TALC EMBOLI AND RETINAL NEOVASCULARIZATION IN A DRUG ABUSER L I N D A J. KRESCA, M.D.,
M O R T O N F. G O L D B E R G , M.D., Chicago,
Peripheral retinal neovascularization has been found in many diseases charac terized by sluggish blood flow, vascular occlusions, and hypoxia, with production of a presumed vasoformative stimulus. 1 Such diseases include sickle cell hemoglobinopathies, 2 - 6 hemoglobin C trait, 7 macroglobulinemia, 8 ' 9 polycythemia, 10 chronic myelogenous leukemia, 11,12 sarcoidosis, 13 ' 14 retrolental fibroplasia,15,16 Eales' disease, uveitis, branch retinal vein occlusion, periphlebitis, diabetes mellitus, incontinentia pigmenti, and others. Neovascularization may represent a reparative effort of new vessels to revascularize ischemic or hypoxic zones. A variety of endogenous (cholesterol, calcium, platelets, fibrin, lipids, bacteria, tumor, amniotic fluid) and exogenous (parasites, fungi, silicone, air, mercury, oil, talc, cornstarch, glass beads) materials have been known to enter the retinal arterial tree, block vessels, and cause reti nal ischemia. We describe herein a case of probable talc microembolization. Although several previous cases with retinal talc emboli have been reported, 17 ' 18 this is the first case associated with peripheral neovas cularization of the retina. From the Department of Ophthalmology, Univer sity of Illinois Eye and Ear Infirmary, Chicago, Illinois. This study was supported in part by grant PHS HL15168 from the National Heart and Lung Institute, National Institutes of Health; an unre stricted grant from Research to Prevent Blindness, Inc., New York City; and a research grant from the Illinois Society for the Prevention of Blindness, Chicago, Illinois. Reprint requests to Lee M. Jampol, M.D...Depart ment of Ophthalmology, University of Illinois Eye and Ear Infirmary, 1855 W. Taylor St., Chicago, IL 60612. 334
AND L E E M. J A M P O L ,
M.D.
Illinois CASE REPORT A 38-year-old man was admitted to the psychiatry service's methadone program in September 1977 and was referred to our ophthalmology clinic for a routine examination. He had been a chronic alcohol and drug abuser for 17 years. He admitted using pentazocine (Talwin), tripelennamine HC1, and heroin, all intravenously. He made an aqueous sus pension from oral medications, and the drugs were then filtered through used cigarette filters. Needles and syringes were used many times. The patient had numerous episodes of chills, fever, and malaise after injecting various drugs. His general health had been good except for a hospitalization in 1972 for pneumonia. There was no history of diabetes mellitus or sickle cell disease. He had no ocular symptoms. Ocular history in cluded a skin laceration in the right medial canthal area in 1969, sustained from a piece of metal that flew out from a grinding machine. The laceration was sutured in the emergency room and he was told that no permanent ocular damage had occurred. Three weeks before admission he was hit with a lawn marker stick in the right eye, which resulted in some eyelid edema but no ocular injection, discom fort, or decreased visual acuity. Visual acuity was 6/6 (20/20) and J l in each eye uncorrected. External and slit-lamp examinations were normal. Applanation tension was 16 mm Hg bilaterally. Goldmann fields were normal, and gonioscopy disclosed wide open angles in both eyes. Ophthalmoscopic examination revealed multiple, glistening, refractile bodies in small retinal vessels throughout both retinas, especially concentrated in the perimacular areas (Figs. 1-3). Retinal neovascu larization was present in the temporal periphery of the left eye and the nasal periphery of the right eye at the junction of the well-perfused and poorly perfused retina (Fig. 4). Additionally, retinal hemor rhage, and old, resolving, inferior vitreous hemor rhage were present in the right eye. The pathogenesis of the retinal neovascularization was related to peripheral retinal vascular occlusions secondary to emboli from intravenous drug abuse. The emboli were considered to be talc particles. Laboratory tests were done to rule out other possible factors such as diabetes mellitus, sickle cell hemoglobinopathies, leukemia, sarcoidosis, syphilis, and polycythemia. The following laboratory results were obtained: two-hour postprandial blood glucose, 112 mg/100 ml; automated chemical analyses (Na + , K+, Ca + + , Cl~, blood urea nitrogen, creatinine), normal; quantitative hemoglobin electrophoresis, 96.8% A, 2.6% A2, and 0.6%F; hemoglobin, 13.7 gm/100 ml;
AMERICAN JOURNAL O F OPHTHALMOLOGY 87:334-339, 1979
Fig. 1 (Kresca, Goldberg, and Jampol). Posterior pole of left eye demonstrating talc emboli.
