Early treatment of cystoid macular edema secondary to branch retinal vein occlusion with intravitreal triamcinolone acetonide.

BACKGROUND AND OBJECTIVE: To determine the efficacy of intravitreal triamcinolone acetonide (IVTA) in the early treatment of severe cystoid macular edema (CME) related to acute branch retinal vein occlusion. PATIENTS AND METHODS: Retrospective, non-comparative case series. Twelve eyes with severe CME (foveal thickness > 450 microm) secondary to acute branch retinal vein occlusion received IVTA. RESULTS: Average follow-up was 15.3 months. Mean visual acuity was 0.88 LogMar units (20/160) initially, 0.55 LogMar units (20/70) at 1 week, 0.46 LogMar units (20/60) at 1 month, and 0.49 LogMar units (20/60) at last follow-up. Visual acuity improved by 3 lines or greater in 42% of patients at 1 week, 50% at 1 month, and 42% at last follow-up. Average foveal thickness was 589 microm (range, 460 to 840 microm) at baseline, 237 microm at 1 week, 196 microm at 1 month, and 235 microm at last follow-up. All eyes showed reduction of foveal thickness as measured by optical coherence tomography. Eight eyes developed recurrent CME at an average of 5.5 months after initial IVTA injection. Ten eyes required additional intervention during the follow-up period. CONCLUSIONS: Early treatment of severe CME secondary to branch retinal vein occlusion with IVTA is effective in reducing foveal thickness as measured by optical coherence tomography and improving visual acuity. However, monotherapy with IVTA can be associated with a significant rate of recurrent CME.

Percutaneous carotid artery angioplasty and stenting for ocular ischemic syndrome.

PURPOSE: To describe percutaneous carotid angioplasty and stenting to treat ocular ischemic syndrome resulting from severe intracranial carotid artery stenosis. DESIGN: Retrospective case series of 3 patients with ocular ischemic syndrome and intracranial carotid artery stenosis. INTERVENTION: All patients underwent carotid artery evaluation, including ultrasound, transcranial Doppler, magnetic resonance imaging or magnetic resonance angiography,and angiography. Carotid angioplasty and stenting was performed in all patients. MAIN OUTCOME MEASURES: Carotid angiography, fluorescein angiography, and transcranial Doppler imaging were used to evaluate cerebral and ocular perfusion. RESULTS: Cerebral perfusion improved in all patients. Fluorescein angiography arteriovenous transit times improved in 2 patients. One patient had a correction in the reversal of flow through the ophthalmic artery. Visual acuity remained stable or improved in all patients. There were no complications associated with the procedure. CONCLUSIONS: Intracranial carotid artery stenosis is a rare cause of ocular ischemic syndrome. With the advent of carotid angioplasty and stenting, stenotic lesions previously not amenable to carotid endarterectomy are now treatable with stenting. A complete work-up of the carotid artery is necessary in all cases of ocular ischemic syndrome to ensure evaluation of the entire carotid artery system. Early diagnosis of intracranial carotid stenosis is important for preservation of visual function and reducing risk of cerebral vascular event.