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Chorioretinal Anastomoses after Argon Laser Photocoagulation
C H O R I O R E T I N A L ANASTOMOSES AFTER ARGON LASER P H O T O C O A G U L A T I O N S P I R O S O. G A L I N O S , M.D., J. W A L L A C E M C M E E L , M.D., C L E M E N T L. T R E M P E , M.D., A N D C H A R L E S L. S C H E P E N S , M.D. Boston,
Massachusetts
Photocoagulation remains the method of choice in treating vascular lesions of diverse etiology, and the introduction of the argon laser in recent years has made this mode of treatment even more popu lar. However, argon laser photocoagulation has been associated with severe com plications such as retinal and choroidal hemorrhages, nerve fiber field defects, ischémie or thermal papillitis, recur rent neovascularization, preretinal mem brane contracture, acute choroidal ische mia, and corneal or lenticular b u r n s . 1 - 5 We treated two patients with argon laser photocoagulation with subsequent com munication between the retinal and cho roidal circulation. CASE REPORTS Case 1—In February 1971, a 41-year-old white man, diabetic for 25 years, had recurrent episodes of blurred vision in both eyes. His diabetes was stable on 40 units of insulin (NPH) daily. Visual acuity was 6/6 (20/20) in each eye. The external ocular structures and anterior segments were normal. Ophthalmoscopy showed moderately dense intraretinal hemorrhages and microaneurysms, a few hard exudates, and multiple areas of flat retinal neovascularization in both eyes. Epipapillary neovascular growth and intravitreous hemor rhages, which caused episodes of blurred vision, were also present in both eyes. The plan was to obliterate the proliferative lesions in both retinas by photocoagulation. The right eye was treated with the xenon arc photocoagulator (MIRA Model 1000). Two hundred applications were delivered without complications From the Eye Research Institute of Retina Foun dation and the Retina Service of the Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. This study was supported by Public Health Service grant EY-00227, National Eye Institute, National Insti tutes of Health, and by the Massachusetts Lions Eye Research, Inc. Reprint requests to Spiros O. Galinos, M.D., Uni versity of Massachusetts Medical Center, Depart ment of Ophthalmology, 55 Lake Ave. North, Worcester, MA 01605.
with the field diaphragm set at normal, a 4.5-degree spot size, the power set at green 1, and an average exposure time of 0.3 seconds. In January and Sep tember 1973, additional photocoagulation treatment was performed to eliminate recurrent neovasculari zation. One neovascular frond was located along the 9:30 o'clock meridian and surrounded by pigment proliferation (Fig. 1). Fluorescein angiography showed that the frond obtained its blood supply from the retinal circulation (Fig. 2). On these last two treatments the monochromatic argon laser was used. T h e wavelength was 514.5 nm (green), the spot size varied from 100 to 500 μ, the intensity was between 100 and 250 mW, and the exposure time was constant at 0.2 seconds. Both sessions were free of complications and visual acuity was 6/6 (20/20). In December 1973, ophthalmoscopy revealed an unusually large (1 disk diameter or 1,500 μ) chorioretinal scar at a laser treatment site (spot size, 100 to 500 μ) just inferior to the superotemporal vein and within 3 disk diameters from the fovea at the 9:30 o'clock meridian. The scar was unpigmented, yellow-white, and slightly elevated. Several new vessels accompanied by dense fibrous tissue emerged from its center and extended inferotemporally and superonasally (Fig. 3). The lesion was partially hidden by a vitreous hemorrhage. Biomicroscopy with a three-mirror contact lens revealed that the vascular tuft emerged from the chorioretinal scar and extended into the vitreous cavity giving a
Fig. 1 (Galinos and associates). Case 1. The area of recurrent neovascularization after xenon arc photocoagulation treatment. Note zone of hyperpigmentation (arrows) surrounding fibrovascular tissue (fv); arterioles (a) and venule (v).
