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Carotid Cavernous Fistula
Laura S Gilmore, MDDepartment of Ophthalmology
TTUHSCFebruary 13, 2004
Discussant: Kenn Freedman, MD
Case Presentation
• 26yo AAM s/p MVA • CHI, L zygoma fracture• Consulted for proptotic, red OS• CT: proptosis OS. No basilar skull
fracture. no retrobulbar hematoma, no superior ophthalmic vein enlargement, no ocular muscle enlargement
Differential Diagnosis
Cavernous Sinus Thrombosis• Retrobulbar Hematoma• Unrecognized intra-orbital FB, with
possible cellulitis• Carotid Cavernous Sinus Fistula• Tumor
Physical Exam
• General: sedated, intubated• Lids: edematous, margins intact• Pupils: 2.5mm->2mm, 7->NR• Conj: chemosis, OS>OD; SCH OS• IOP: 16, 28• Cornea 2+ edema OS, clear OD• + gross proptosis OS• + bruit OS on auscultation, no neck bruit• DFE: discs flat with sharp edges, vessels
normal, retina flat OU
MRI of CC Fistula
Carotid Cavernous Fistula
• Abnormal communication between previously normal carotid artery and cavernous sinus
• Characterized as:-Direct vs. Indirect-High vs. Low Flow-Traumatic vs. Spontaneous
Types of CC Fistula
Mechanisms of CCSF
• Trauma• Spontaneous causes:
– rupture of intracavernous aneurysms– neurofibromatosis– atherosclerotic disease– collagen vascular disease
• Iatrogenic
Direct Carotid Cavernous Fistula
• Arterial blood passes directly through a defect in the wall of intracavernous portion of ICA
• Blood in vein becomes arterialized• Venous pressure increases• Arterial pressure and perfusion
decreases
Signs of Direct CCSF• Ptosis• Very red, chemotic conj• Increased IOP from increased
episcleral venous pressure• Anterior segment ischemia in 20%
– Corneal edema, cell/flare, iris atrophy, rubeosis, cataract
• Proptosis is pulsatile• Bruit and thrill• Muscle palsies• Visual loss
Etiologies of Direct CCSF• From trauma in 75% of all cases
– Basal skull fracture tears ICA within cavernous sinus
– Traumatic fistulae-high flow rates, sudden and dramatic onset of symptoms
• Spontaneous rupture of aneurysm or atherosclerotic artery in 25%– Post-menopausal, hypertensive females– Lower flow rates, less severe symptoms
Mechanisms of Traumatic CCSF
• direct injury from basilar skull fracture
• injury from torsion or stretching of the carotid siphon upon impact
• impingement of the vessel on bony prominences
Indirect Carotid Cavernous Fistula
• Fistulous connection is within the wall of the cavernous sinus
• Tend to be low-flow• Small meningeal arteries supplying dural
wall of cavernous sinus can rupture spontaneously, while ICA itself remains intact
• Insidious onset, mild orbital congestion, proptosis, low or no bruit
• Lesions may fluctuate, and may resolve spontaneously
Clinical Presentation of CCSF• Ophthalmic consequences of CCSF are
caused by compression and ischemia related to increased venous pressure and reduced arterial pressure– flow reversal leads to engorged
ophthalmic veins causing proptosis, conjunctival injection, chemosis.
– Patients complain of retro-orbital headache, or a bruit. Facial pain with V1 and V2 involvement
Clinical Presentation of CCSF
• Other manifestations:– congestion of the opposite orbit– diplopia– ptosis, mydriasis– corneal ulceration– loss of visual acuity– transient neurological deficits– subarachnoid hemorrhage
Radiological Evaluation of CCSF
• Angiography is the definitive diagnostic examination
• CT and MRI may show– Enlarged superior ophthalmic vein– Enlarged muscles– Enlarged cavernous sinus with a
convex shape to the lateral wall
Treatment of CCSF• Most are not life-threatening
– Only involved eye is at risk typically• Main indicators for treatment
– Glaucoma– Diplopia– Intolerable bruit or HA– Severe proptosis causing exposure
keratopathy– Spontaneous closure from thrombosis
of cavernous sinus is unlikely (as in trauma, high-flow)
Treatment of CCS Fistulas
• 99% of treatment is done by interventional neuroradiologists– Intravascular approach-placement of
thrombogenic materials, eg coils
• Other therapies include:– carotid artery ligation– surgical exposure with clipping of the
fistula
Summary
• Direct CCSF usually results from trauma
• Patients typically present with proptosis, conjunctival injection, and a bruit
• Angiography when pt stable• Transarterial embolization