Onyx embolization of carotid-cavernous fistulas

Abstract

The authors conducted a study to determine the safety and efficacy of embolization of carotid-cavernous fistulas (CCFs) with the ethylene vinyl alcohol copolymer, Onyx. They prospectively collected data in all patients with CCFs who underwent Onyx-based embolization at their institution over a 3-year period. The type of fistula, route of embolization, viscosity of Onyx, additional use of coils, extent of embolization, procedural complications, and clinical follow-up were recorded. A total of 12 patients (5 men and 7 women who were age 24-88 years) underwent embolization in which Onyx was used. There were 1 Barrow Type A, 1 Type B, 3 Type C, and 7 Type D fistulas. Embolization was performed via a transvenous route in 8 cases and a transarterial route in 4 cases. Onyx 34 was used in all but 2 cases: a direct Type A fistula embolized with Onyx 500 and an indirect Type C fistula embolized with Onyx 18. Adjuvant embolization with framing coils was performed in 7 cases. All procedures were completed in a single session. Immediate fistula obliteration was achieved in all cases. Clinical resolution of presenting symptoms occurred in 100% of the patients by 2 months. Neurological complications occurred in 3 patients. One patient developed a complete cranial nerve (CN) VII palsy that has not resolved. Two patients developed transient neuropathies--1 a Horner syndrome and partial CN VI palsy, and 1 a complete CN III and partial CN V palsy. Radiographic follow-up (mean 16 months, range 4-35 months) was available in 6 patients with complete resolution of the lesion in all. Onyx is a liquid embolic agent that is effective in the treatment of CCFs but not without hazards. Postembolization cavernous sinus thrombosis and swelling may result in transient compressive cranial neuropathies. The inherent gradual polymerization properties of Onyx allow for casting of the cavernous sinus but may potentially result in deep penetration within arterial collaterals that can cause CN ischemia/infarction. Although not proven, the angiotoxic effects of dimethyl sulfoxide may also play a role in postembolization CN deficits.