- Email: [email protected]
Retinal Neovascularization After Branch Retinal Arterial Obstruction
Retinal Neovascularization After Branch Retinal Arterial Obstruction Marvin F. Kraushar, M . D . , and Gary C. Brown, M . D .
We examined two eyes from two noninsulindependent diabetic patients that developed vitreous hemorrhage secondary to retinal neovascularization after branch retinal arterial obstruction. Although there was no ophthalmoscopic evidence of diabetic retinopathy, diabetes mellitus may have predisposed the retinas to a neovascular response, which was precipitated by the arterial obstruction. ALTHOUGH RETINAL NEOVASCULARIZATION in
association with branch retinal arterial obstruction is rare, 1 this complication is encountered more frequently in carotid artery disease 2 and occasionally after central retinal arterial obstruction. 3 We examined two eyes with retinal neovascularization that developed after branch retinal arterial obstruction. These cases are significantly similar to a previously reported case, 1 and thus provide additional insight into the pathogenesis of the retinal neovascularization.
Case Reports
tion (Fig. 1). There was segmentation of the blood column. Mild opacification of the superficial retina could be seen in the distribution of the superotemporal artery. No neovascularization was noted at the disk or elsewhere in the retina. Changes suggestive of diabetic retinopathy were not present in either eye. Ophthalmoscopic examination of the left eye was unremarkable. No carotid system disease was seen on Doppler sonography. Results of echocardiography were unremarkable. The patient was reexamined on May 9, 1985, because of decreased vision in the right eye, noted on March 22. Visual acuity in the right eye was hand motions because of a vitreous hemorrhage, and only the superior peripheral retina was visible. The patient was examined every two months thereafter, and a slowly progressive clearing of the blood was noted. On March 10, 1986, nearly a year after the hemorrhage, ophthalmoscopy and fluorescein angiography disclosed neovascularization of the retina in the area of the first bifurcation of the superotemporal retinal artery (Fig. 2).
Case 1 A 69-year-old woman with a ten-year history of diabetes mellitus controlled by diet was examined on Oct. 25, 1984, because of a sudden decrease in vision in the right eye for five days. Visual acuity was 20/40 in both eyes with a myopic correction. Slit-lamp examination showed mild cortical lens changes in both eyes. Intraocular pressures were 16 mm Hg. Ophthalmoscopic examination of the right eye disclosed sheathing of the superotemporal retinal artery from the disk to the first major bifurca-
Accepted for publication May 19, 1987. From the Department of Ophthalmology, University of Medicine and Dentistry of New Jersey, Newark, New Jersey (Dr. Kraushar), and the Retina Vascular Unit, Wills Eye Hospital, Thomas Jefferson University, Philadelphia, Pennsylvania (Dr. Brown). Reprint requests to Marvin F. Kraushar, M.D., 600 South Ave. W., Westfield, NJ 07090. 294
Fig. 1 (Kraushar and Brown). Patient 1. Superotemporal branch retinal arterial obstruction (arrow).
©AMERICAN JOURNAL OF OPHTHALMOLOGY 104:294-296, SEPTEMBER, 1987
Vol. 104, No. 3
Retinal Neovascularization
295
Fig. 2 (Kraushar and Brown). Patient 1. Fluorescein angiogram demonstrating retinal neovascularization (arrow).
Fig. 3 (Kraushar and Brown). Patient 2. Inferotemporal branch retinal arterial obstruction.
There was mild staining of some branches of the inferotemporal vein suggesting possible previous venous involvement. There was no evidence of impaired perfusion of the choroid or the retinal capillary bed in the area immediately adjacent to the arterial obstruction. Retinal laser ablation was performed in the superotemporal quadrant, which resulted in complete involution of the neovascularization. The postoperative visual acuity was 20/70.
of his right eye for two days. Visual acuity was R.E.: 20/40, corrected with a contact lens. Ophthalmoscopic examination disclosed elevated retinal neovascularization at the site of the previous retinal arterial obstruction, with intraretinal and vitreous hemorrhage. Fluorescein angiography (Fig. 4) disclosed leakage from the neovascularization and no evidence of impaired perfusion of the choroid. There was some evidence of capillary nonperfusion immediately superior to the neovascularization, but this area appeared perfused in the late venous phase. Laser retinal ablation was performed in the inferotemporal quadrant. On Dec. 16, 1985, a second vitreous hemorrhage was noted in the right eye. By Feb. 13, 1986, the hemorrhage had cleared and a traction detachment of the retina was visible extending from the area of neovascularization into the inferior portion of the macula. Visual acuity improved to 20/30 after vitrectomy.