Fig. 2 (Kresca, Goldberg, and Jampol). Macula of left eye demonstrating talc emboli.
Fig. 3 (Kresca, Goldberg, and Jampol). Posterior pole of right eye demonstrating talc emboli.
Fig. 4 (Kresca, Goldberg, and Jampol). Temporal periphery of left eye showing neovascularization (arrows) and demarcation zone between normal and ischemic retina.
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hematocrit, 42.1%, white blood cell count, 5,900/ mm 3 with 39% polymorphonuclear leukocytes, 47% lymphocytes, and 14% monocytes; and VDRL, neg ative. Because of lack of patient cooperation, ade quate fluorescein angiography, further laboratory evaluation, and argon laser treatment could not be done. We cannot completely exclude the possibility of a leukemic process based on the slightly abnor mal differential white blood cell count obtained, but the peripheral smear was normal. DISCUSSION
Attempts to embolize retinal vessels experimentally have been made since the late 1800s by using various methods. 1 9 " 2 1 In one case, graded glass ballotini were injected into the common carotid artery of cats. 19 Retinal vascular changes included visible ballotini in the arterioles, sludging phenomena in the blocked arterioles and adjacent venules, arteriolar anastomoses, and venular anastomoses. Visible anasto moses appeared several days after occlu sion of an arteriolar branch. The vascular communications appeared to be enlarged interarteriolar capillary channels, rather than newly formed vessels. Peripheral neovascularization occurred only after ballotini embolization in the immature retina of an 8-day-old kitten. When injection of the external carotid artery in dogs with latex microspheres of known sizes resulted in isolated occlu sion of small retinal vessels (capillaries and precapillary arterioles), there were apparently no histologic changes in the retina. 22 Occlusion of large retinal vessels (arterioles), however, caused atrophic changes in the inner retinal layers (gan glion and bipolar cells). Flat preparations of the retina revealed no evidence of neovascularization or new anastomotic vessels during a three- to nine-month follow-up period. The absence of anasto moses differs with the findings of other observers. Blood flow rates were determined by injecting radioactively labeled microspheres 15 JJL in diameter through the femoral veins of monkeys. 2 1 This method is based on the assumption that the
337
spheres are evenly mixed in arterial blood and are trapped in the blood vessels of a tissue in proportion to blood flow in that particular tissue. Blood flow (in milliliters per minute per square millimeter) through various regions of the fundus was calculated from the radioactivity of rectangular pieces cut out from flatmount preparations. The retina and choroid were divided into four regions: foveal, peripapillary, intermediary, and peripheral. Results showed that blood flow was greatest to the foveal area for both retinal and choroidal vasculatures, followed by the peripapillary, interme diary, and peripheral areas, in decreasing order. Thus, the distribution of blood flow within the monkey choroid and retina was different from that seen in cats, for which the flow was evenly distributed. 2 3 The uneven distribution of the spheres in pri mates is probably caused by an uneven blood flow distribution with increased flow to the macular and peripapillary re gions. This interpretation is supported by the observation that in the submacular area of the choroid a greater density of arteries is present than in any other area equidistant from the disk. 24 Furthermore, Michaelson 2 5 reported a denser retinal capillary net in the peripapillary and perimacular regions than in the periphery of the human retina. Oral medications including those used by our patient contain inert filler material (usually talc or starch) which, if not fil tered properly before intravascular injec tion, can act as emboli in the microcirculation. The appearance of the emboli in our patient is most consistent with talc. 17,18 Most of the talc emboli apparent ly settled out in the retinal circulation of the posterior pole because of the denser capillary net in that area, 25 and the greater blood flow to that region. 21 The occur rence of neovascularization at the inter face between perfused and nonperfused portions of the peripheral retina is consis tent with other, similar clinical reports. 26
