RHEGMATOGENOUS RETINAL DETACHMENT AFTER TRIBUTARY RETINAL VEIN OCCLUSION H O W A R D C. J O O N D E P H , M.D.,
A N D M O R T O N F . GOLDBERG,
M.D.
Chicago, Illinois T h e retinopathic manifestations of tribu tary retinal vein occlusion, characterized b y hemorrhages, edema, intraretinal microvascular abnormalities and neovascularization, form a clinical picture that is generally well recognized. T h e natural course and pathogenesis of complications arising from this condition, however, remain relatively uncertain. A m o n g these complications, rhegmatogenous retinal detachment due to tribu tary retinal vein occlusion is an infrequent phenomenon with a poorly denned patho genic mechanism. W e encountered two patients whose tribu tary vein occlusion was complicated by the development of neovascular tissue, retinal hole formation, and subsequent rhegmatogenous retinal detachment. C A S E REPORTS
Case 1—A 63-year-old white man was referred in September 1972 for evaluation of poor vision in the right eye. In 1968 he had sustained a superotemporal branch vein occlusion in the right eye and was treated with anticoagulants for six months. Discontinuation of the anticoagulant therapy was followed by a vitreous hemorrhage in the right eye. His vision gradually improved and was re corded as 6/8 in July 1972. Two weeks prior to consultation he noted a "sharp drop" in the vision of his right eye associated with a central scotoma and, in the last few days prior to consultation, a further decrease in vision of the right eye. His medical history included systemic hyper tension of many years' duration, presently requiring diuretics and a reserpine derivative for control, and "glaucoma for three to four years" treated with pilocarpine 4% and an epinephrine derivative. Visual acuity was 6/120 in the right eye with —1.75 sph and 6/8 in the left eye with —1.S0 sph.
Results of external, slit-lamp, and gonioscopic examinations were normal in both eyes. Goldmann fields, performed with a II«e test object, revealed a 7-degree central scotoma in the right eye, which was confirmed with the Amsler grid. Ophthalmoscopic examination of the dilated fundus revealed a normal left eye. The optic disks and cups were normal in both eyes. The right vitreous body contained asteroid hyalosis. The superotemporal vein had an irregular diameter along its length. A rhegmatogenous retinal detachment extended from the disk margin to 2 disk diameters temporal to the fovea and from above the superior temporal vessels to below the macula (Figs. 1 and 2). There was a full-thickness retinal hole between the superotemporal artery and vein. A tuft of neo vascular tissue was adherent to the posterior hya loid face, just anterior to the retinal hole. The vitreous body was collapsed, and the posterior hyaloid face was attached only at the site of the neovascularization. Two additional patches of flat neovascular tissue were noted superior to the superotemporal vein. In September 1972, the patient was treated with xenon arc photocoagulation without complication. Lesions were applied to surround the area of neo vascularization and retinal hole. During the fourday hospitalization after treatment, the subretinal fluid showed "slight resolution." Reexamination in October 1972 revealed conjunctival injection and bullous keratopathy, which
From the Department of Ophthalmology, Uni versity of Illinois Eye and Ear Infirmary, Chicago, Fig. 1 (Joondeph and Goldberg). Case 1. Rheg Illinois. This study was supported in part by an unrestricted grant from Research to Prevent Blind matogenous retinal detachment involving the macula ness, Inc., and by training grant PHS EY24/16 of the right eye. Note retinal hole (RH) with overlying plug of retinal tissue adherent to neo from the National Eye Institute. Reprint requests to Morton F. Goldberg, M.D., vascular tissue ( R P - f NV). RD indicates retinal University of Illinois Eye and Ear Infirmary, 1855 detachment; M indicates macula; D indicates optic disk. W. Taylor St., Chicago, IL 60612. 253
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Fig. 2 (Joondeph and Goldberg). Case 1. Verti cal cross section through retinal hole (RH) and macula (M) of Figure 1. Note retinal plug (RP) adherent to neovascular tissue (NV) which, in turn, is adherent to the detached posterior hyaloid ( P H ) . V indicates vitreous; RD indicates retinal detachment. necessitated the use of topical glycerine to visualize the anterior chamber. There was + 1 aqueous flare without cells and + 4 brown pigment dusting on the corneal endothelium. Intraocular pressure by ap planation tonometry was 38 mm Hg. The disk was barely visible. The patient was treated with topical atropine, dexamethasone, an epinephrine derivative, and an oral carbonic anhydrase inhibitor. Two weeks later the corneal edema had subsided slightly. The aqueous flare disappeared and the intraocular pressure by applanation tonometry was 22 mm Hg. The disk was slightly more visible. In January 1973 the patient's vision had returned to its pretreatment level. The corneal endothelial pigment dusting was unchanged, and the intra ocular pressure by applanation tonometry was 28 mm Hg. The area of previous rhegmatogenous detachment was flat; the area of photocoagulation revealed typical pigmentary changes. The tuft of neovascular tissue was still elevated from the retina and was still adherent to the posterior hyaloid face. Fluorescein angiography showed only a hyperfluorescent point corresponding with the tented venule; the neovascular tissue was not per fused. In July 1973, visual acuity in the right eye re mained unchanged. The applanation pressure was