Case 2 This 40-year-old man with a four-year history of diabetes mellitus controlled by an oral hypoglycemic agent was examined on Feb. 7, 1985. He complained of a sudden onset of decreased vision in the superonasal quadrant of the right eye for two days. Visual acuity was 20/20 in both eyes with contact lenses. The anterior ocular segments were normal. There was no evidence of diabetic retinopathy in either eye. The right inferotemporal retinal artery (Fig. 3) was sheathed at a bifurcation between the disk and the macula. Segmentation of the blood column was noted peripherally in the inferotemporal quadrant; no embolus was visible. There was marked superficial retinal opacification extending into the inferior portion of the fovea. Results of echocardiography and Doppler studies of the carotid systems were normal. The patient was reexamined on Nov. 13, 1985. He had been seeing "red spots" in front
Discussion Brown and Reber1 described a patient who developed neovascularization of the retina and optic disk after branch retinal arterial obstruction. Their patient and our two patients were all noninsulin-dependent diabetics. There was no evidence of diabetic retinopathy ophthalmoscopically or with retinal fluorescein angiogra-
296
September, 1987
AMERICAN JOURNAL OF OPHTHALMOLOGY
Fig. 4 (Krausharand Brown). Patient 2. Fluorescein angiogram demonstrating retinal neovascularization with vitreous hemorrhage. phy. Brown and Reber's patient was the only one with demonstrable carotid artery disease, although the stenosis found was not of sufficient degree to be hemodynamically important. The interval between branch retinal arterial obstruction and vitreous hemorrhage in the three eyes ranged from seven to 13 months (average, ten months). Brown and Reber's patient was the only one who developed optic disk neovascularization. Our Patient 2 developed a fibrovascular response on the retinal surface, as did Brown and Reber's patient. There was no ophthalmoscopic evidence of diabetic retinopathy in any of the eyes before the development of retinal neovascularization. Choroidal filling defects were not demonstrated on retinal fluorescein angiography in any of the three eyes. The only evidence of retinal capillary nonperfusion was an area of delayed filling in Patient 2 (Fig. 4). In all three eyes the retinal neovascularization originated from the venous system. Brown and Reber's patient was the only one to show venous beading. Chronic retinal hypoxia is the most likely pathogenic factor in the production of retinal neovascularization. New blood vessel formation may be a direct response to retinal ischemia or it may be the result of an angiogenic substance produced by the hypoxic retina. 4 Brown and Reber1 believed that the relative rarity of retinal neovascularization after branch and central retinal arterial obstruction, as com-
pared with branch and central vein obstruction, is caused by the rapid tissue death of the hypoxic inner retina or the reestablishment of the retinal circulation as the arterial obstruction is spontaneously relieved. Both of these events may end the production of any theoretical angiogenic factor. In the eyes described herein, a chronic low-flow state may have developed that was of insufficient severity to kill the involved retina, but instead made the retina hypoxic, thus predisposing it to the growth of new blood vessels. Carotid artery stenosis has been seldom implicated in retinal neovascularization. 2 The incidence of retinal neovascularization after central retinal arterial obstruction without carotid stenosis is even less common. The normal carotid studies in the two patients in this series, in addition to the normal choroidal circulation demonstrated by retinal fluorescein angiography, suggests that carotid disease did not play a role in the development of the neovascularization. The two pathologic factors shared by the three patients are diabetes mellitus and branch retinal arterial obstruction. The striking lack of diabetic retinopathy in each patient makes it difficult to consider diabetes as the primary cause of the neovascularization. The diabetes may have predisposed the retina to a neovascular response after the arterial obstruction. However, the neovascularization did not develop until after the arterial obstruction, which suggests that the vascular accident was the primary causative factor. The fundi of diabetic patients who develop branch retinal arterial obstruction should be closely observed for at least one year for the development of retinal neovascularization.
References 1. Brown, G. C , and Reber, R.: An unusual presentation of branch retinal artery obstruction in association with ocular neovascularization. Can. J. Ophthalmol. 21:103, 1986. 2. Brown, G. C , Magargal, L. E., Simeone, F. A., Goldberg, R. E., Federman, J. L., and Benson, W. E.: Arterial obstruction and ocular neovascularization. Ophthalmology 89:139, 1982. 3. Benton, C. D., Jr.: Glaucoma following occlusion of central retinal artery. Arch. Ophthalmol. 49:280, 1953. 4. Henkind, P.: Ocular neovascularization. The Krill Memorial Lecture. Am. J. Ophthalmol. 85:287, 1978.