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It suggests that blood flow had been re duced to a more critical level in the retinal periphery than in the posterior pole, even though a greater number of talc emboli had been filtered out in the posterior pole. This is not surprising in view of the poor perfusion of the peripheral retina as com pared with the rich blood supply of the posterior pole. Wise, Dollery, and Henkind 2 7 stated that retinal neovascularization does not occur after central retinal artery or branch arterial occlusion. Recent reports suggest that this is not always the case, however. Jampol, Isenberg, and Goldberg 2 8 de scribed retinal arteriolitis in a 34-year-old woman, which led to a superotemporal branch arteriolar occlusion, with the sub sequent development of retinal neovascu larization. Manschot 29 described two cases of central retinal artery obstruction with the histopathologic finding of a thick prepapillary and peripapillary neovascular layer. Other occlusive arterial dis eases such as carotid artery disease and aortic arch syndromes can lead to ocular ischemia and subsequent retinal neovas cularization. 30 Sickle-cell retinopathy, an occlusive disease of peripheral retinal arterioles, 31 ' 32 is frequently characterized by the development of peripheral retinal sea fan neovascularization. Our case of talc embolization can be considered a model of proliferative sickle-cell retinop athy, 26 in that the initiating event was vaso-occlusion and the neovasculariza tion was located at the equator and oc curred at the junction between perfused (proximal, posterior) and nonperfused (distal, anterior) portions of the retina. In both diseases peripheral vaso-occlusion appears to be initiated by embolization of the retinal vascular tree (by sickled erythrocytes in proliferative sickle cell retinop athy, and by talc particles in the present case). Addendum—Additional cases of retinal talc emboli have been reported. 33 No neovascularization was noted.
MARCH, 1979
SUMMARY
A 38-year-old male drug abuser had multiple emboli in the retinal circulation of the posterior pole of both eyes. He showed widespread peripheral retinal capillary nonperfusion and neovascular proliferation at the junction of perfused and nonperfused retina. The emboli were considered to be talc particles from the intravenous administration of suspen sions of oral medications. The presumed mechanism of development of neovascu larization in this case was the filtering out of the particles by the retinal vasculature with vaso-occlusion, ischemia and subse quent retinal neovascularization. REFERENCES 1. Wise, G. N.: Factors influencing retinal new vessel formation. Am. J. Ophthalmol. 52:637, 1961. 2. Condon, P. I., and Serjeant, G. R.: Ocular findings in sickle-cell thalassemia in Jamaica. Am J. Ophthalmol. 74:1105, 1972. 3. Nagpal, K. C., Asdourian, G. K., Patrianakos, D., Goldberg.M. F., Rabb, M. F., Goldbaum, M., and Raichand, M.: Proliferative retinopathy in sickle-cell trait. Report of seven cases. Arch. Intern. Med. 137:325, 1977. 4. Welch, R. B., and Goldberg, M. F.: Sickle-cell hemoglobin and its relation to fundus abnormality. Arch. Ophthalmol. 75:353, 1966. 5. Goldberg, M. F., Charache, S., and Acacio, I.: Ophthalmologic manifestations of sickle-cell thalas semia. Arch. Intern. Med. 128:33, 1971. 