AUGUST, 197S
26 mm Hg while the patient was receiving a car bonic anhydrase inhibitor, topical pilocarpine, phospholine iodide, and an epinephrine derivative. Ex amination of the anterior segment showed some iris atrophy, but it was otherwise unchanged. Fundus findings were unchanged from the previous exami nation. Case 2—A 57-year-old white woman was re ferred in April 1973 for evaluation of an episode of vitreous hemorrhage in the right eye. From 1957 to June 1962 she had been seen by her oph thalmologist who reported normal findings. On June 6, 1962, after hospitalization for an episode of severe frontal and occipital headaches and weak ness of the left arm, she was noted to have "a patch of angiomatosis retinae in the temporal ret ina." She remained asymptomatic until September 1968 when she was seen for reduced vision that had started as "cobwebs" five days before. The previously noted angiomatosis was now accom panied by "clouding of the vitreous," and she was referred to another ophthalmological center. The diagnostic opinion, confirmed with fluorescein angi ography, was "branch occlusion of the superior temporal vein in the past" followed by "localized retinitis proliferans with vitreous extension" and subsequent vitreous hemorrhage. In November 1968, corrected visual acuity in the right eye returned to 20/20, the "angiomatosis" was unchanged, and "a few cells in the vitreous" were noted. She was then seen by us in April 1973 complaining of "terrific pain in the right eye" of three days' duration. Her past medical history revealed no systemic disease, including hypertension and diabetes mellitus; however, her mother, aunt, and uncle had all died of strokes. Physical examination revealed visual acuity of 6/6 bilaterally with +3.00 sph in the right eye and +3.25 sph in the left eye. Ex ternal, slit-lamp, and gonioscopic examinations and Goldmann fields all gave normal results bilaterally. Applanation pressure was 16 mm Hg in both eyes. Onhthalmoscopk examination showed the left eye to be normal with a cup/disk ratio of 0.4. In the right eye the cup/disk ratio was 0.6. The fundus was normal except in the superotemporal quadrant. At 10:30 o'clock, a large plug of retinal tissue was adherent to the detached posterior hyaloid overlyirg a large full-thickness retinal hole. The hole was surrounded by a localized retinal detachment without pigmentary changes. Adjacent to the plug of retinal tissue and adherent to the posterior hyaloid face was a patch of white, occluded, old neovascular tissue, with a sea-fan appearance (Figs. 3 and4). A tense vitreous band projected from this intravitreal vascular tissue toward the retina. Immedi ately above the retina, the band bifurcated with one arm attaching to a retinal venule and the other to an adjacent retinal arteriole. Both the artery and vein were tented at the point of attachment of the vitreous band. On close examination these bands
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were found to be the ghost remnants of branches of the retinal vessels. Dilated, tortuous retinal capil laries were noted within this immediate area. In January 1974, the retinal hole was sealed with argon laser photocoagulation. Laser lesions were also applied to surround the region of traction on the retinal arteriole and venule. Reexamination one month later revealed a com pletely obliterated retinal hole. Some retinal trac tion was still present; however, the area of trac tion was well surrounded with photocoagulation scars. The patient has been asymptomatic. DISCUSSION
The pathogenesis of rhegmatogenous ret inal detachment complicating tributary reti nal vein occlusion has not been well described. Zauberman1 reported four cases of retinal hole formation, three of which progressed to retinal detachments associated with oc clusion of a major venous channel. The ret inal breaks were all peripheral; one was associated with snail-track degeneration, two with peripheral microcystoid degeneration, and one was a horseshoe tear. He proposed the following sequence: venous occlusion causing or aggravating peripheral micro cystoid degeneration along with atrophic retinal degeneration, leading, in turn, to ret-
Fig. 4 (Joondeph and Goldberg). Case 2. Oblique cross section through detached retina (RD). Note retinal plug (RP) adherent to neovascular tissue (NV), which in turn is adherent to the detached posterior hyaloid (PH). B indicates fibrous band (occluded retinal vessel) joining the neovascular tissue with the tented retinal vessels causing a tractional retinal detachment (RD) ; A indicates retinal arteriole; V indicates retinal venule.