We examined two eyes from two noninsulindependent diabetic patients that developed vitreous hemorrhage secondary to retinal neovascularization after branch retinal arterial obstruction. Although there was no ophthalmoscopic evidence of diabetic retinopathy, diabetes mellitus may have predisposed the retinas to a neovascular response, which was precipitated by the arterial obstruction. ALTHOUGH RETINAL NEOVASCULARIZATION in
association with branch retinal arterial obstruction is rare, 1 this complication is encountered more frequently in carotid artery disease 2 and occasionally after central retinal arterial obstruction. 3 We examined two eyes with retinal neovascularization that developed after branch retinal arterial obstruction. These cases are significantly similar to a previously reported case, 1 and thus provide additional insight into the pathogenesis of the retinal neovascularization.
Case Reports
tion (Fig. 1). There was segmentation of the blood column. Mild opacification of the superficial retina could be seen in the distribution of the superotemporal artery. No neovascularization was noted at the disk or elsewhere in the retina. Changes suggestive of diabetic retinopathy were not present in either eye. Ophthalmoscopic examination of the left eye was unremarkable. No carotid system disease was seen on Doppler sonography. Results of echocardiography were unremarkable. The patient was reexamined on May 9, 1985, because of decreased vision in the right eye, noted on March 22. Visual acuity in the right eye was hand motions because of a vitreous hemorrhage, and only the superior peripheral retina was visible. The patient was examined every two months thereafter, and a slowly progressive clearing of the blood was noted. On March 10, 1986, nearly a year after the hemorrhage, ophthalmoscopy and fluorescein angiography disclosed neovascularization of the retina in the area of the first bifurcation of the superotemporal retinal artery (Fig. 2).
Case 1 A 69-year-old woman with a ten-year history of diabetes mellitus controlled by diet was examined on Oct. 25, 1984, because of a sudden decrease in vision in the right eye for five days. Visual acuity was 20/40 in both eyes with a myopic correction. Slit-lamp examination showed mild cortical lens changes in both eyes. Intraocular pressures were 16 mm Hg. Ophthalmoscopic examination of the right eye disclosed sheathing of the superotemporal retinal artery from the disk to the first major bifurca-
Accepted for publication May 19, 1987. From the Department of Ophthalmology, University of Medicine and Dentistry of New Jersey, Newark, New Jersey (Dr. Kraushar), and the Retina Vascular Unit, Wills Eye Hospital, Thomas Jefferson University, Philadelphia, Pennsylvania (Dr. Brown). Reprint requests to Marvin F. Kraushar, M.D., 600 South Ave. W., Westfield, NJ 07090. 294
Fig. 1 (Kraushar and Brown). Patient 1. Superotemporal branch retinal arterial obstruction (arrow).
©AMERICAN JOURNAL OF OPHTHALMOLOGY 104:294-296, SEPTEMBER, 1987
Vol. 104, No. 3
Retinal Neovascularization
295
Fig. 2 (Kraushar and Brown). Patient 1. Fluorescein angiogram demonstrating retinal neovascularization (arrow).
Fig. 3 (Kraushar and Brown). Patient 2. Inferotemporal branch retinal arterial obstruction.
There was mild staining of some branches of the inferotemporal vein suggesting possible previous venous involvement. There was no evidence of impaired perfusion of the choroid or the retinal capillary bed in the area immediately adjacent to the arterial obstruction. Retinal laser ablation was performed in the superotemporal quadrant, which resulted in complete involution of the neovascularization. The postoperative visual acuity was 20/70.
of his right eye for two days. Visual acuity was R.E.: 20/40, corrected with a contact lens. Ophthalmoscopic examination disclosed elevated retinal neovascularization at the site of the previous retinal arterial obstruction, with intraretinal and vitreous hemorrhage. Fluorescein angiography (Fig. 4) disclosed leakage from the neovascularization and no evidence of impaired perfusion of the choroid. There was some evidence of capillary nonperfusion immediately superior to the neovascularization, but this area appeared perfused in the late venous phase. Laser retinal ablation was performed in the inferotemporal quadrant. On Dec. 16, 1985, a second vitreous hemorrhage was noted in the right eye. By Feb. 13, 1986, the hemorrhage had cleared and a traction detachment of the retina was visible extending from the area of neovascularization into the inferior portion of the macula. Visual acuity improved to 20/30 after vitrectomy.