6. Condon, P. I., and Serjeant, G. R.: Ocular findings in homozygous sickle-cell anemia in Jamai ca. Am. J. Ophthalmol. 73:533, 1972. 7. Moschandreou, M., Galinos, S., Valenzuela, R., Constantaras, A. A., Goldberg, M. F., and Adams, J.: Retinopathy in hemoglobin C trait (AC hemoglobinopathy). Am. J. Ophthalmol. 77:465, 1974. 8. Anderson, B., and Samuelson, A.: A case of hyperglobulinemia with pronounced eye changes and acrocyanosis. Acta Med. Sci. 117:248, 1944. 9. Carr, R. E., and Henkind, P.: Retinal findings associated with serum hyperviscosity. Am. J. Oph thalmol. 56:23, 1963. 10. Nagy, F.: Changes in the fundus caused by polycythaemia. Br. J. Ophthalmol. 34:380, 1950. 11. Frank, R. N., and Ryan, S. J., Jr.: Peripheral retinal neovascularization with chronic myelogenous leukemia. Arch. Ophthalmol. 87:585, 1972. 12. Morse, P. H., and McCready, J. L.: Peripheral retinal neovascularization in chronic myelocytic leukemia. Am. J. Ophthalmol. 72:975, 1971. 13. Algvere, P.: Fluorescein studies of retinal vasculitis in sarcoidosis. Report of a case. Acta Ophthalmol. 48:1129, 1970.
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14. Asdourian, G. K., Goldberg, M. F., and Busse, B. J.: Peripheral retinal neovascularization in sarcoidosis. Arch. Ophthalmol. 93:787, 1975. 15. Ashton, N., Ward B., and Serpell, G.: Effect of oxygen on developing retinal vessels with particular reference to the problem of retrolental fibroplasia. Br. J. Ophthalmol. 38:397, 1954. 16. Patz, A.: Retrolental fibroplasia. Survey Oph thalmol. 14:1, 1969. 17. Lee, J., and Sapira, J.: Retinal and cerebral microembolization of talc in a drug abuser. Am. J. Med. Sci. 265:75, 1973. 18. Atlee, W.: Talc and cornstarch emboli in eyes of drug abusers. J. A. M. A. 219:49, 1972. 19. Ashton, N., and Henkind, P.: Experimental occlusion of retinal arterioles. Br. J. Ophthalmol. 49:225, 1965. 20. Gay, A. J., Goldor, H., and Smith, M.: Chorioretinal vascular occlusions with latex spheres. Invest. Ophthalmol. 3:647, 1964. 21. Aim, A., and Bill, A.: Ocular and optic nerve blood flow at normal and increased intraocular pres sures in monkeys. A study with radioactively la belled microspheres including flow determinations in brain and some other tissues. Exp. Eye Res. 15:15, 1973. 22. Goldor, H., and Gay, A. J.: Chorioretinal vas cular occlusions with latex microspheres (a longterm study). Pt. 2. Invest. Ophthalmol. 6:51, 1967. 23. Aim, A., and Bill, A.: The oxygen supply to the retina. 2. Effects of high intraocular pressure and of increased arterial carbon dioxide tension on uveal
339
and retinal blood flow in cats. A study with radioac tively labelled microspheres including flow deter mination in brain and some other tissues. Acta Physiol. Scand. 84:306, 1972. 24. Ring, H. G., and Fujino, T.: Observations on the anatomy and pathology of the choroidal vasculature. Arch. Ophthalmol. 78:431, 1967. 25. Michaelson, I. C.: Retinal Circulation in Man and Animals. Springfield, Charles C Thomas, 1954, pp. 74-100. 26. Goldberg, M. F.: Classification and pathogenesis of proliferative sickle retinopathy. Am. J. Ophthalmol. 71:649, 1971. 27. Wise, G. N., Dollery, C. T., and Henkind, P.: The Retinal Circulation. New York, Harper and Row, 1971, p . 299. 28. Jampol, L. M., Isenberg, S. J., and Goldberg, M. F.: Occlusive retinal arteriolitis with neovascu larization. Am. J. Ophthalmol. 81:583, 1976. 29. Manschot, W. A.: Retinal vascular obstruc tion. Doc. Ophthalmol. 40:383, 1976. 30. Knox, D. L.: Ischemic ocular inflammation. Am. J. Ophthalmol. 60:996, 1965. 31. Goldberg, M. F.: Retinal vaso-occlusion in sickling hemoglobinopathies. Birth Defects 12:475, 1976. 32. Goldberg, M. F.: Retinal neovascularization in sickle-cell retinopathy. Trans. Am. Acad. Oph thalmol. Otolaryngol. 83:409, 1977. 33. Murphy, S. B., Jackson, W. B., and Pare, J. A. P.: Talc retinopathy. Can. J. Ophthalmol. 13: 152, 1978.