inal cyst formation, breakdown of the cyst wall with hole formation, and subsequent detachment. To indict venous occlusion as the predisposing factor in this chain of events may not be necessary, as the same sequence of events occurs in connection with peripheral retinal breaks without the pres ence of major vascular occlusion. In a study of 95 patients with tributary retinal vein occlusion, Archer, Ernest, and Newell2 proposed a classification based on arterial perf usion, microvascular competence, retinal ischemia, and neovascularization. Under this classification, their Group 4 had arterial insufficiency and retinal ischemia as predominant features. Of 12 patients in this group, two developed retinal traction bands and hole formation, and one developed a retinal detachment, the cause of which was not clearly defined, although it was assumed to be tractional. Gutman and Zegarra 3 described the natu ral course of temporal tributary vein oc clusion in 40 patients. One patient developed Fig. 3 (Joondeph and Goldberg). Case 2. Retinal hole (RH) with overlying neovascular tissue a rhegmatogenous retinal detachment sec (NV) and adherent retinal plug (RP). B indicates ondary to two operculated tears in an area fibrous band (occluded retinal vessel) leading from adjacent to preretinal neovascularization. neovascular tissue to tented retinal vessels; A in dicates retinal arteriole; V indicates retinal venule; They ascribed the pathogenesis of the detach1 RD indicates localized tractional retinal detach ments to that described by Zauberman ment. (vascular occlusion, microcystoid degenera-
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tion, retinal cyst formation, hole formation, and finally detachment). Davis* described the natural course of proliferative diabetic retinopathy in 89 pa tients and divided it into three stages. In Stage 1, new vessels always appeared either on the retinal surface or within its most superficial layers and, in the absence of pos terior vitreous detachment, did not extend into the vitreous more than 0.5 mm. Stage 2 began with the onset of posterior vitreous detachment. The posterior vitreous surface was adherent to the retina at the site of neovascular tissue and pulled the latter for ward with or without the underlying retina. Preretinal or vitreous hemorrhages were "commonly" associated with vitreous detach ment and the "frequently" occurring retinal detachments were "always" related to a site of neovascular tissue. When retinal breaks occurred, they were "located adjacent to the vitreoretinal adhesions." The author made two additional comments worthy of note: (1) that vitreoretinal adhesions were "so commonly present along the superior temporal vessels," and (2) that "the regions of earliest detectable vitreous detachment" were noted "along the superior temporal vessels above the macula" in six of 21 eyes. Both patients reported here developed rhegmatogenous retinal detachments after tributary retinal vein occlusions through ap parently identical pathogenic mechanisms. Occlusion of a tributary venous channel led to ischemia within its drainage area through the mechanism of capillary nonperfusion (and subsequent loss of the actual capil laries). The ischemia or hypoxia, or both, then presumably served as a stimulus for the development of neovascularization by an as yet undetermined mechanism. In other clinical settings characterized by retinal ischemia and subsequent neovascularization, such as diabetic retinopathy and sickle cell retinopathy, it has been speculated that a vasotactic factor released by the hypoxic retina is the neovasculogenic factor. These
AUGUST, 1975
