35 Carotid-Cavernous Fistula Embolization

10.1055/b-0040-175282

35 Carotid-Cavernous Fistula Embolization

Stephan A. Munich, Giuseppe Lanzino, and Leonardo Rangel-Castilla

General Description

Carotid cavernous fistulas (CCFs) are characterized by an abnormal connection between the internal carotid artery (ICA) or external carotid artery (ECA) and the cavernous sinus. Most broadly, they can be divided into direct or indirect types. Direct CCFs are formed when a hole in the cavernous segment of the ICA results in a direct connection with the cavernous sinus (Barrow type A classification of CCFs), as is seen when a cavernous ICA aneurysm ruptures. Indirect CCFs are characterized by abnormal shunting to the cavernous sinus from a dural or meningeal branch of the ICA (Barrow type B), a dural or meningeal branch of the ECA (Barrow type C), or dural or meningeal branches from both the ICA and ECA (Barrow type D).

Evidence

Spontaneous occlusion of indirect CCFs may occur in 20%–60% of patients. Manual compression of the ipsilateral carotid artery results in similar rates of occlusion for indirect CCFs but results in occlusion of only 17% of direct CCFs.

Since detachable balloons were removed from the market, endovascular treatment of CCFs has consisted of coiling or liquid embolic occlusion. In most series, the success of these techniques is > 85% with < 10% morbidity. However, it is not uncommon for patients to experience an immediate post-procedure worsening of symptoms, followed by long-term resolution.

Indications

Indirect fistulas are low flow and may thrombose spontaneously or with carotid compression. However, most physicians recommend treatment of these lesions to avoid potential visual symptoms. Direct CCFs require intervention because they are high-flow lesions and will not thrombose spontaneously.

Urgent intervention for any CCF is necessary under the following circumstances:

Elevated intraocular pressure (> 25 cm H₂O).
Impaired visual acuity.
Elevated intracranial pressure with cortical venous hypertension.

Although indirect CCFs may thrombose without treatment, spontaneous resolution of visual symptoms or increased intraocular pressure warrants investigation with angiography. Either of these findings may represent thrombosis of the superior ophthalmic vein (SOV) and development of retrograde cortical venous drainage, which increases risk of hemorrhage.

Neuroendovascular Anatomy

As previously mentioned, the Barrow classification of CCFs is based on their arterial anatomy (see General Description). The clinical presentation is much more affected by the venous anatomy. Drainage of the fistula through the SOV results in venous hypertension within the orbit, leading to the typical visual complaints experienced by these patients. However, when the SOV is thrombosed or severely engorged, venous drainage may occur retrogradely through cortical veins, increasing intracranial pressure and putting patients at risk for hemorrhage.

The venous anatomy associated with the cavernous sinus also has relevance for treatment strategies. Transvenous embolization is the method of choice for indirect fistulas ( Fig. 35.1, Video 35.1 ). The preferred transvenous route of access to the cavernous sinus is the inferior petrosal sinus (IPS) ( Fig. 35.2, Video 35.2 ). Alternative venous conduits to the cavernous sinus include the contralateral IPS, facial vein, superior petrosal sinus, and SOV.

Periprocedure Medications

We routinely administer systemic heparin to an activated coagulation time of 250–300 s. If transarterial treatment is pursued with a stent (e.g., flow-diverting stent), dual antiplatelet therapy is administered. For elective cases, aspirin (325 mg) and clopidogrel (75 mg) are administered daily for 5–7 days before the procedure. For emergent cases, loading doses are administered before the procedure (aspirin 650 mg and clopidogrel 600 mg).

Post-procedure cranial nerve palsies may occur following embolization or packing of the cavernous sinus. Ophthalmoplegia has been reported in the literature to occur in 2%–5% of patients. In cases in which this occurs, we typically administer a short course of dexamethasone.

Specific Technique and Key Steps

Transarterial Route

Identification of the direct fistula. Transarterial embolization carries significant risk in Barrow types B–D CCFs because of the risk of embolic reflux into the ICA ( Fig. 35.1, Video 35.1 ).
Placement of guide catheter in the distal cervical ICA. The inner diameter of the guide catheter should be large enough to accommodate two microcatheter systems.
Identification of the fistulous point. The inflation of a balloon within the ICA and a microinjection may help to identify the exact location of the fistulous point.
Microcatheterization through the fistulous point into the cavernous sinus ( Fig. 35.1, 35.2, Video 35.1, 35.2 ).
Injection of liquid embolic or deployment of coils into the cavernous sinus. This should begin as deep into the cavernous sinus (as far away from the fistulous point) as possible.
During injection of liquid embolic or deployment of coils, a balloon can be inflated within the ICA to protect it ( Fig. 35.2, Video 35.2 ).

Transvenous Route

Transfemoral venous and arterial access. Arterial access is needed to help identify the site of the fistula and to confirm obliteration following embolization.
Navigation through the heart and into the internal jugular vein with a guide catheter.
Microcatheterization of the IPS. The IPS can often be catheterized even when it does not opacify with contrast injections.
Injection of liquid embolic or deployment of coils into the cavernous sinus ( Fig. 35.2, Video 35.2 ).