Fig. 16.4 Slit lamp photograph of the right eye of a patient who suffered a HCRVO 7 years before. Iris atrophy from previous phacoemulsification cataract extraction is present (the green arrow). Anterior chamber clot covers the front of the intraocular lens implant (the yellow arrows). There is no iris neovascularization. Vitreous hemorrhage was present, but is not evident in this photograph

hemorrhage were present (Fig. 16.4). Neovascularization of the iris (NVI) was not present. Gonioscopy of the right eye showed no neovascularization of the angle (NVA), but there was an inferior hyphema. Ultrasonography of the right eye showed no retinal detachment or intraocular tumor. How would you manage this case?

had been needed. The hyphema and vitreous hemorrhage spontaneously cleared over the next month. Neither ophthalmoscopy nor FA showed retinal or disc neovascularization, nor was NVI found when the hyphema cleared. However, the pupil dilated poorly, and the FA could not capture views of the peripheral retina well.

If neovascularization had been recognized, then in extrapolation to the results of the BVOS, laser panretinal photocoagulation (PRP) of the involved retina would be advisable in an attempt to cause regression of the neovascularization.1 The BVOS did not study eyes with HCRVO, but the underlying principles of pathogenesis and treatment of retinal and disc neovascularization are the same for BRVO and HCRVO. If the patient had alternatively noted significant degradation in quality of life, then early intervention with pars plana vitrectomy and sector PRP could have been offered.

Although no bleeding source was found, it was suspected that an unidentified focus of neovascularization was the likely source of the bleeding. PRP was given to the involved hemiretina as a treatment for that inferred diagnosis. Over 1 year of subsequent follow-up, there has been no further vitreous hemorrhage. Continued observation would have been another rational management option.

Although it is possible that the vitreous hemorrhage and spillover hyphema in this case represent the effect of a hemorrhagic posterior vitreous detachment or an acute retinal break with associated vitreous hemorrhage, the history of previous inferior HCRVO raises the probability of secondary disc or retinal neovascularization and consequent vitreous hemorrhage as the more plausible explanation for the clinical findings. Because the patient noted the change in VA, but did not note significant disturbance in quality of life, he elected an option of watchful waiting for the hemorrhage to clear and identification of the bleeding source by ophthalmoscopy or FA. Topical hypotensive drops controlled the intraocular pressure. An IVBI could have been offered if the blood failed to clear or if more rapid clearing

16.4Case 16.4: Spontaneous Improvement of a Nonischemic Central Retinal Vein Occlusion

A 65-year-old man with hypertension and hypercholesterolemia complained of acute, painless loss of vision in the right eye. A nonischemic CRVO was discovered with VA of 20/100. No relative afferent pupillary defect (RAPD) was present, there was no NVI, and the fundus examination showed ME as the cause of loss of VA (Fig. 16.5). FA showed good capillary perfusion. One month later, the situation was unchanged and, after discussing alternatives, the patient elected to undergo laser chorioretinal venous anastomosis (LCRVA). Two sites were chosen