• Stage III = neovascular and fibrous proliferation; stage IV = vitreous hemorrhage; stage V = retinal detachment. Arabic numerals = substages: 0 none; 1= 30° of circumferential fundus involvement (and 3 proliferations or hemorrhages); 2 = 31°-60° of circumferential fundus involvement (or 4-6 proliferations or hemorrhages); 3 = 61°-90° of circumferential fundus involvement (or 7-9 proliferations or hemorrhage 91° of circumferential fundus involvement (or 10 proliferatio hemorrhages). CLASSIFICATION OF PROLIFERATIVE SICKLE RETINOPATHY (FOR USE WITH INDIRECT OPHTHALMOSCOPY AND FLUORESCEIN ANGIOGRAPHY) Stage I. Peripheral arteriolar occlusions Substages 0. None 1. 30° circumferential involvement and <3 occluded arterioles Stage II. Peripheral arteriolar-venular anastomoses Substages 0. None 1. 30° circumferential involvement and 3 discrete anastomoses Stage III. Neovascular and fibrous proliferation Substages 0. None 1. 30° circumferential involvement and 3 discrete proliferations Stage IV. Vitreous Hemorrhage Substages 0. None 1. 30° circumferential involvement Stage V. Retinal detachment Substages 0. None 1. 30° circumferential involvement 538 MORTON F. GOLDBERG The lesions of stages III, IV, and V are the ones which are responsible for visual symptomatology in PSR. Consequently, for purposes of this report, only these stages were assessed precoagulation and postcoagulation (Tables 1 and 3 through 5). Stage III lesions were not considered to be obliterated unless complete absence of fluorescein leakage into the vitreous could be demonstrated by fundus photography 10 to 15 minutes after intravenous injection of dye. Twenty-five eyes were treated by photocoagulation with the West German Zeiss xenon arc photocoagulator. In most instances, the regular "green" load setting was utilized, with 3°, 4.5°, or 6° apertures in the image field diaphragm, and with a slightly constricted iris diaphragm (approximately setting No. 4). Photocoagulation lesions of moderate intensity (gray-white retinal reaction) were considered desirable. Retrobulbar anesthesia was used in all patients. One eye was treated with transconjunctival cryocoagulation, and one eye was treated with argon laser coagulation. When a neovascular lesion lay flat on the retina, therapy was usually directed at the abnormal capillary bed. When a neovascular lesion was found to be elevated from the retina, therapy was directed to the feeding arterioles at its posterior edge (between the lesion and the optic disc), where these vessels were flat on the retina. Because of the characteristic manner of development of neovascular lesions in PSR, arteriolar feeder vessels are almost never found at these lesions' anterior borders (that is, between the neovascular lesions and the ora serrata).1,2 Thus, in practical terms, there is no need for photocoagulation between the neovascularized retina and the ora serrata. When more than one photocoagulation was indicated, as evidenced by persistent perfusion of the neovascular lesion with intravenously TR AM ACAD OPHTH & OTOL FIG 2-(4) Schematic appearance of left eye of patient 15. Large preretinal neovascular and fibrous prolifera tion ("sea fan'2) is present superotemporally, a characteristic location., (B) Fluorescein angiogram of superotemporal neovascularization in early arteriovenous phase. Numerous arteriolar feeder vessels and complex capillary bed are revealed. (C) Late arteriovenous phase shows leakage of fluorescein from neovascular capillary bed into vitreous. (D) Late arteriovenous phase after one photocoagulation of arteriolar feeder vessels reveals slight diminution in capillary vessels. fans"10) were completely obliterated or were rendered harmless by having their arteriolar supply shut off, as shown by fluorescein fundus photography (Fig 4). Fluorescein angiography was essential in determining if the neovascular tissues were still carrying blood following photocoagulation. With With ophthalmoscopy alone, perfused neovascular channels were easily camouflaged by the surrounding, hyperpigmented photocoagulation scar (Fig 5). Small sea fans (stage III-1), particularly when they lay flat on the retina, were easily obliterated, often with only one photocoagulation treatment (Fig 6). Larger sea fans (such as stage III4), particularly when elevated into a preretinal location, or when supplied by more than one arteriolar feeder vessel, were considerably more difficult to treat successfully (Figs 7 and 8). In such instances, cessation of perfusion of the sea fans was more difficult to obtain, and (F) Schematic appearance of fundus after eight photocoagulations. (G) Following eighth photocoagulation, fluorescein angiogram during late arteriovenous phase confirms complete absence of perfusion of neovascular tissue (seen as dark area in upper right of photo). Mottled appearance is created by retinal pigment migration. There is no leakage of dye. photocoagulation-induced vitreous hemorrhage seemed more likely to occur. Of the 58 treatment episodes, three (5.2%) were complicated by vitreous hemorrhag within 24 hours, and all three occurred with large, elevated, complex sea fans (Fig 2). Two of the hemorrhages were minor and cleared rapidly. The third re mained ophthalmoscopically visible and caused symptoms for at least six months. During the course of photocoagulation, three other eyes rebled spontaneously; that is, there was no apparent temporal relationship to a previous photocoagulation episode. |