M O R T O N F. G O L D B E R G , M.D., Chicago,
Peripheral retinal neovascularization has been found in many diseases charac terized by sluggish blood flow, vascular occlusions, and hypoxia, with production of a presumed vasoformative stimulus. 1 Such diseases include sickle cell hemoglobinopathies, 2 - 6 hemoglobin C trait, 7 macroglobulinemia, 8 ' 9 polycythemia, 10 chronic myelogenous leukemia, 11,12 sarcoidosis, 13 ' 14 retrolental fibroplasia,15,16 Eales' disease, uveitis, branch retinal vein occlusion, periphlebitis, diabetes mellitus, incontinentia pigmenti, and others. Neovascularization may represent a reparative effort of new vessels to revascularize ischemic or hypoxic zones. A variety of endogenous (cholesterol, calcium, platelets, fibrin, lipids, bacteria, tumor, amniotic fluid) and exogenous (parasites, fungi, silicone, air, mercury, oil, talc, cornstarch, glass beads) materials have been known to enter the retinal arterial tree, block vessels, and cause reti nal ischemia. We describe herein a case of probable talc microembolization. Although several previous cases with retinal talc emboli have been reported, 17 ' 18 this is the first case associated with peripheral neovas cularization of the retina. From the Department of Ophthalmology, Univer sity of Illinois Eye and Ear Infirmary, Chicago, Illinois. This study was supported in part by grant PHS HL15168 from the National Heart and Lung Institute, National Institutes of Health; an unre stricted grant from Research to Prevent Blindness, Inc., New York City; and a research grant from the Illinois Society for the Prevention of Blindness, Chicago, Illinois. Reprint requests to Lee M. Jampol, M.D...Depart ment of Ophthalmology, University of Illinois Eye and Ear Infirmary, 1855 W. Taylor St., Chicago, IL 60612. 334
AND L E E M. J A M P O L ,
M.D.
