bubble_chart Overview

Traumatic carotid-cavernous sinus fistula refers to the rupture of the internal carotid artery or its branches within the cavernous sinus due to trauma, leading to direct communication with venous structures and the formation of an arteriovenous fistula. The primary cause is often skull base fractures, with an incidence of approximately 2.5% in traumatic brain injuries. Since the cavernous segment of the internal carotid artery is firmly anchored by the dura mater at its entry and exit points, fractures traversing the middle cranial fossa or extending near the sella turcica can tear this segment of the artery or its branches. Occasionally, the injury may result from fracture fragments, penetrating wounds, or projectiles. Statistics indicate that over 75% of carotid-cavernous sinus fistulas are trauma-related. The damaged artery may rupture immediately or experience delayed rupture, resulting in variable intervals between the injury and the onset of arteriovenous fistula symptoms—ranging from immediate manifestation to delays of days or weeks. Often, there is an asymptomatic interval before symptoms appear.

bubble_chart Clinical Manifestations

When the internal carotid artery is ruptured into the cavernous sinus, not only does the blood from the damaged carotid artery directly flow into the venous system, forming a short-circuit circulation that causes dilation of all veins draining into the cavernous sinus, but also due to the stealing of blood at the fistula, the branches of the internal carotid artery experience reversed blood flow, leading to ischemia in the related brain regions. In severe cases, this can result in brain dysfunction and increased intracranial pressure, or even compensatory cardiac enlargement due to the large shunt of the arteriovenous fistula. Sometimes, bleeding through the fracture lines of the skull base into the sphenoid sinus can cause fatal massive epistaxis. If bleeding enters the subarachnoid space, it can lead to acute intracranial hypertension, ultimately causing brain herniation and death.

The typical initial symptom of an internal carotid artery-cavernous sinus fistula is often a continuous bruit heard by the patient themselves, which intensifies with cardiac contraction, disturbing them day and night and making it difficult to rest. Due to the obstruction of venous return in the ophthalmic vein, sphenoparietal sinus, lateral fissure, and basal veins, within 24 hours after the injury, the affected eye may exhibit conjunctival congestion, edema, ectropion, and proptosis accompanied by pulsations synchronized with the heartbeat. At this time, auscultation over the affected orbit, temporal fossa, and forehead may reveal a blowing murmur and a palpable thrill. Approximately 70% of patients experience restricted eye movement, particularly due to involvement of the abducens and oculomotor nerves, which can cause diplopia. In severe cases, it may lead to conjunctivitis, corneal ulceration, glaucoma due to eyeball compression, optic nerve atrophy, and even blindness. Occasionally, patients may exhibit symptoms of the ophthalmic branch of the trigeminal nerve, such as pain in the forehead, temple, or orbit on the affected side, sensory disturbances in the forehead skin, and weakened corneal reflexes. Additionally, in some patients, due to the large size of the cavernous sinus and easy communication between the two sides, bilateral ocular symptoms and signs may occur.

bubble_chart Diagnosis

The diagnosis of traumatic carotid-cavernous fistula is relatively easy, but determining the type and location of the fistula is not straightforward. From a treatment perspective, the diagnostic objectives and requirements should also include the location and size of the fistula, the degree of blood stealing, the blood supply source of the fistula, the condition of the cerebral arterial circle (Willis Circle), and the direction of venous drainage, to facilitate the selection of appropriate treatment methods. Therefore, femoral artery catheterization for selective cerebral angiography is often required. In addition to angiography of the affected internal and external carotid arteries, images of the contralateral internal carotid artery and vertebral artery must also be taken while compressing the affected carotid artery to temporarily block blood flow. On the angiogram of the affected internal carotid artery, only a shadow of contrast agent in the cavernous sinus is visible, with poor filling of distal cerebral vessels, making it difficult to determine the exact location of the fistula. However, vertebral artery angiography combined with compression of the affected carotid artery often clearly shows the contrast agent flowing retrograde through the posterior communicating artery and spilling out of the carotid-cavernous fistula. Angiography of the healthy internal carotid artery can also assess the integrity of the Willis Circle and estimate the compensatory capacity of cerebral circulation, helping to determine whether blood flow in the affected internal carotid artery can be safely interrupted. Additionally, selective external carotid angiography can reveal whether any branches of the internal carotid artery anastomose with the meningeal arteries, accessory meningeal arteries, or ascending pharyngeal arteries at the base of the cavernous sinus, forming an external carotid blood supply. Parkinson (1967) classified traumatic carotid-cavernous fistulas into two types: those caused by rupture of the internal carotid artery itself within the cavernous sinus, and those caused by rupture of branches of the internal carotid artery in the cavernous sinus. The latter type is often difficult to treat effectively with simple balloon embolization.

bubble_chart Treatment Measures

Traumatic carotid-cavernous fistulas have a low spontaneous healing rate of only 5–10%. Occasionally, compression of the affected carotid artery (Mata's Test) may reduce fistula blood flow and promote healing. However, the majority of cases require surgical intervention. The goals of surgery are to restore the normal physiological state of the cavernous sinus, relieve pressure in the venous system, reduce proptosis, preserve vision, eliminate bruits, and prevent cerebral ischemia. Various surgical methods exist, but simple ligation of the affected internal carotid artery in the neck has largely been abandoned. Currently, two main treatment approaches are employed: surgical embolization and endovascular embolization.