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Fig. 2 (Galinos and associates). Case 1. Fluorescein angiogram of same lesion as in Figure 1, 11 seconds after injection, showing neovascular tissue (arrow) filling from retinal arteriole (a). few communicating branches to the surrounding retinal vessels inferiorly. To determine the origin of this neovascular frond, rapid-sequence fluorescein angiography (two frames per second) was performed (Fig. 4). The vascular tufts filled with fluorescein earlier than the sur rounding retinal vessels, proving that their blood supply was from the choroid. A communication between these tufts and retinal vessels was noted in late frames of the angiogram. To arrest this florid growth two argon laser ses sions were performed under topical anesthesia, first in January 1974 (150 to 200 mW, 100 to 500 μ, 0.2 seconds, 645 applications) and again in October 1974 (400 to 500 mW, 250 to 500 μ, 0.5 seconds, 710 applications). At each session, treatment was directed to the peripheral arcades, avoiding the central vascular channels, in an attempt to decrease the vascularity of the growth. Although the neovascular tufts were not obliterated, both the vascularity of the growth and the leakage of dye markedly decreased. Subsequent ly, vitreous hemorrhages recurred and visual acuity was 6/60 (20/200). Hazy media precluded further treatment. The left eye had argon laser photocoagu lation treatments without complications. Case 2—A 26-year-old white man in January 1973 complained of cloudy vision of two months' dura tion in his right eye. He denied previous ocular problems and his past medical history was unre markable. Visual acuity was 6/7.5 (20/25) and the anterior segments were normal in both eyes. Ophthalmoscopy of the right eye revealed a yel lowish circinate intraretinal exudate whose nasal aspect encroached on the temporal portion of the macula. Within the ring of exudation minimal reti nal edema and a glistening aneurysmal dilatation of the inferior temporal artery were seen (Fig. 5). Distal to the aneurysm the artery became dilated and tortuous. Additional dot-like aneurysmal formations
AUGUST, 1976
were noted outside the ring of exudation superotemporal to the macula. Fluorescein angiography revealed total obstruc tion of the inferior temporal retinal artery distal to the aneurysmal dilatation (Fig. 6, top). Retrograde filling of the inferior temporal artery as well as of the aneurysm itself occurred in later angiograms (Fig. 6, bottom). Minimal leakage of fluorescein was seen along the nasal edge of the exudative ring that spread over to the macular area. The tentative diag nosis was Leber's multiple miliary aneurysms. Because of retinal edema and exudates that com promised macular function, argon laser photoco agulation was applied to the right eye. At two separate treatment sessions (one month apart) and under topical anesthesia only, 130 laser applications (514.5 nm, 100 to 250 mW, 50 to 100 μ, 0.2 seconds) were made within the ring of exudation surrounding the dilated arterial segment. The aneurysm-like for mation was spared from treatment since no visible dye leakage had been detected. After photocoagulation the retinal exudates and edema decreased markedly (Fig. 7). Two months after photocoagulation, rapid-sequence fluorescein angiography revealed an anastomosis between the uveal circulation and the inferotemporal retinal ar tery. The choroidal vessel clearly emerged from a whitish, unpigmented, photocoagulation scar, filled with dye ten seconds after injection (Fig. 8), and showed no communication with the surrounding retinal vasculature (Fig. 9). No untoward effects were noted secondary to this abnormal vascular communication. DISCUSSION
A recently recognized complication fol lowing argon laser photocoagulation has
Fig. 3 (Galinos and associates). Case 1. Same area as in Figure 1 after two argon laser treatments. Note new fibrovascular growths (cfv) emanating from center of scar (s) and taut fibrous band (arrow).
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Fig. 4 (Galinos and associates). Case 1. Sequential fluorescein angiograms (13, 14, and 15 seconds after injection) of vascular growth shown in Figure 3. Note progressive filling of main vascular channels first and of peripheral arcades later while surround ing retinal vessels are still unperfused. Top right, White line (arrow) represents fibrous band. Bottom left, T h e retinal vessels (arrowheads) are barely visible while the peripheral arcades already leak profusely.
Fig. 5 (Galinos and associates). Case 2. Vascular lesion (arrow) along inferior retinal artery. The marked intraretinal exudation (ie) extends toward the fovea (f).
been the development of choriovitreous neovascular tufts appearing through photocoagulation scars. Galinos and coworkers 6 have reported three of these cases after treating retinal neovascularization in two cases of sickle cell retinopathy and one case of ocular sarcoidosis. More recently François and co-workers 7 report ed three cases where argon laser photoco agulation, performed to destroy subretinal vascular lesions, enhanced and, in one case, induced choroidal neovascularization. These cases differ in that they relate to diseases affecting the choroidal circula tion rather than the retinal circulation (two patients had angioid streaks and one had macular disciform degeneration) demonstrating vascular lesions that pre dated the laser treatment.
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Fig. 7 (Galinos and associates). Case 2. The same area as in Figure 5 after treatment shows dense scarring, marked decrease of intraretinal exudation, and a visible site of anastomosis (arrow).