Illinois CASE REPORT A 38-year-old man was admitted to the psychiatry service's methadone program in September 1977 and was referred to our ophthalmology clinic for a routine examination. He had been a chronic alcohol and drug abuser for 17 years. He admitted using pentazocine (Talwin), tripelennamine HC1, and heroin, all intravenously. He made an aqueous sus pension from oral medications, and the drugs were then filtered through used cigarette filters. Needles and syringes were used many times. The patient had numerous episodes of chills, fever, and malaise after injecting various drugs. His general health had been good except for a hospitalization in 1972 for pneumonia. There was no history of diabetes mellitus or sickle cell disease. He had no ocular symptoms. Ocular history in cluded a skin laceration in the right medial canthal area in 1969, sustained from a piece of metal that flew out from a grinding machine. The laceration was sutured in the emergency room and he was told that no permanent ocular damage had occurred. Three weeks before admission he was hit with a lawn marker stick in the right eye, which resulted in some eyelid edema but no ocular injection, discom fort, or decreased visual acuity. Visual acuity was 6/6 (20/20) and J l in each eye uncorrected. External and slit-lamp examinations were normal. Applanation tension was 16 mm Hg bilaterally. Goldmann fields were normal, and gonioscopy disclosed wide open angles in both eyes. Ophthalmoscopic examination revealed multiple, glistening, refractile bodies in small retinal vessels throughout both retinas, especially concentrated in the perimacular areas (Figs. 1-3). Retinal neovascu larization was present in the temporal periphery of the left eye and the nasal periphery of the right eye at the junction of the well-perfused and poorly perfused retina (Fig. 4). Additionally, retinal hemor rhage, and old, resolving, inferior vitreous hemor rhage were present in the right eye. The pathogenesis of the retinal neovascularization was related to peripheral retinal vascular occlusions secondary to emboli from intravenous drug abuse. The emboli were considered to be talc particles. Laboratory tests were done to rule out other possible factors such as diabetes mellitus, sickle cell hemoglobinopathies, leukemia, sarcoidosis, syphilis, and polycythemia. The following laboratory results were obtained: two-hour postprandial blood glucose, 112 mg/100 ml; automated chemical analyses (Na + , K+, Ca + + , Cl~, blood urea nitrogen, creatinine), normal; quantitative hemoglobin electrophoresis, 96.8% A, 2.6% A2, and 0.6%F; hemoglobin, 13.7 gm/100 ml;
AMERICAN JOURNAL O F OPHTHALMOLOGY 87:334-339, 1979
Fig. 1 (Kresca, Goldberg, and Jampol). Posterior pole of left eye demonstrating talc emboli.
Fig. 2 (Kresca, Goldberg, and Jampol). Macula of left eye demonstrating talc emboli.
Fig. 3 (Kresca, Goldberg, and Jampol). Posterior pole of right eye demonstrating talc emboli.
Fig. 4 (Kresca, Goldberg, and Jampol). Temporal periphery of left eye showing neovascularization (arrows) and demarcation zone between normal and ischemic retina.
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hematocrit, 42.1%, white blood cell count, 5,900/ mm 3 with 39% polymorphonuclear leukocytes, 47% lymphocytes, and 14% monocytes; and VDRL, neg ative. Because of lack of patient cooperation, ade quate fluorescein angiography, further laboratory evaluation, and argon laser treatment could not be done. We cannot completely exclude the possibility of a leukemic process based on the slightly abnor mal differential white blood cell count obtained, but the peripheral smear was normal. DISCUSSION
Attempts to embolize retinal vessels experimentally have been made since the late 1800s by using various methods. 1 9 " 2 1 In one case, graded glass ballotini were injected into the common carotid artery of cats. 19 Retinal vascular changes included visible ballotini in the arterioles, sludging phenomena in the blocked arterioles and adjacent venules, arteriolar anastomoses, and venular anastomoses. Visible anasto moses appeared several days after occlu sion of an arteriolar branch. The vascular communications appeared to be enlarged interarteriolar capillary channels, rather than newly formed vessels. Peripheral neovascularization occurred only after ballotini embolization in the immature retina of an 8-day-old kitten. When injection of the external carotid artery in dogs with latex microspheres of known sizes resulted in isolated occlu sion of small retinal vessels (capillaries and precapillary arterioles), there were apparently no histologic changes in the retina. 22 Occlusion of large retinal vessels (arterioles), however, caused atrophic changes in the inner retinal layers (gan glion and bipolar cells). Flat preparations of the retina revealed no evidence of neovascularization or new anastomotic vessels during a three- to nine-month follow-up period. The absence of anasto moses differs with the findings of other observers. Blood flow rates were determined by injecting radioactively labeled microspheres 15 JJL in diameter through the femoral veins of monkeys. 2 1 This method is based on the assumption that the