Case 2 This 40-year-old man with a four-year history of diabetes mellitus controlled by an oral hypoglycemic agent was examined on Feb. 7, 1985. He complained of a sudden onset of decreased vision in the superonasal quadrant of the right eye for two days. Visual acuity was 20/20 in both eyes with contact lenses. The anterior ocular segments were normal. There was no evidence of diabetic retinopathy in either eye. The right inferotemporal retinal artery (Fig. 3) was sheathed at a bifurcation between the disk and the macula. Segmentation of the blood column was noted peripherally in the inferotemporal quadrant; no embolus was visible. There was marked superficial retinal opacification extending into the inferior portion of the fovea. Results of echocardiography and Doppler studies of the carotid systems were normal. The patient was reexamined on Nov. 13, 1985. He had been seeing "red spots" in front
Discussion Brown and Reber1 described a patient who developed neovascularization of the retina and optic disk after branch retinal arterial obstruction. Their patient and our two patients were all noninsulin-dependent diabetics. There was no evidence of diabetic retinopathy ophthalmoscopically or with retinal fluorescein angiogra-
296
September, 1987
AMERICAN JOURNAL OF OPHTHALMOLOGY
Fig. 4 (Krausharand Brown). Patient 2. Fluorescein angiogram demonstrating retinal neovascularization with vitreous hemorrhage. phy. Brown and Reber's patient was the only one with demonstrable carotid artery disease, although the stenosis found was not of sufficient degree to be hemodynamically important. The interval between branch retinal arterial obstruction and vitreous hemorrhage in the three eyes ranged from seven to 13 months (average, ten months). Brown and Reber's patient was the only one who developed optic disk neovascularization. Our Patient 2 developed a fibrovascular response on the retinal surface, as did Brown and Reber's patient. There was no ophthalmoscopic evidence of diabetic retinopathy in any of the eyes before the development of retinal neovascularization. Choroidal filling defects were not demonstrated on retinal fluorescein angiography in any of the three eyes. The only evidence of retinal capillary nonperfusion was an area of delayed filling in Patient 2 (Fig. 4). In all three eyes the retinal neovascularization originated from the venous system. Brown and Reber's patient was the only one to show venous beading. Chronic retinal hypoxia is the most likely pathogenic factor in the production of retinal neovascularization. New blood vessel formation may be a direct response to retinal ischemia or it may be the result of an angiogenic substance produced by the hypoxic retina. 4 Brown and Reber1 believed that the relative rarity of retinal neovascularization after branch and central retinal arterial obstruction, as com-
pared with branch and central vein obstruction, is caused by the rapid tissue death of the hypoxic inner retina or the reestablishment of the retinal circulation as the arterial obstruction is spontaneously relieved. Both of these events may end the production of any theoretical angiogenic factor. In the eyes described herein, a chronic low-flow state may have developed that was of insufficient severity to kill the involved retina, but instead made the retina hypoxic, thus predisposing it to the growth of new blood vessels. Carotid artery stenosis has been seldom implicated in retinal neovascularization. 2 The incidence of retinal neovascularization after central retinal arterial obstruction without carotid stenosis is even less common. The normal carotid studies in the two patients in this series, in addition to the normal choroidal circulation demonstrated by retinal fluorescein angiography, suggests that carotid disease did not play a role in the development of the neovascularization. The two pathologic factors shared by the three patients are diabetes mellitus and branch retinal arterial obstruction. The striking lack of diabetic retinopathy in each patient makes it difficult to consider diabetes as the primary cause of the neovascularization. The diabetes may have predisposed the retina to a neovascular response after the arterial obstruction. However, the neovascularization did not develop until after the arterial obstruction, which suggests that the vascular accident was the primary causative factor. The fundi of diabetic patients who develop branch retinal arterial obstruction should be closely observed for at least one year for the development of retinal neovascularization.
References 1. Brown, G. C , and Reber, R.: An unusual presentation of branch retinal artery obstruction in association with ocular neovascularization. Can. J. Ophthalmol. 21:103, 1986. 2. Brown, G. C , Magargal, L. E., Simeone, F. A., Goldberg, R. E., Federman, J. L., and Benson, W. E.: Arterial obstruction and ocular neovascularization. Ophthalmology 89:139, 1982. 3. Benton, C. D., Jr.: Glaucoma following occlusion of central retinal artery. Arch. Ophthalmol. 49:280, 1953. 4. Henkind, P.: Ocular neovascularization. The Krill Memorial Lecture. Am. J. Ophthalmol. 85:287, 1978.