With regard to the genesis of such le sions, preliminary experimental evidence in monkeys 8 indicates that a laser beam of high power density invariably destroys Bruch's membrane by excessive heating. The elimination of a section of that natur al barrier between the retina and the choroid sets the stage for the formation of chorioretinal anastomoses. Once such Fig. 6 (Galinos and associates). Case 2. Top, Fluorescein angiogram (19 seconds after injection) of same area as in Figure 5. Note total obstruction of distal portion of artery (a), loss of capillary bed (cb), and aneurysmal dilatations along empty arterial lumen (arrowheads). Bottom, Late phase of fluores cein angiogram (62 seconds after injection). Note retrograde filling of artery (a) and of aneurysm (arrow). More aneurysmal dilatations (d) are evident in an area not visible in top photograph.
In our patients, rapid-sequence fluores cein angiography proved the choroidal origin of the neovascular lesions. The vascular lesions were detected one to six months after the final laser treatment. In the second case, the formation of a true chorioretinal anastomosis had no unto ward sequelae, possibly because it oc curred in the absence of vasoproliferative retinopathy.
Fig. 8 (Galinos and associates). Case 2. Fluores cein angiogram (ten seconds after injection) of lesion shown in Figure 7. Arteriole (a) at the center of the chorioretinal scar (arrow) fluoresces while the sur rounding retinal vessels are still devoid of dye.
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photocoagulation treatment to eliminate abnormal retinal vasculature. In both in stances rapid-sequence fluorescein angiography documented the choroidal origin of the anastomoses. Such anastomoses developed in areas where an excessively dense laser beam aimed at occluding reti nal vessels presumably destroyed the un derlying Bruch's membrane and permit ted invasion of the retina by fibrovascular growth from the choroid. The occurrence of such growths is a potential complica tion of argon laser photocoagulation di rectly related to the power density used. Fig. 9 (Galinos and associates). Case 2. Fluorescein angiogram (15 seconds after injection) shows absence of communication between anastomosed retinal arteriole (a) and surrounding retinal vasculature.
communications are established, new vessels and fibrous tissue grow rapidly into the retina and may even invade the vitreous body, a complication that is apt to occur in retinas already compromised by proliferative retinopathy. The absence of normal pigmentation at the site of the anastomosis as well as rapid blood flow through the chorioretinal shunt make these growths particularly resistant to successful closure by photocoagulation. Finally the diversity of the clinical en tities in which such chorioretinal commu nications have been documented sup ports previous observations 6 that such lesions are a complication of argon laser treatment rather than a manifestation of the underlying retinal vascular disease. SUMMARY
Communication between the retinal and the choroidal circulation occurred in one case of proliferative diabetic retinop athy and one case of Leber's disease (mul tiple miliary aneurysms) after argon laser
ACKNOWLEDGMENT
H. M. Freeman, M.D., referred Case 2.
REFERENCES 1. L'Espérance, F . A., Jr.: The treatment of oph thalmic vascular disease by argon laser photocoagu lation. Trans. Am. Acad. Ophthalmol. Otolaryngol. 73:1077, 1969. 2. Little, H. L., and Zweng, H. C : Complications of argon laser retinal photocoagulation. Trans. Pac. Coast Otoophthalmol. Soc. 52:115, 1971. 3. Patz, A., Maumenee, E. A., and Ryan, S. J.: Argon laser photocoagulation. Advantages and limi tations. Trans. Am. Acad. Ophthalmol. Otolaryngol. 75:569, 1971. 4. Zweng, H. C , Little, H. L., and Hammond, A. H.: Complications of argon laser photocoagulation. Trans. Am. Acad. Ophthalmol. Otolaryngol. 78:195, 1974. 5. Goldbaum, M. H., Galinos, S. O., Apple, D., Asdourian, G. K., Nagpal, K., Jampol, L., Woolf, M. B., and Busse, B.: Acute choroidal ischemia as a complication of photocoagulation. Arch. Ophthal mol. In press. 6. Galinos, S. O., Asdourian, G. A., Woolf, M. B., Goldberg, M. F., and Busse, B. J.: Choroido-vitreal neovascularization after argon laser photocoagula tion. Arch. Ophthalmol. 93:524, 1975. 7. François, J., De Laey, J. J., Cambie, E., Hanssens, M., and Victoria-Troncoso, V.: Neovasculari zation after argon laser photocoagulation of macular lesions. Am. J. Ophthalmol. 79:206, 1975. 8. Goldbaum, M. H., Goldberg, M. F., Nagpal, K., Asdourian, G. K. and Galinos, S.O.: Quantitative photocoagulation and the treatment of proliferative sickle retinopathy. In Proceedings of the First Inter national Photocoagulation Congress. St. Louis, C.V. Mosby. In press.