337
spheres are evenly mixed in arterial blood and are trapped in the blood vessels of a tissue in proportion to blood flow in that particular tissue. Blood flow (in milliliters per minute per square millimeter) through various regions of the fundus was calculated from the radioactivity of rectangular pieces cut out from flatmount preparations. The retina and choroid were divided into four regions: foveal, peripapillary, intermediary, and peripheral. Results showed that blood flow was greatest to the foveal area for both retinal and choroidal vasculatures, followed by the peripapillary, interme diary, and peripheral areas, in decreasing order. Thus, the distribution of blood flow within the monkey choroid and retina was different from that seen in cats, for which the flow was evenly distributed. 2 3 The uneven distribution of the spheres in pri mates is probably caused by an uneven blood flow distribution with increased flow to the macular and peripapillary re gions. This interpretation is supported by the observation that in the submacular area of the choroid a greater density of arteries is present than in any other area equidistant from the disk. 24 Furthermore, Michaelson 2 5 reported a denser retinal capillary net in the peripapillary and perimacular regions than in the periphery of the human retina. Oral medications including those used by our patient contain inert filler material (usually talc or starch) which, if not fil tered properly before intravascular injec tion, can act as emboli in the microcirculation. The appearance of the emboli in our patient is most consistent with talc. 17,18 Most of the talc emboli apparent ly settled out in the retinal circulation of the posterior pole because of the denser capillary net in that area, 25 and the greater blood flow to that region. 21 The occur rence of neovascularization at the inter face between perfused and nonperfused portions of the peripheral retina is consis tent with other, similar clinical reports. 26
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It suggests that blood flow had been re duced to a more critical level in the retinal periphery than in the posterior pole, even though a greater number of talc emboli had been filtered out in the posterior pole. This is not surprising in view of the poor perfusion of the peripheral retina as com pared with the rich blood supply of the posterior pole. Wise, Dollery, and Henkind 2 7 stated that retinal neovascularization does not occur after central retinal artery or branch arterial occlusion. Recent reports suggest that this is not always the case, however. Jampol, Isenberg, and Goldberg 2 8 de scribed retinal arteriolitis in a 34-year-old woman, which led to a superotemporal branch arteriolar occlusion, with the sub sequent development of retinal neovascu larization. Manschot 29 described two cases of central retinal artery obstruction with the histopathologic finding of a thick prepapillary and peripapillary neovascular layer. Other occlusive arterial dis eases such as carotid artery disease and aortic arch syndromes can lead to ocular ischemia and subsequent retinal neovas cularization. 30 Sickle-cell retinopathy, an occlusive disease of peripheral retinal arterioles, 31 ' 32 is frequently characterized by the development of peripheral retinal sea fan neovascularization. Our case of talc embolization can be considered a model of proliferative sickle-cell retinop athy, 26 in that the initiating event was vaso-occlusion and the neovasculariza tion was located at the equator and oc curred at the junction between perfused (proximal, posterior) and nonperfused (distal, anterior) portions of the retina. In both diseases peripheral vaso-occlusion appears to be initiated by embolization of the retinal vascular tree (by sickled erythrocytes in proliferative sickle cell retinop athy, and by talc particles in the present case). Addendum—Additional cases of retinal talc emboli have been reported. 33 No neovascularization was noted.
