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Case Report This patient avoided follow-up for CRVO
by Andrew Gurwood, O.D., Contributing Editor and John Mileski, O.D., Philadelphia A 67-year-old white male presented following a sudden onset of blurred vision in his left eye. He said it was like looking through wax paper. His
ocular history included hypertensive retinopathy grade II and atherosclerotic changes in both eyes. His medical history was remarkable for hypertension, for which he was taking oral catopril. Clinical Findings
Confrontation fields uncovered a relative central scotoma in the left eye, confirmed by Amsler grid. Refraction revealed stable myopia with presbyopia: -1.50 O.D./+2.50 and -1.75 O.S./+2.50. Biomicros-copy demonstrated normal anterior segment structures and grade IV Van Herick angles. Goldmann applanation tonometry measured intraocular pressures of 16mm Hg O.U. Dilated fundus evaluation found normal nerves and peripheries and grade II atherosclerotic and hypertensive changes O.U. The posterior pole O.S. exhibited multiple flame-shaped hemorrhages emanating from the disc into all four quadrants with scattered cotton-wool patches (figure 1). Diagnosis Management The patient cancelled his appointment with the retina service and all other follow-up visits for over four months. He failed to answer phone calls, return messages or respond to registered mail. When the patient finally returned, his chief complaint was painful, blurry vision in the left eye. His history was unchanged, but the laboratory tests we recommended hadn't been done. Visual acuity in his right eye was stable, but in his left eye was now 20/200. External examination revealed normal motilities. Confrontation fields found a deeper relative central scotoma. The swinging-flashlight test demonstrated a grade II relative afferent pupillary defect in the left eye.
At this visit we diagnosed neovascular glaucoma secondary to ischemic central retinal vein occlusion. We started the patient on atropine 1 percent, Iopidine (apraclonidine 1 percent), timolol 0.5 percent BID and prednisolone 1 percent every two hours O.S. We also prescribed two 250mg tablets of Diamox (acetazolamide) by mouth. Dilated fundus examination was consistent with previous findings, with no neovascularization of the retina or disc. Within 50 minutes the intraocular pressure measured 27mm Hg O.S. We explained to the patient that this was a serious ocular problem requiring immediate attention. We arranged for him to see our retinal specialist and continued him on atropine 1 percent BID, timolol 0.5 percent BID, prednisolone every two hours O.S. and a 500mg sequel of Diamox BID. The retinal specialist confirmed our diagnosis. Panretinal photocoagulation was performed to arrest the neovascularization. Today the patient is comfortable with 20/300 vision O.S., grade I cells and flare O.S. and IOPs of 13mm Hg O.D. and 20mm Hg O.S. He remains on the topical medications described previously. The Diamox was discontinued. Discussion
Pathophysiology. CRVO may be ischemic (nonperfused) or nonischemic (perfused). Thirty percent of CRVO become ischemic. Neovas-cular glaucoma occurs in 40-60 percent of these cases.9 Progression from the nonischemic to ischemic form occurs in 5-20 percent of such cases.8 The CRVO Study Group identified four factors associated with anterior segment neovascularization: retinal capillary nonperfusion on fluorescein angiography, retinal hemorrhage, acute nature and male gender.7 The mechanism behind iris neovascularization and the subsequent glaucoma is complex. The ischemic retina produces hypoxia-induced angiogenic factors.17 Vasoproliferative material may diffuse anteriorly through the vitreous to initiate vessel growth.11 The nature of the angiogenesis factors is unknown.11,12 Antiangiogenic factors from the RPE regulate and reverse ocular neovascularization.1 New vessel growth results from an imbalance between these stimulatory and inhibitory factors.1,11,12 The process begins at the minor circle of the iris. Capillary buds progress to become vascular tufts, composed of fenestrated endothelial cells yet lack muscular layers and supportive tissues.1 These vessels extend radially over the iris surface toward the angle. When rubeosis reaches the angle it branches out across the trabecular meshwork as a fibrovascular membrane. The tissue ultimately contracts, pulling the iris toward the trabecular meshwork and forming localized peripheral anterior synechiae. The synechiae eventually coalesce and produce secondary angle closure. Traction along the iris surface can pull the posterior pigmented epithelium of the iris around the pupillary margin. Signs and symptoms. Normal IOP and the presence of new vessel tufts at the pupillary margin mark the preglaucoma stage. These vessels may enlarge, coursing along the iris surface toward the angle, or they may regress. Gonioscopy can rule out angle neovascularization. The open angle glaucoma stage results when the fibrovascular membrane occludes significant trabecular meshwork. Biomicroscopy may reveal anterior chamber inflammation with or without hyphema. This typically occurs 8-15 weeks after the initial occlusive event, hence the term "90-day glaucoma."2 The synechial angle closure stage presents with pain and photophobia. Visual acuity declines and IOP may be as high as 60mm Hg.1 You may observe a steamy, edematous cornea, iris neovascularization, cells, flare, peripheral anterior synechiae and ectropion uvea. Management. The CRVO Study Group found no benefit in performing panretinal photocoagulation before observing iris or angle neovascularization in patients who had frequent follow-up exams.7 Monthly follow-ups during the first 6-8 months are indicated. The investigators recommend monthly follow-ups after photocoagulation until the anterior segment neovascularization regresses.18 Medical therapy for neovascular glaucoma includes topical beta blockers, alpha2 agonists and oral carbonic anhydrase inhibitors. Atropine 1 percent and topical corticosteroids are indicated for the pain and inflammation. Miotics are contraindicated. Early detection of the neovascularization is critical. Prompt panretinal photocoagulation can cause the neovascularization to regress and, thus, prevent glaucoma. It seems to work by reducing retinal hypoxia and the release of angiogenic factors. Peripheral retinal cryotherapy is an alternative. Other modalities to reduce IOP include filtration shunts and cyclodestructive procedures.19-22 When vision fails, therapy is redirected toward pain management. Topical atropine and corticosteroids are common choices. Retrobulbar alcohol injection and enucleation are final measures.
Dr. Gurwood is associate professor at Pennsylvania College of Optometry and attending optometrist at its Eye Institute. Dr. Mileski is in private practice.
1. Wand M. Neovascular Glaucoma. In: Ritch R, Shields MB, Krupin T (eds). The Glaucomas, 2nd ed. St. Louis: Mosby-Year Book Inc. 1996:1073-1130. |