Massachusetts
Photocoagulation remains the method of choice in treating vascular lesions of diverse etiology, and the introduction of the argon laser in recent years has made this mode of treatment even more popu lar. However, argon laser photocoagulation has been associated with severe com plications such as retinal and choroidal hemorrhages, nerve fiber field defects, ischémie or thermal papillitis, recur rent neovascularization, preretinal mem brane contracture, acute choroidal ische mia, and corneal or lenticular b u r n s . 1 - 5 We treated two patients with argon laser photocoagulation with subsequent com munication between the retinal and cho roidal circulation. CASE REPORTS Case 1—In February 1971, a 41-year-old white man, diabetic for 25 years, had recurrent episodes of blurred vision in both eyes. His diabetes was stable on 40 units of insulin (NPH) daily. Visual acuity was 6/6 (20/20) in each eye. The external ocular structures and anterior segments were normal. Ophthalmoscopy showed moderately dense intraretinal hemorrhages and microaneurysms, a few hard exudates, and multiple areas of flat retinal neovascularization in both eyes. Epipapillary neovascular growth and intravitreous hemor rhages, which caused episodes of blurred vision, were also present in both eyes. The plan was to obliterate the proliferative lesions in both retinas by photocoagulation. The right eye was treated with the xenon arc photocoagulator (MIRA Model 1000). Two hundred applications were delivered without complications From the Eye Research Institute of Retina Foun dation and the Retina Service of the Massachusetts Eye and Ear Infirmary, Boston, Massachusetts. This study was supported by Public Health Service grant EY-00227, National Eye Institute, National Insti tutes of Health, and by the Massachusetts Lions Eye Research, Inc. Reprint requests to Spiros O. Galinos, M.D., Uni versity of Massachusetts Medical Center, Depart ment of Ophthalmology, 55 Lake Ave. North, Worcester, MA 01605.
with the field diaphragm set at normal, a 4.5-degree spot size, the power set at green 1, and an average exposure time of 0.3 seconds. In January and Sep tember 1973, additional photocoagulation treatment was performed to eliminate recurrent neovasculari zation. One neovascular frond was located along the 9:30 o'clock meridian and surrounded by pigment proliferation (Fig. 1). Fluorescein angiography showed that the frond obtained its blood supply from the retinal circulation (Fig. 2). On these last two treatments the monochromatic argon laser was used. T h e wavelength was 514.5 nm (green), the spot size varied from 100 to 500 μ, the intensity was between 100 and 250 mW, and the exposure time was constant at 0.2 seconds. Both sessions were free of complications and visual acuity was 6/6 (20/20). In December 1973, ophthalmoscopy revealed an unusually large (1 disk diameter or 1,500 μ) chorioretinal scar at a laser treatment site (spot size, 100 to 500 μ) just inferior to the superotemporal vein and within 3 disk diameters from the fovea at the 9:30 o'clock meridian. The scar was unpigmented, yellow-white, and slightly elevated. Several new vessels accompanied by dense fibrous tissue emerged from its center and extended inferotemporally and superonasally (Fig. 3). The lesion was partially hidden by a vitreous hemorrhage. Biomicroscopy with a three-mirror contact lens revealed that the vascular tuft emerged from the chorioretinal scar and extended into the vitreous cavity giving a
Fig. 1 (Galinos and associates). Case 1. The area of recurrent neovascularization after xenon arc photocoagulation treatment. Note zone of hyperpigmentation (arrows) surrounding fibrovascular tissue (fv); arterioles (a) and venule (v).
