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We present a series of nine cases involving primary intraocular lens implantation in congenital cataracts. Because of the problems encountered with the technique used in the earlier cases, we developed a new surgical technique that may be described as primary epilenticular posterior chamber lens implantation followed by pars plana endocapsular lensectomy. This new technique ensures a clear pupillary area, minimizes postoperative complications, and ultimately prevents amblyopia, resulting in useful vision.

Since the number of cases for each of the conditions in our study was small, only preliminary conclusions can be made; in order to establish the fluorescein pattern of each of these peripheral retinal lesions, additional studies will be required. The following summarizes our preliminary observations. 1. Areas of retinal white-with-pressure or without and peripheral retinal cystoid degeneration did not reveal remarkable fluorescein angiographic findings. One exception was in an area of pigment epithelial disturbance characterized by atrophy and proliferation, which showed a "window and masking" effect of choroidal fluorescence. 2. Fluorescein angiography of areas of the fundus with lattice retinal degeneration showed little or no findings in early or mild cases. In severe or advanced cases, the affected retina revealed poor or absent perfusion caused by vascular occlusion. The retinal and choroidal circulation was devoid of fluorescein leakage. Advanced lesions displayed choroidal hypofluorescence in areas of pigment proliferation and hyperfluorescence in areas of pigment atrophy. 3. In advanced cases, occlusive vascular changes over areas of acquired retinoschisis were observed. There was intraretinal leakage of the dye from deep capillaries and pooling of the dye in cystic cavities near the margin of the retinoschisis. 4. There was no perfusion of the choroid and retina in the area of the hole and in the retina surrounding it. This finding suggests choroidal and retinal ischemia in the pathogenesis of a retinal hole. 5. Fluorescein angiography of retinal tears revealed fluorescein leakage along the edge of the tear and absent perfusion of the retinal flap. The retinal and choroidal circulation-around the tear was otherwise unremarkable. The choroidal fluorescein underlying the retinal flap was not visible, perhaps because it was masked by the retinal flap. 6. Our fluorescein angiographic findings in cases of rhegmatogenous retinal detachment confirmed those of others [7, 8, 10]. Transit of fluorescein through the retinal circulation was sluggish. The retinal capillaries were dilated. 7. In cases of rhegmatogenous retinal detachment which had become reattached surgically, areas treated with diathermy or cryoapplications showed absent or diminished choroidal and retinal perfusion. Leakage of the fluorescein from capillaries in the optic disc and retina in the posterior pole was sometimes persistent several months postoperatively.

One hundred twenty-eight consecutive aphakic glaucomatous eyes of 91 patients were examined by fluorescein angiography. Macular edema was present in 16 (28%) of 56 eyes currently being treated with epinephrine and 9 (13%) of 72 eyes not currently being treated with epinephrine. This difference is statistically significant at the 95% confidence level. Epinephrine therapy was discontinued in seven eyes with macular edema. A follow-up of these patients for six months to one year with serial anglograms showed resolution of edema in six of seven eyes. In one eye without macular edema, administration of epinephrine was associated with appearance of edema. Discontinuing epinephrine therapy was associated with resolution of edema. No significant correlation was found between use of other antiglaucomatous medications and macular edema. It is evident from this study that there is statistical support for the concept of an epinephrine-induced macular edema.

Peripapillary subretinal neovascularization progressively developed in both eyes of a 17-year-old black woman with bilateral chronic granulomatous uveitis. Despite intensive medical therapy, central vision was lost in the left eye due to disciform scarring that extended to the macula. When a similar process was discovered in the right eye, argon laser therapy was started and was successful in eliminating all areas of subretinal neovascularization in the right eye while maintaining good cental vision. Chronic uveitis is probably another cause of peripapillary subretinal neovascularization, which can be treated with photocoagulation in spite of the presence of inflammation.

A 30-year-old black woman with biopsy-proven sarcoidosis and sickle cell anemia had peripheral retinal neovascularization. Elevated fibrovascular proliferations and distal retinal ischemia with nonperfused ghost vessels passing through the area of neovascularization were found at the temporal periphery. No signs of intraocular inflammation were present. Both diseases occur in black patients and should always be considered in the presence of peripheral retinal neovascularization.