new vessels advance through the internal limiting membrane and attach to (or, rarely, penetrate) the posterior hyaloid membrane where they continue to proliferate. As the posterior hyaloid membrane detaches from the internal limiting membrane and retracts, it pulls the tuft of neovascular tissue along with it away from the retina.4'5 This traction on the new vessels leads either to their rupture with subsequent vitreous hemor rhage or to traction on the retina itself causing a tractional detachment or operculated hole formation, as in the two cases presented here. The development of sub sequent rhegmatogenous retinal detachment then becomes a distinct possibility. Krill, Archer, and Newell6 suggested de struction of neovascular tissue in branch vein occlusion by photocoagulation to pre vent secondary vitreous hemorrhage and macular edema. Michels and Gass7 and Archer, Ernest, and Newell2 suggested the use of photocoagulation to treat neovascular tissue that has caused previous vitreous hemorrhage in an attempt to prevent re peated hemorrhage. Patz 8 described the use of argon laser photocoagulation to prevent the development of neovascularization by de stroying ischemic retinal tissue in areas of nonperfusion after tributary vein occlusion. In this report, we stress the importance of adhesion of neovascular tissue to the posterior hyaloid. Traction from collapsed vitreous led to avulsion of retinal plugs and localized rhegmatogenous detachments of the retina. Photocoagulation was successful in obliterating the retinal holes and in pre venting extension of the retinal detachments. SUMMARY
Two patients had rhegmatogenous retinal detachment after tributary retinal vein oc clusion. Neovascularization adherent to the posterior hyaloid was avulsed, along with a plug of retinal tissue, as the vitreous body collapsed. Localized retinal detachments re sulted. Photocoagulation successfully oblit-
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4. Davis, M. D.: Vitreous contraction in proerated the retinal holes and prevented ex , liferative diabetic retinopathy. Arch. Ophthalmol. tension of the retinal detachments in both 74:741,1965. 5. Tolentino, F. I., Lee, P. F., and Schepens, cases. REFERENCES
1. Zauberman, H.: Retinopathy of retinal detach ment after major vascular occlusion. Br. J. Oph thalmol. 52:117,1968. 2. Archer, D. B., Ernest, J. T., and Newell, F. W.: Classification of branch retinal vein ob struction. Trans. Am. Acad. Ophthalmol. Oto laryngol. 78:148,1974. 3. Gutman, F. A., and Zegarra, H.: The natural course of temporal retinal branch vein occlusion. Trans. Am. Acad. Ophthalmol. Otolaryngol. 78:178, 1974.
C. L.: Biomicroscopic study of vitreous cavity in diabetic retinopathy. Arch. Ophthalmol. 75:238, 1966. 6. Krill, A. E, Archer, D., and Newell, F. W.: Photocoagulation in complications secondary to branch vein occlusion. Arch. Ophthalmol. 85:48, 1971. 7. Michels, R. G., and Gass, J. D. M.: The natural course of retinal branch vein occlusion. Trans. Am. Acad. Ophthalmol. Otolaryngol. 78:166, 1974. 8. Patz, A.: A guide to argon laser photocoagu lation. Survey Ophthalmol. 16:249, 1972.
O P H T H A L M I C MINIATURE
The fallacy of ostensive definition: This is a form of an incomplete definition as pointing to one overt characteristic or to one individual in a class in an attempt to explain and define. To prove existence does not give full meaning. Even more extensive identification of overt character istics may not fully define phenomena, such as those that are mental and have both public and subjective aspects. Public demonstration does have a superior but exclusive claim to proof. When ostension cannot be per formed, it should not be concluded that no other demonstrative act—as subjective report—is of use as evidence of existence. . . . suddenly a footman in livery came running out of the wood (she consid ered him to be a footman because he was in livery; otherwise she would have called him a fish).