**I. Surgical Embolization Therapy** This involves craniotomy to perform fistula isolation, copper wire embolization, or direct fistula repair. Regardless of the method, preoperative Mata's training and cerebral angiography with cross-circulation assessment are essential to confirm adequate collateral circulation. Without this, internal carotid artery occlusion risks paralysis or aphasia.

1. **Isolation Embolization**: The internal carotid artery is ligated both intracranially and in the neck, isolating and closing the fistula. However, this completely blocks carotid blood flow and is only considered if collateral circulation is established and contralateral vision is intact, as the affected eye's blood supply may be compromised, risking blindness. Additionally, if other branches of the cavernous carotid artery provide collateral flow, the fistula may recur. To improve efficacy, muscle emboli may be injected via the neck to occlude the fistula. **Surgical Technique**: Under general anesthesia, the affected internal carotid artery is exposed in the neck and prepared for occlusion. A frontotemporal craniotomy is performed, the dura is opened, and cerebrospinal fluid is drained. The optic nerve is exposed along the sphenoid ridge, and the orbital roof and optic canal are partially removed to visualize the ophthalmic artery origin. During carotid occlusion, the ophthalmic artery should also be clipped to minimize retrograde flow. If venous engorgement hinders intracranial exposure, temporary carotid occlusion may facilitate the procedure. After intracranial closure, the neck is revisited. The common, internal, and external carotid arteries are temporarily occluded, and a 4mm plastic tube is inserted into the internal carotid artery. Muscle emboli are then injected to block the fistula. Finally, the tube is removed, and the carotid arteries are ligated.

2. **Copper Wire Embolization of the Cavernous Sinus Fistula**: Bare copper wire, carrying a positive charge, is inserted into the fistula via craniotomy, attracting negatively charged blood cells and fibrin to form an embolus. This method preserves carotid patency and avoids distal ischemia, making it suitable for bilateral fistulas. **Surgical Technique**: Under general anesthesia, a frontotemporal craniotomy exposes the lateral wall of the cavernous sinus. Sterilized thin copper wire (0.15–0.2mm diameter, 4–5cm long) is inserted into the sinus wall using a conductive needle. The wire is advanced ~1cm until resistance is met, then cut. Additional wires are inserted at other pulsating or bulging sites until the sinus becomes firm and pulsation ceases.

**II. Endovascular Embolization Therapy** This involves direct embolus injection or interventional neuroradiology using specialized catheters to occlude the fistula. The latter, developed in the 1970s, is the simplest and most reliable method, with a cure rate exceeding 90%. However, it requires specialized equipment and expertise, limiting widespread adoption. Two techniques are briefly described for reference: internal carotid artery embolus injection and detachable balloon embolization.

1. Internal carotid artery embolization: This involves exposing the internal carotid artery through the neck. While temporarily blocking the common carotid, internal carotid, and external carotid arteries, a small incision is made at the origin of the external carotid artery. A muscle embolus slightly smaller than the diameter of the internal carotid artery is pushed into the internal carotid artery using a dissector. The proximal end of the external carotid artery incision is then clamped, and the common carotid and internal carotid arteries are reopened, allowing the muscle embolus to be flushed to the fistula site. Repeating this process 2–3 times often seals the fistula. However, due to the risks of occluding the internal carotid artery or the embolus migrating distally, this method is now rarely used. Alternatively, a "kite-flying" technique has been employed, where a nylon monofilament is tied to the muscle embolus and a clip is attached as a marker. After placing the embolus into the internal carotid artery, its position is adjusted under fluoroscopic guidance via X-ray until satisfactory. The nylon thread is then secured to the soft tissue outside the vessel, and the external carotid artery incision and neck incision are sutured as usual.

2. Detachable balloon embolization: Through retrograde catheterization of the femoral artery, a specially designed microcatheter is inserted into the affected internal carotid artery under fluoroscopic guidance. Then, a suitable detachable balloon catheter is selected and advanced through the microcatheter to the fistula site. A small amount of contrast agent is injected to partially inflate the balloon, allowing blood flow to carry the balloon out of the fistula. Once the balloon is confirmed to be in the cavernous sinus, it is slowly filled with isotonic iodinated contrast agent until the bruit disappears, the cavernous sinus is no longer visualized, and the internal carotid artery blood flow remains unobstructed. Finally, the balloon microcatheter is gently and continuously pulled to detach the balloon from the Teflon catheter. After the procedure, the catheter is withdrawn, and the puncture site is compressed for 10-20 minutes to prevent local hematoma formation.