MARCH, 1979
SUMMARY
A 38-year-old male drug abuser had multiple emboli in the retinal circulation of the posterior pole of both eyes. He showed widespread peripheral retinal capillary nonperfusion and neovascular proliferation at the junction of perfused and nonperfused retina. The emboli were considered to be talc particles from the intravenous administration of suspen sions of oral medications. The presumed mechanism of development of neovascu larization in this case was the filtering out of the particles by the retinal vasculature with vaso-occlusion, ischemia and subse quent retinal neovascularization. REFERENCES 1. Wise, G. N.: Factors influencing retinal new vessel formation. Am. J. Ophthalmol. 52:637, 1961. 2. Condon, P. I., and Serjeant, G. R.: Ocular findings in sickle-cell thalassemia in Jamaica. Am J. Ophthalmol. 74:1105, 1972. 3. Nagpal, K. C., Asdourian, G. K., Patrianakos, D., Goldberg.M. F., Rabb, M. F., Goldbaum, M., and Raichand, M.: Proliferative retinopathy in sickle-cell trait. Report of seven cases. Arch. Intern. Med. 137:325, 1977. 4. Welch, R. B., and Goldberg, M. F.: Sickle-cell hemoglobin and its relation to fundus abnormality. Arch. Ophthalmol. 75:353, 1966. 5. Goldberg, M. F., Charache, S., and Acacio, I.: Ophthalmologic manifestations of sickle-cell thalas semia. Arch. Intern. Med. 128:33, 1971. 6. Condon, P. I., and Serjeant, G. R.: Ocular findings in homozygous sickle-cell anemia in Jamai ca. Am. J. Ophthalmol. 73:533, 1972. 7. Moschandreou, M., Galinos, S., Valenzuela, R., Constantaras, A. A., Goldberg, M. F., and Adams, J.: Retinopathy in hemoglobin C trait (AC hemoglobinopathy). Am. J. Ophthalmol. 77:465, 1974. 8. Anderson, B., and Samuelson, A.: A case of hyperglobulinemia with pronounced eye changes and acrocyanosis. Acta Med. Sci. 117:248, 1944. 9. Carr, R. E., and Henkind, P.: Retinal findings associated with serum hyperviscosity. Am. J. Oph thalmol. 56:23, 1963. 10. Nagy, F.: Changes in the fundus caused by polycythaemia. Br. J. Ophthalmol. 34:380, 1950. 11. Frank, R. N., and Ryan, S. J., Jr.: Peripheral retinal neovascularization with chronic myelogenous leukemia. Arch. Ophthalmol. 87:585, 1972. 12. Morse, P. H., and McCready, J. L.: Peripheral retinal neovascularization in chronic myelocytic leukemia. Am. J. Ophthalmol. 72:975, 1971. 13. Algvere, P.: Fluorescein studies of retinal vasculitis in sarcoidosis. Report of a case. Acta Ophthalmol. 48:1129, 1970.
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14. Asdourian, G. K., Goldberg, M. F., and Busse, B. J.: Peripheral retinal neovascularization in sarcoidosis. Arch. Ophthalmol. 93:787, 1975. 15. Ashton, N., Ward B., and Serpell, G.: Effect of oxygen on developing retinal vessels with particular reference to the problem of retrolental fibroplasia. Br. J. Ophthalmol. 38:397, 1954. 16. Patz, A.: Retrolental fibroplasia. Survey Oph thalmol. 14:1, 1969. 17. Lee, J., and Sapira, J.: Retinal and cerebral microembolization of talc in a drug abuser. Am. J. Med. Sci. 265:75, 1973. 18. Atlee, W.: Talc and cornstarch emboli in eyes of drug abusers. J. A. M. A. 219:49, 1972. 19. Ashton, N., and Henkind, P.: Experimental occlusion of retinal arterioles. Br. J. Ophthalmol. 49:225, 1965. 20. Gay, A. J., Goldor, H., and Smith, M.: Chorioretinal vascular occlusions with latex spheres. Invest. Ophthalmol. 3:647, 1964. 21. Aim, A., and Bill, A.: Ocular and optic nerve blood flow at normal and increased intraocular pres sures in monkeys. A study with radioactively la belled microspheres including flow determinations in brain and some other tissues. Exp. Eye Res. 15:15, 1973. 22. Goldor, H., and Gay, A. J.: Chorioretinal vas cular occlusions with latex microspheres (a longterm study). Pt. 2. Invest. Ophthalmol. 6:51, 1967. 23. Aim, A., and Bill, A.: The oxygen supply to the retina. 2. Effects of high intraocular pressure and of increased arterial carbon dioxide tension on uveal
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