Dwight J. Ingle Fallacies and errors in the Wonderlands of Biology, Medicine, and Lewis Carroll Perspectives in Biology and Medicine 15:261 1972
A N D M O R T O N F . GOLDBERG,
M.D.
Chicago, Illinois T h e retinopathic manifestations of tribu tary retinal vein occlusion, characterized b y hemorrhages, edema, intraretinal microvascular abnormalities and neovascularization, form a clinical picture that is generally well recognized. T h e natural course and pathogenesis of complications arising from this condition, however, remain relatively uncertain. A m o n g these complications, rhegmatogenous retinal detachment due to tribu tary retinal vein occlusion is an infrequent phenomenon with a poorly denned patho genic mechanism. W e encountered two patients whose tribu tary vein occlusion was complicated by the development of neovascular tissue, retinal hole formation, and subsequent rhegmatogenous retinal detachment. C A S E REPORTS
Case 1—A 63-year-old white man was referred in September 1972 for evaluation of poor vision in the right eye. In 1968 he had sustained a superotemporal branch vein occlusion in the right eye and was treated with anticoagulants for six months. Discontinuation of the anticoagulant therapy was followed by a vitreous hemorrhage in the right eye. His vision gradually improved and was re corded as 6/8 in July 1972. Two weeks prior to consultation he noted a "sharp drop" in the vision of his right eye associated with a central scotoma and, in the last few days prior to consultation, a further decrease in vision of the right eye. His medical history included systemic hyper tension of many years' duration, presently requiring diuretics and a reserpine derivative for control, and "glaucoma for three to four years" treated with pilocarpine 4% and an epinephrine derivative. Visual acuity was 6/120 in the right eye with —1.75 sph and 6/8 in the left eye with —1.S0 sph.
Results of external, slit-lamp, and gonioscopic examinations were normal in both eyes. Goldmann fields, performed with a II«e test object, revealed a 7-degree central scotoma in the right eye, which was confirmed with the Amsler grid. Ophthalmoscopic examination of the dilated fundus revealed a normal left eye. The optic disks and cups were normal in both eyes. The right vitreous body contained asteroid hyalosis. The superotemporal vein had an irregular diameter along its length. A rhegmatogenous retinal detachment extended from the disk margin to 2 disk diameters temporal to the fovea and from above the superior temporal vessels to below the macula (Figs. 1 and 2). There was a full-thickness retinal hole between the superotemporal artery and vein. A tuft of neo vascular tissue was adherent to the posterior hya loid face, just anterior to the retinal hole. The vitreous body was collapsed, and the posterior hyaloid face was attached only at the site of the neovascularization. Two additional patches of flat neovascular tissue were noted superior to the superotemporal vein. In September 1972, the patient was treated with xenon arc photocoagulation without complication. Lesions were applied to surround the area of neo vascularization and retinal hole. During the fourday hospitalization after treatment, the subretinal fluid showed "slight resolution." Reexamination in October 1972 revealed conjunctival injection and bullous keratopathy, which
From the Department of Ophthalmology, Uni versity of Illinois Eye and Ear Infirmary, Chicago, Fig. 1 (Joondeph and Goldberg). Case 1. Rheg Illinois. This study was supported in part by an unrestricted grant from Research to Prevent Blind matogenous retinal detachment involving the macula ness, Inc., and by training grant PHS EY24/16 of the right eye. Note retinal hole (RH) with overlying plug of retinal tissue adherent to neo from the National Eye Institute. Reprint requests to Morton F. Goldberg, M.D., vascular tissue ( R P - f NV). RD indicates retinal University of Illinois Eye and Ear Infirmary, 1855 detachment; M indicates macula; D indicates optic disk. W. Taylor St., Chicago, IL 60612. 253
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Fig. 2 (Joondeph and Goldberg). Case 1. Verti cal cross section through retinal hole (RH) and macula (M) of Figure 1. Note retinal plug (RP) adherent to neovascular tissue (NV) which, in turn, is adherent to the detached posterior hyaloid ( P H ) . V indicates vitreous; RD indicates retinal detachment. necessitated the use of topical glycerine to visualize the anterior chamber. There was + 1 aqueous flare without cells and + 4 brown pigment dusting on the corneal endothelium. Intraocular pressure by ap planation tonometry was 38 mm Hg. The disk was barely visible. The patient was treated with topical atropine, dexamethasone, an epinephrine derivative, and an oral carbonic anhydrase inhibitor. Two weeks later the corneal edema had subsided slightly. The aqueous flare disappeared and the intraocular pressure by applanation tonometry was 22 mm Hg. The disk was slightly more visible. In January 1973 the patient's vision had returned to its pretreatment level. The corneal endothelial pigment dusting was unchanged, and the intra ocular pressure by applanation tonometry was 28 mm Hg. The area of previous rhegmatogenous detachment was flat; the area of photocoagulation revealed typical pigmentary changes. The tuft of neovascular tissue was still elevated from the retina and was still adherent to the posterior hyaloid face. Fluorescein angiography showed only a hyperfluorescent point corresponding with the tented venule; the neovascular tissue was not per fused. In July 1973, visual acuity in the right eye re mained unchanged. The applanation pressure was
