May the Inferior Petrosal Sinus Recanalization During Endovascular Treatment for Carotid-Cavernous Fistulas Increase the Risk of Sixth Nerve Palsy?

BACKGROUND: Sixth nerve palsy is a common complication of endovascular treatment for carotid-cavernous fistulas (CCF). Two hypotheses are evoked: the spontaneous venous congestion into the cavernous sinus and the direct compression of the nerve by the embolic agent into the cavernous sinus. Nevertheless, the evidence is still uncertain. Knowing the vicinity of the sixth nerve with the inferior petrosal sinus (IPS) in the Dorello canal, we hypothesized that the recanalization of the IPS increased the risk of nerve damage. METHODS: We analyzed a prospective database of patients treated for CCFs from March 2009 to April 2016. We excluded patients who did not need treatment, cases of high-flow CCF, and patients lost to follow-up, obtaining a homogeneous population of 82 patients with indirect CCFs. This population was divided in 2 groups: patients without new-onset/worsening of sixth nerve palsy and patients with this postprocedural complication. RESULTS: Our main endpoints were the potential differences between patients with or without recanalization of IPS and between those who underwent or not an embolization with Onyx-18. We did not find any statistically meaningful difference between the 2 groups concerning the necessity of IPS recanalization (P > 0.999, odds ratio 0.97, 95% confidence interval 0.32-2.96) or with the use of Onyx-18 as an embolic agent (P = 0.56; odds ratio 1.41, 95% confidence interval 0.41-2.45). CONCLUSIONS: The recanalization of a thrombosed IPS does not increase the risk of procedural sixth nerve damage. The initial injury seems to relate with development/worsening of a sixth nerve palsy.

Thrombosis of venous outflows of the cavernous sinus: possible aetiology of the cortical venous reflux in case of indirect carotid-cavernous fistulas.

BACKGROUND: The presence of a cortical venous reflux (CVR) in a carotid-cavernous fistula (CCF) is well described and is considered to be a criterion for urgent treatment. This reflux is often associated with direct/traumatic CCF and the high-flow of the fistula alone explains the reflux. For indirect CCF, the pathophysiology of a CVR is unclear. METHODS: All patients treated endovascularly for an indirect CCF with a cortical venous reflux between 2003 and 2015 were included. We retrospectively analysed data focusing on whether venous outflows of the cavernous sinus would opacify or not with the local injection of contrast, in order to locate those that could explain the venous reflux. RESULTS: Twenty consecutive patients (male/female ratio, 2/3) were included in this series with a mean age of 63 years. All patients presented ocular signs and no patients showed any neurological sign secondary to the CVR. We distinguished four patterns of CVR: in the superficial middle cerebral vein (75%), in the uncal vein (15%), in the superior petrosal vein (5%) and in the inferior petrosal vein (5%). Seventy percent of the cases presented a lack of opacification in more than three venous outflows of the CS involved. Each patient received an endovascular therapy by venous approach with a success rate of 76.9% per embolisation session. Two patients (10%) presented a permanent ocular paresis and two others a transient deficit. CONCLUSIONS: CVR is directly correlated with the thrombosis of multiple venous outflows of the CS. The "non-opacification" of at least three of the CS venous outflows is necessary for the development of CVR. Such thrombosis may be explained by the combination of haemodynamic and inflammatory changes of the venous wall.