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Fig. 2 (Galinos and associates). Case 1. Fluorescein angiogram of same lesion as in Figure 1, 11 seconds after injection, showing neovascular tissue (arrow) filling from retinal arteriole (a). few communicating branches to the surrounding retinal vessels inferiorly. To determine the origin of this neovascular frond, rapid-sequence fluorescein angiography (two frames per second) was performed (Fig. 4). The vascular tufts filled with fluorescein earlier than the sur rounding retinal vessels, proving that their blood supply was from the choroid. A communication between these tufts and retinal vessels was noted in late frames of the angiogram. To arrest this florid growth two argon laser ses sions were performed under topical anesthesia, first in January 1974 (150 to 200 mW, 100 to 500 μ, 0.2 seconds, 645 applications) and again in October 1974 (400 to 500 mW, 250 to 500 μ, 0.5 seconds, 710 applications). At each session, treatment was directed to the peripheral arcades, avoiding the central vascular channels, in an attempt to decrease the vascularity of the growth. Although the neovascular tufts were not obliterated, both the vascularity of the growth and the leakage of dye markedly decreased. Subsequent ly, vitreous hemorrhages recurred and visual acuity was 6/60 (20/200). Hazy media precluded further treatment. The left eye had argon laser photocoagu lation treatments without complications. Case 2—A 26-year-old white man in January 1973 complained of cloudy vision of two months' dura tion in his right eye. He denied previous ocular problems and his past medical history was unre markable. Visual acuity was 6/7.5 (20/25) and the anterior segments were normal in both eyes. Ophthalmoscopy of the right eye revealed a yel lowish circinate intraretinal exudate whose nasal aspect encroached on the temporal portion of the macula. Within the ring of exudation minimal reti nal edema and a glistening aneurysmal dilatation of the inferior temporal artery were seen (Fig. 5). Distal to the aneurysm the artery became dilated and tortuous. Additional dot-like aneurysmal formations
AUGUST, 1976
were noted outside the ring of exudation superotemporal to the macula. Fluorescein angiography revealed total obstruc tion of the inferior temporal retinal artery distal to the aneurysmal dilatation (Fig. 6, top). Retrograde filling of the inferior temporal artery as well as of the aneurysm itself occurred in later angiograms (Fig. 6, bottom). Minimal leakage of fluorescein was seen along the nasal edge of the exudative ring that spread over to the macular area. The tentative diag nosis was Leber's multiple miliary aneurysms. Because of retinal edema and exudates that com promised macular function, argon laser photoco agulation was applied to the right eye. At two separate treatment sessions (one month apart) and under topical anesthesia only, 130 laser applications (514.5 nm, 100 to 250 mW, 50 to 100 μ, 0.2 seconds) were made within the ring of exudation surrounding the dilated arterial segment. The aneurysm-like for mation was spared from treatment since no visible dye leakage had been detected. After photocoagulation the retinal exudates and edema decreased markedly (Fig. 7). Two months after photocoagulation, rapid-sequence fluorescein angiography revealed an anastomosis between the uveal circulation and the inferotemporal retinal ar tery. The choroidal vessel clearly emerged from a whitish, unpigmented, photocoagulation scar, filled with dye ten seconds after injection (Fig. 8), and showed no communication with the surrounding retinal vasculature (Fig. 9). No untoward effects were noted secondary to this abnormal vascular communication. DISCUSSION
A recently recognized complication fol lowing argon laser photocoagulation has
Fig. 3 (Galinos and associates). Case 1. Same area as in Figure 1 after two argon laser treatments. Note new fibrovascular growths (cfv) emanating from center of scar (s) and taut fibrous band (arrow).
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Fig. 4 (Galinos and associates). Case 1. Sequential fluorescein angiograms (13, 14, and 15 seconds after injection) of vascular growth shown in Figure 3. Note progressive filling of main vascular channels first and of peripheral arcades later while surround ing retinal vessels are still unperfused. Top right, White line (arrow) represents fibrous band. Bottom left, T h e retinal vessels (arrowheads) are barely visible while the peripheral arcades already leak profusely.
Fig. 5 (Galinos and associates). Case 2. Vascular lesion (arrow) along inferior retinal artery. The marked intraretinal exudation (ie) extends toward the fovea (f).
been the development of choriovitreous neovascular tufts appearing through photocoagulation scars. Galinos and coworkers 6 have reported three of these cases after treating retinal neovascularization in two cases of sickle cell retinopathy and one case of ocular sarcoidosis. More recently François and co-workers 7 report ed three cases where argon laser photoco agulation, performed to destroy subretinal vascular lesions, enhanced and, in one case, induced choroidal neovascularization. These cases differ in that they relate to diseases affecting the choroidal circula tion rather than the retinal circulation (two patients had angioid streaks and one had macular disciform degeneration) demonstrating vascular lesions that pre dated the laser treatment.
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Fig. 7 (Galinos and associates). Case 2. The same area as in Figure 5 after treatment shows dense scarring, marked decrease of intraretinal exudation, and a visible site of anastomosis (arrow).