AUGUST, 197S
26 mm Hg while the patient was receiving a car bonic anhydrase inhibitor, topical pilocarpine, phospholine iodide, and an epinephrine derivative. Ex amination of the anterior segment showed some iris atrophy, but it was otherwise unchanged. Fundus findings were unchanged from the previous exami nation. Case 2—A 57-year-old white woman was re ferred in April 1973 for evaluation of an episode of vitreous hemorrhage in the right eye. From 1957 to June 1962 she had been seen by her oph thalmologist who reported normal findings. On June 6, 1962, after hospitalization for an episode of severe frontal and occipital headaches and weak ness of the left arm, she was noted to have "a patch of angiomatosis retinae in the temporal ret ina." She remained asymptomatic until September 1968 when she was seen for reduced vision that had started as "cobwebs" five days before. The previously noted angiomatosis was now accom panied by "clouding of the vitreous," and she was referred to another ophthalmological center. The diagnostic opinion, confirmed with fluorescein angi ography, was "branch occlusion of the superior temporal vein in the past" followed by "localized retinitis proliferans with vitreous extension" and subsequent vitreous hemorrhage. In November 1968, corrected visual acuity in the right eye returned to 20/20, the "angiomatosis" was unchanged, and "a few cells in the vitreous" were noted. She was then seen by us in April 1973 complaining of "terrific pain in the right eye" of three days' duration. Her past medical history revealed no systemic disease, including hypertension and diabetes mellitus; however, her mother, aunt, and uncle had all died of strokes. Physical examination revealed visual acuity of 6/6 bilaterally with +3.00 sph in the right eye and +3.25 sph in the left eye. Ex ternal, slit-lamp, and gonioscopic examinations and Goldmann fields all gave normal results bilaterally. Applanation pressure was 16 mm Hg in both eyes. Onhthalmoscopk examination showed the left eye to be normal with a cup/disk ratio of 0.4. In the right eye the cup/disk ratio was 0.6. The fundus was normal except in the superotemporal quadrant. At 10:30 o'clock, a large plug of retinal tissue was adherent to the detached posterior hyaloid overlyirg a large full-thickness retinal hole. The hole was surrounded by a localized retinal detachment without pigmentary changes. Adjacent to the plug of retinal tissue and adherent to the posterior hyaloid face was a patch of white, occluded, old neovascular tissue, with a sea-fan appearance (Figs. 3 and4). A tense vitreous band projected from this intravitreal vascular tissue toward the retina. Immedi ately above the retina, the band bifurcated with one arm attaching to a retinal venule and the other to an adjacent retinal arteriole. Both the artery and vein were tented at the point of attachment of the vitreous band. On close examination these bands
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were found to be the ghost remnants of branches of the retinal vessels. Dilated, tortuous retinal capil laries were noted within this immediate area. In January 1974, the retinal hole was sealed with argon laser photocoagulation. Laser lesions were also applied to surround the region of traction on the retinal arteriole and venule. Reexamination one month later revealed a com pletely obliterated retinal hole. Some retinal trac tion was still present; however, the area of trac tion was well surrounded with photocoagulation scars. The patient has been asymptomatic. DISCUSSION
The pathogenesis of rhegmatogenous ret inal detachment complicating tributary reti nal vein occlusion has not been well described. Zauberman1 reported four cases of retinal hole formation, three of which progressed to retinal detachments associated with oc clusion of a major venous channel. The ret inal breaks were all peripheral; one was associated with snail-track degeneration, two with peripheral microcystoid degeneration, and one was a horseshoe tear. He proposed the following sequence: venous occlusion causing or aggravating peripheral micro cystoid degeneration along with atrophic retinal degeneration, leading, in turn, to ret-
Fig. 4 (Joondeph and Goldberg). Case 2. Oblique cross section through detached retina (RD). Note retinal plug (RP) adherent to neovascular tissue (NV), which in turn is adherent to the detached posterior hyaloid (PH). B indicates fibrous band (occluded retinal vessel) joining the neovascular tissue with the tented retinal vessels causing a tractional retinal detachment (RD) ; A indicates retinal arteriole; V indicates retinal venule.
