Abstract
Carotid–cavernous fistulas (CCF) are a specific type of dural arteriovenous fistula and have abnormal communications between the arterial system and the venous cavernous sinus at the wall of the cavernous sinus. The cavernous sinus (CS) is different from other venous sinuses according to its location and structure. It is situated outside of the dura, but other dural sinuses are located between two dural walls. It is where an artery is completely surrounded by a venous structure. There are various cranial nerves in the CS. It has rich communications with the other sinuses and veins, with the transverse and sigmoid sinuses through the superior and inferior petrosal sinuses, with the cerebral cortical veins through the sphenoparietal sinus and with pterygoid plexus, and with the facial veins through the superior and inferior ophthalmic veins. CCF can demonstrate wide-range clinical presentations according to these communications, like ophthalmic signs and symptoms (proptosis, chemosis, and visual loss); cranial nerve pareses; bleeding from the mouth, nose, or ears; and intracranial hemorrhage. High-pressure arterial blood moves directly into the cavernous sinus and ophthalmic veins, leads to venous hypertensions after CCF, and causes the sign and symptoms above. CCFs are classified as direct and indirect based on etiology and pathophysiology. Direct CCFs may occur following a traumatic tear in the cavernous segment of the internal carotid artery (ICA) or aneurysmic rupture within this segment. Direct CCFs account for 70–80% of all cases. Indirect CCFs occur spontaneously and are abnormal communications between the smaller meningeal arterial branches of the internal or external carotid system and cavernous sinus. Indirect CCFs account for 20% of all cases.
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