Cavernous Carotid Fistulas (CCFs) represent abnormal arteriovenous communication between the cavernous sinus and the carotid arterial system (internal and external carotid arteries) [1-3]. They can be characterized by high or low flow, direct or indirect (dural), traumatic or spontaneous. The clinical manifestations can vary according to the type of FCC and the venous drainage pattern [1-4].
Barrow classification categorizes the CFF into direct (type A) and indirect (types B, C and D) types. Type A is a direct high-flow shunt between the internal carotid artery and the cavernous sinus. Type B is a dural shunt between meningeal branches of the internal carotid artery and the cavernous sinus. Type C is a dural shunt between meningeal branches of the external carotid artery and the cavernous sinus. Type D is a dural shunt between meningeal branches of the internal and external carotid arteries and the cavernous sinus [5].
Direct FCCs have a rapid flow. They are more common in young men, frequently caused by traumatic insult, by rupture of an internal carotid artery aneurysm within the cavernous sinus, associated with an underlying connective tissue disorder (Ehlers-Danlos syndrome type IV), or iatrogenic intervention [1-4].
Indirect FCCs usually have a low flow and are more common in middle-aged women, with 25% of these fistulas being spontaneous; other causes include hypertension, fibromuscular dysplasia, Ehlers-Danlos type IV, and dissection of the internal carotid artery [1-3].
The FCCs symptoms are related to size, duration, location, presence of venous or arterial collaterals, and venous drainage. They include headache, intracranial haemorrhages (subarachnoid and subdural), cephalic bruit, trigeminal nerve dysfunction and epistaxis, resulting from venous hypertension in the dura mater sinuses. The most frequent ocular signs and symptoms are exophthalmos, proptosis, conjunctival chemosis (red eye), ophthalmoplegia, ocular pain, increased intraocular pressure and decreased visual acuity, resulting from the reversal of blood flow to the ophthalmic veins due to overload and dilation of the cavernous sinus [3-6].
Treatment depends on flow velocity through the fistula, arterial supply, and venous drainage routes. Endovascular intervention or stereotactic radiosurgery can be performed when invasive treatment is necessary. Modern endovascular techniques offer the ability to treat CCF with low morbidity successfully [7,8].
In this case report, we aimed to describe a case report of high-flow complex indirect FCC that underwent endovascular treatment via transarterial and transvenous.
Click and see the full case report