inal cyst formation, breakdown of the cyst wall with hole formation, and subsequent detachment. To indict venous occlusion as the predisposing factor in this chain of events may not be necessary, as the same sequence of events occurs in connection with peripheral retinal breaks without the pres ence of major vascular occlusion. In a study of 95 patients with tributary retinal vein occlusion, Archer, Ernest, and Newell2 proposed a classification based on arterial perf usion, microvascular competence, retinal ischemia, and neovascularization. Under this classification, their Group 4 had arterial insufficiency and retinal ischemia as predominant features. Of 12 patients in this group, two developed retinal traction bands and hole formation, and one developed a retinal detachment, the cause of which was not clearly defined, although it was assumed to be tractional. Gutman and Zegarra 3 described the natu ral course of temporal tributary vein oc clusion in 40 patients. One patient developed Fig. 3 (Joondeph and Goldberg). Case 2. Retinal hole (RH) with overlying neovascular tissue a rhegmatogenous retinal detachment sec (NV) and adherent retinal plug (RP). B indicates ondary to two operculated tears in an area fibrous band (occluded retinal vessel) leading from adjacent to preretinal neovascularization. neovascular tissue to tented retinal vessels; A in dicates retinal arteriole; V indicates retinal venule; They ascribed the pathogenesis of the detach1 RD indicates localized tractional retinal detach ments to that described by Zauberman ment. (vascular occlusion, microcystoid degenera-
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tion, retinal cyst formation, hole formation, and finally detachment). Davis* described the natural course of proliferative diabetic retinopathy in 89 pa tients and divided it into three stages. In Stage 1, new vessels always appeared either on the retinal surface or within its most superficial layers and, in the absence of pos terior vitreous detachment, did not extend into the vitreous more than 0.5 mm. Stage 2 began with the onset of posterior vitreous detachment. The posterior vitreous surface was adherent to the retina at the site of neovascular tissue and pulled the latter for ward with or without the underlying retina. Preretinal or vitreous hemorrhages were "commonly" associated with vitreous detach ment and the "frequently" occurring retinal detachments were "always" related to a site of neovascular tissue. When retinal breaks occurred, they were "located adjacent to the vitreoretinal adhesions." The author made two additional comments worthy of note: (1) that vitreoretinal adhesions were "so commonly present along the superior temporal vessels," and (2) that "the regions of earliest detectable vitreous detachment" were noted "along the superior temporal vessels above the macula" in six of 21 eyes. Both patients reported here developed rhegmatogenous retinal detachments after tributary retinal vein occlusions through ap parently identical pathogenic mechanisms. Occlusion of a tributary venous channel led to ischemia within its drainage area through the mechanism of capillary nonperfusion (and subsequent loss of the actual capil laries). The ischemia or hypoxia, or both, then presumably served as a stimulus for the development of neovascularization by an as yet undetermined mechanism. In other clinical settings characterized by retinal ischemia and subsequent neovascularization, such as diabetic retinopathy and sickle cell retinopathy, it has been speculated that a vasotactic factor released by the hypoxic retina is the neovasculogenic factor. These
AUGUST, 1975
