculate that stasis of venous flow and loss of venous pressure in TCCF may lead to stasis of blood flow in the superior petrosal sinus. Similar conditions have been reported in carotid-cavernous dural arteriovenous fistula (19,20) and in the ophthalmic vein following TCCF (21); therefore, thrombus formation due to stasis of the venous flow likely contributes to occlusion of the superior petrosal sinus in TCCF.…”

Section: Discussionmentioning

confidence: 86%

Brainstem edema caused by traumatic carotid-cavernous fistula: A case report and review of the literature

Guo

Zhao

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Brainstem edema caused by traumatic carotid-cavernous fistula (TCCF) is rare, and there is little information available regarding its clinical characteristics. The present report describes the case of a 51-year-old man with TCCF, who presented with right exophthalmos and intracranial bruit for 1 week. One month prior to admission at hospital, he fractured the frontal and ethmoid sinuses. Digital subtraction angiography confirmed the diagnosis of TCCF, and magnetic resonance imaging (MRI) suggested edema on the right side of the pons. Five days after admission, the patient exhibited left hemiparesis, and MRI revealed aggravation of the brainstem edema. Following treatment with transarterial balloon embolization, the clinical symptoms, including hemiparesis, were relieved; at the 1-month follow-up, the brain edema had disappeared. The patient was normal at the 6-month follow-up. Following the report of the present case, we reviewed six additional cases previously reported in the literature and discussed the potential mechanisms of TCCF-associated brainstem edema. We conclude that occlusion of the superior petrosal sinus may contribute to brainstem edema caused by TCCF. Relief of the brainstem edema and brainstem edema-associated clinical symptoms can be achieved with transarterial coil or balloon embolization of the TCCF to reduce the drainage pressure in the brainstem veins.

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“…SOVT is seen in patients with flow alterations in the orbital vascular system, such as in dural arteriovenous fistulae in the direct vicinity of the cavernous sinus. [1][2][3][4][5] Facial trauma is another aseptic cause of SOVT, reported in literature. [6][7][8] Systemic diseases reporting SOVT in literature include Graves' Orbitopathy, systemic lupus erythematosus, and ulcerative colitis.…”

Section: Discussionmentioning

confidence: 99%