Indirect carotid-cavernous sinus fistulas (CCFs) are defined as low-flow communication between the cavernous sinus and cavernous artery branches arising from the internal carotid artery (ICA) and/or the external carotid artery (ECA). Transvenous endovascular embolization is the standard approach to treating these CCFs. As with all transvenous embolization strategies for CCFs, a microcatheter must be positioned within the cavernous sinus. Access to the cavernous sinus depends on the angioarchitecture of each patient. In general, the inferior petrosal sinus is the preferred and most commonly used endovascular route to the cavernous sinus; however, if this route is not available, other endovascular access routes such as the facial vein, superior petrosal sinus, superficial middle cerebral vein or pterygoid plexus can be considered. Suppose purely endovascular approaches are not feasible or technically limited. In that case, access to the cavernous sinus can be gained by direct puncture (mainly direct puncture of the ophthalmic veins or the cavernous sinus) or by direct surgical strategies (mainly exposure of the ophthalmic, facial or Sylvian veins). Here we present our experience with a 32-year-old woman who suffered from mental retardation but had an otherwise unremarkable medical history. She presented to the emergency department with a right “red eye” and orbital discomfort that had developed over the previous 6 months. Consultant ophthalmologists treated her with topical solutions and creams containing various steroids and antibiotics. Two days prior to admission, her parents noticed a sudden protrusion of the “swollen eye” and took the patient to the emergency department. On admission, the patient had a painful, disfiguring proptosis of the right eye with marked conjunctival hyperemia and chemosis. Ophthalmological and neurological examinations revealed blurred vision in the right eye, strabismus and diplopia, and exposure keratopathy secondary to the proptosis. Elevated intraocular pressure (38 mmHg) was confirmed. Careful auscultation revealed no orbital bruit. Color Doppler confirmed flow reversal in the superior ophthalmic vein. Head CT, MRI, and MR angiography (MRA) suggested a diagnosis of low-flow dural-type CCF based on the proptosis, enlargement of the superior ophthalmic vein, bulging cavernous sinus, and rich dural rete in the right cavernous sinus. A diagnostic angiogram of the right ECA revealed an indirect CCF supplied by the dural branches of the ECA and draining predominantly through the superior ophthalmic vein via the angular, anterior facial, common facial, and internal jugular veins (Barrow type C CCF: dural shunts between the meningeal branches of the external carotid artery and the cavernous sinus). The anterior facial vein showed a remarkably tortuous course. The patient underwent endovascular embolization of the CCF via transfacial, superior ophthalmic vein, and cavernous sinus embolization using coils and Onyx. The procedure’s success was based on robust proximal support that allowed easy microcatheter navigation through a tortuous facial venous complex. Diagnostic angiography immediately after embolization confirmed complete disconnection of the arteriovenous shunt. The patient progressed satisfactorily with progressive improvement of her ophthalmic signs and symptoms and was discharged after an ophthalmic evaluation confirmed the resolution of blurred vision with normal intraocular pressure (18 mmHg) 3 days after the procedure. Follow-up angiography at 3 months showed no evidence of the CCF. This case illustrates the embolization of a dural CCF via a transvenous facial-ophthalmic approach and discusses relevant anatomical and technical concepts required for this transvenous embolization approach.