new vessels advance through the internal limiting membrane and attach to (or, rarely, penetrate) the posterior hyaloid membrane where they continue to proliferate. As the posterior hyaloid membrane detaches from the internal limiting membrane and retracts, it pulls the tuft of neovascular tissue along with it away from the retina.4'5 This traction on the new vessels leads either to their rupture with subsequent vitreous hemor rhage or to traction on the retina itself causing a tractional detachment or operculated hole formation, as in the two cases presented here. The development of sub sequent rhegmatogenous retinal detachment then becomes a distinct possibility. Krill, Archer, and Newell6 suggested de struction of neovascular tissue in branch vein occlusion by photocoagulation to pre vent secondary vitreous hemorrhage and macular edema. Michels and Gass7 and Archer, Ernest, and Newell2 suggested the use of photocoagulation to treat neovascular tissue that has caused previous vitreous hemorrhage in an attempt to prevent re peated hemorrhage. Patz 8 described the use of argon laser photocoagulation to prevent the development of neovascularization by de stroying ischemic retinal tissue in areas of nonperfusion after tributary vein occlusion. In this report, we stress the importance of adhesion of neovascular tissue to the posterior hyaloid. Traction from collapsed vitreous led to avulsion of retinal plugs and localized rhegmatogenous detachments of the retina. Photocoagulation was successful in obliterating the retinal holes and in pre venting extension of the retinal detachments. SUMMARY
Two patients had rhegmatogenous retinal detachment after tributary retinal vein oc clusion. Neovascularization adherent to the posterior hyaloid was avulsed, along with a plug of retinal tissue, as the vitreous body collapsed. Localized retinal detachments re sulted. Photocoagulation successfully oblit-
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4. Davis, M. D.: Vitreous contraction in proerated the retinal holes and prevented ex , liferative diabetic retinopathy. Arch. Ophthalmol. tension of the retinal detachments in both 74:741,1965. 5. Tolentino, F. I., Lee, P. F., and Schepens, cases. REFERENCES
1. Zauberman, H.: Retinopathy of retinal detach ment after major vascular occlusion. Br. J. Oph thalmol. 52:117,1968. 2. Archer, D. B., Ernest, J. T., and Newell, F. W.: Classification of branch retinal vein ob struction. Trans. Am. Acad. Ophthalmol. Oto laryngol. 78:148,1974. 3. Gutman, F. A., and Zegarra, H.: The natural course of temporal retinal branch vein occlusion. Trans. Am. Acad. Ophthalmol. Otolaryngol. 78:178, 1974.
C. L.: Biomicroscopic study of vitreous cavity in diabetic retinopathy. Arch. Ophthalmol. 75:238, 1966. 6. Krill, A. E, Archer, D., and Newell, F. W.: Photocoagulation in complications secondary to branch vein occlusion. Arch. Ophthalmol. 85:48, 1971. 7. Michels, R. G., and Gass, J. D. M.: The natural course of retinal branch vein occlusion. Trans. Am. Acad. Ophthalmol. Otolaryngol. 78:166, 1974. 8. Patz, A.: A guide to argon laser photocoagu lation. Survey Ophthalmol. 16:249, 1972.
O P H T H A L M I C MINIATURE
The fallacy of ostensive definition: This is a form of an incomplete definition as pointing to one overt characteristic or to one individual in a class in an attempt to explain and define. To prove existence does not give full meaning. Even more extensive identification of overt character istics may not fully define phenomena, such as those that are mental and have both public and subjective aspects. Public demonstration does have a superior but exclusive claim to proof. When ostension cannot be per formed, it should not be concluded that no other demonstrative act—as subjective report—is of use as evidence of existence. . . . suddenly a footman in livery came running out of the wood (she consid ered him to be a footman because he was in livery; otherwise she would have called him a fish).
Dwight J. Ingle Fallacies and errors in the Wonderlands of Biology, Medicine, and Lewis Carroll Perspectives in Biology and Medicine 15:261 1972