With regard to the genesis of such le sions, preliminary experimental evidence in monkeys 8 indicates that a laser beam of high power density invariably destroys Bruch's membrane by excessive heating. The elimination of a section of that natur al barrier between the retina and the choroid sets the stage for the formation of chorioretinal anastomoses. Once such Fig. 6 (Galinos and associates). Case 2. Top, Fluorescein angiogram (19 seconds after injection) of same area as in Figure 5. Note total obstruction of distal portion of artery (a), loss of capillary bed (cb), and aneurysmal dilatations along empty arterial lumen (arrowheads). Bottom, Late phase of fluores cein angiogram (62 seconds after injection). Note retrograde filling of artery (a) and of aneurysm (arrow). More aneurysmal dilatations (d) are evident in an area not visible in top photograph.
In our patients, rapid-sequence fluores cein angiography proved the choroidal origin of the neovascular lesions. The vascular lesions were detected one to six months after the final laser treatment. In the second case, the formation of a true chorioretinal anastomosis had no unto ward sequelae, possibly because it oc curred in the absence of vasoproliferative retinopathy.
Fig. 8 (Galinos and associates). Case 2. Fluores cein angiogram (ten seconds after injection) of lesion shown in Figure 7. Arteriole (a) at the center of the chorioretinal scar (arrow) fluoresces while the sur rounding retinal vessels are still devoid of dye.
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photocoagulation treatment to eliminate abnormal retinal vasculature. In both in stances rapid-sequence fluorescein angiography documented the choroidal origin of the anastomoses. Such anastomoses developed in areas where an excessively dense laser beam aimed at occluding reti nal vessels presumably destroyed the un derlying Bruch's membrane and permit ted invasion of the retina by fibrovascular growth from the choroid. The occurrence of such growths is a potential complica tion of argon laser photocoagulation di rectly related to the power density used. Fig. 9 (Galinos and associates). Case 2. Fluorescein angiogram (15 seconds after injection) shows absence of communication between anastomosed retinal arteriole (a) and surrounding retinal vasculature.
communications are established, new vessels and fibrous tissue grow rapidly into the retina and may even invade the vitreous body, a complication that is apt to occur in retinas already compromised by proliferative retinopathy. The absence of normal pigmentation at the site of the anastomosis as well as rapid blood flow through the chorioretinal shunt make these growths particularly resistant to successful closure by photocoagulation. Finally the diversity of the clinical en tities in which such chorioretinal commu nications have been documented sup ports previous observations 6 that such lesions are a complication of argon laser treatment rather than a manifestation of the underlying retinal vascular disease. SUMMARY
Communication between the retinal and the choroidal circulation occurred in one case of proliferative diabetic retinop athy and one case of Leber's disease (mul tiple miliary aneurysms) after argon laser
ACKNOWLEDGMENT
H. M. Freeman, M.D., referred Case 2.
REFERENCES 1. L'Espérance, F . A., Jr.: The treatment of oph thalmic vascular disease by argon laser photocoagu lation. Trans. Am. Acad. Ophthalmol. Otolaryngol. 73:1077, 1969. 2. Little, H. L., and Zweng, H. C : Complications of argon laser retinal photocoagulation. Trans. Pac. Coast Otoophthalmol. Soc. 52:115, 1971. 3. Patz, A., Maumenee, E. A., and Ryan, S. J.: Argon laser photocoagulation. Advantages and limi tations. Trans. Am. Acad. Ophthalmol. Otolaryngol. 75:569, 1971. 4. Zweng, H. C , Little, H. L., and Hammond, A. H.: Complications of argon laser photocoagulation. Trans. Am. Acad. Ophthalmol. Otolaryngol. 78:195, 1974. 5. Goldbaum, M. H., Galinos, S. O., Apple, D., Asdourian, G. K., Nagpal, K., Jampol, L., Woolf, M. B., and Busse, B.: Acute choroidal ischemia as a complication of photocoagulation. Arch. Ophthal mol. In press. 6. Galinos, S. O., Asdourian, G. A., Woolf, M. B., Goldberg, M. F., and Busse, B. J.: Choroido-vitreal neovascularization after argon laser photocoagula tion. Arch. Ophthalmol. 93:524, 1975. 7. François, J., De Laey, J. J., Cambie, E., Hanssens, M., and Victoria-Troncoso, V.: Neovasculari zation after argon laser photocoagulation of macular lesions. Am. J. Ophthalmol. 79:206, 1975. 8. Goldbaum, M. H., Goldberg, M. F., Nagpal, K., Asdourian, G. K. and Galinos, S.O.: Quantitative photocoagulation and the treatment of proliferative sickle retinopathy. In Proceedings of the First Inter national Photocoagulation Congress. St. Louis, C.V. Mosby. In press.