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Abstract #6082 Published in IGR 2-2
Ultrasound biomicroscope findings in carotid-cavernous fistula
Jackson DW; Lee AG; Gross RLJournal of Glaucoma 2000; 9: 340-342
This paper describes a 65-year-old white man who presented in 1998 with redness of the right eye, binocular diplopia and ipsilateral eyelid edema. His visual acuity was optimal in both eyes. The Hertel exophthalmometer showed a 3-mm increase in the right eye over the left eye. The visual fields were normal. Eye movements were somewhat restricted in the right eye. There was no orbital or carotid bruit. There were engorged, dilated and tortuous episcleral and conjunctival blood vessels. Intraocular pressure was 15 mmHg in both eyes. Ophthalmoscopy showed tortuous retinal veins in the right eye. No optic disc edema. MRI showed mild proptosis and ipsilateral engorgement of the cavernous sinus and enlargement of the superior ophthalmic vein. Cerebral angiography showed a slow flow of the right internal carotid artery, presumed atherosclerotic carotid cavernous fistula between multiple small dural branches of the internal carotid artery and the right cavernous sinus. Endovascular embolization was not considered. The situation worsened after the angiography with a rise of intraocular pressure to 24 mmHg. The anterior chamber became shallow. The deterioration was thought to be caused by spontaneous thrombosis of the carotid-cavernous-fistula. The increased intraocular pressure was treated with latanoprost. Several months later there was another deterioration of the situation with worsening edema, proptosis and an intraocular pressure of 38 mmHg. On gonioscopy, there was progressive narrowing of the angle. On brimonidine treatment, the pressure went down to 15 mmHg. Ultrasound biomicroscopy showed anterior rotation of the ciliary body and narrowing of the angle with a small choroidal effusion. Visual acuity was further decreased and this was thought to be due to macular edema. A venous stasis retinopathy was also seen. Repeated cerebral angiography showed interval obliteration and presumed thrombosis of the previously noted dural feeders to the carotid-cavernous-fistula. The deterioration was thought to be due to the venous outflow obstruction. In cases of carotid-cavernous-fistulae the abnormal arterial blood flow in the venous cavernous sinus needs to increase the venous pressure in the draining vein of the orbit, superior ophthalmic vein, and outflow obstruction to the orbital and episcleral venous drainage. The orbital venous obstruction results in the clinical findings of proptosis, extra ocular muscle enlargement, ophthalmoplegia, episcleral and conjunctival injection and retinal venous obstruction. The increased intraocular pressure is usually caused by episcleral venous pressure, however, neovascular glaucoma and angle closure may also develop. In this particular case, ultrasound biomicroscopy showed that the mechanism of the increased intraocular pressure was increased episcleral venous pressure and apposition of the angle as a result of ciliary body rotation and choroidal effusion.
Dr. Andrew Lee, Department of Ophthalmology, Neurology and Neurosurgery, 200 Hawkins Drive, The University of Iowa Hospitals and Clinics, Iowa City, IA 52242, USA
Classification:
6.12 Ultrasonography and ultrasound biomicroscopy (Part of: 6 Clinical examination methods)
9.4.9 Glaucomas associated with elevated episcleral venous pressure (Part of: 9 Clinical forms of glaucomas > 9.4 Glaucomas associated with other ocular and systemic disorders)
