Neovascular Glaucoma

Etiologic Considerations

GARY C. BROWN, MD, LARRY E. MAGARGAL, MD, ANDREW SCHACHAT, MD, HARSHAD SHAH, MD

Abstract: A review of 208 patients with neovascular glaucoma (NVG) is pre­sented. The most common primary etiologic associations included retinal venous obstructive disease (36.1%), diabetic retinopathy (32.2%), and carotid artery obstructive disease (12.9%). Systemic arterial hypertension was present in 51 % and diabetes mellitus was noted in 46% of all patients. Among the 25 bilateral cases of NVG, 24 occurred in patients with diabetic retinopathy. Women com­prised 65% of patients with NVG secondary to diabetes, and 57% of the venous obstruction group, while men accounted for 74% of cases in which NVG occurred secondary to carotid artery obstructive disease. Overall, 97% of eyes with NVG had a disease process that produced extensive retinal ischemia and preceded the onset of iris neovascularization. Patients with NVG, but without an obvious precipitating fundus condition, should be suspected of having severe carotid artery obstructive disease. [Key words: etiologic associations, neovascular glaucoma.] Ophthalmology 91 :315-320, 1984

Neovascular glaucoma (NVG) is a serious sequela of a number of disease processes that affect the eye. The common factor present in most of these diseases is pos­terior segment ischemia. Several authors1

-s have previ­

ously elucidated etiologic entities associated with NVG, the most frequent causes being retinal vein obstruction, diabetic retinopathy, iritis, central retinal artery obstruc­tion, and choroidal melanoma. Presented herein are the presumed etiologic factors in 208 consecutive patients with NVG who were evaluated by the authors.

MATERIALS AND METHODS

The consecutive cases of all patients presenting with neovascular glaucoma to the Retina Vascular Unit over a 4-year period from 1978 through 1981 were reviewed. Included were only those cases in which iris neovascu-

From the Retina Vascular Unit, Wills Eye Hospital, Thomas Jefferson University, Philadelphia, Pennsylvania.

Presented at the Eighty-eighth Annual meeting of the American Academy of Ophthalmology, Chicago, Illinois, October 3D-November 3, 1983.

Supported in part by the Retina Research and Development Foundation, Philadelphia, and the Research Department, Wills Eye Hospital.

Reprint requests to Gary C. Brown, MD, 910 East Willow Grove Avenue, Wyndmoor, PA 19118.

larization was present in association with increased in­traocular pressure (greater than 22 mmHg). Each patient underwent a complete ophthalmologic examination, in­cluding indirect ophthalmoscopy, when clarity of the me­dia permitted. In every instance an attempt was made to ascertain the underlying etiology of the NVG. Fundus­iris fluorescein angiography was performed when possible in each case, and carotid angiographic evaluation was obtained in patients with clinical features suggestive of the ocular ischemic syndrome.6 Statistical analyses were performed using the chi-square test and the Z test.

RESULTS

Included in the study were 208 patients ranging in age from 19 years to 89 years, with a mean age of 61. 5 years. Of the 208 patients, 112 (53.8%) were women and 96 (46.2%) were men. The presumed etiologic factors found in the series follow and are also listed in Table 1.

RETINAL VENOUS OBSTRUCfION

Retinal venous obstruction was the most common pri­mary factor predisposing to the development of NVG and accounted for 36.1 % (75/208) of the cases. Central vein obstruction (CRVO) occurred in 67 cases, hemi­spheric vein obstruction occurred in 5 eyes, and branch

315

OPHTHALMOLOGY • APRIL 1984 • VOLUME 91 • NUMBER 4

Table 1. Presumed Etiologic Factors Associated with Neovascular Glaucoma (NVG)

No. of Cases No. of Cases with Associated with Systemic

Primary Contributing Cause of No. of Cases Mean Age in Years Diabetes Mellitus Arterial Hypertension NVG (% of Total) (Range) (% of Each Subgroup) (% of Each Subgroup)

Retinal venous obstruction 75 (36.1%) 69.1 (19-89) 15 (20%) 40 (53%) a. Central a. 67 (32.2%) a. 69.3 (19-89) a. 12 (18%) a. 34 (51%) b. Hemispheric b. 5 (2.4%) b. 67.4 (61-81) b. 2 (40%) b. 3 (60%) c. Branch c. 3 (1.5%) c. 68.0 (60-76) c. 1 (33%) c. 3 (100%)

Diabetic retinopathy 67 (32.2%) 54.7 (19-73) 67 (100%) 40 (60%) Carotid artery obstruction 27 (12.9%) 64.2 (51-82) 8 (30%) 14 (52%) Unknown 9 (4.4%) 55.2 (29-73) 0 2 (25%) Central retinal artery

obstruction 8 (3.8%) 68.4 (46-84) 2 (25%) 5 (63%) Combined retinal arterial/

venous obstruction 8 (3.8%) 59.4 (29-77) 2 (25%) 4 (50%) Rhegmatogenous retinal

detachment 3 (1.5%) 51.0 (35-66) 1 (33%) 0(0%) Uveitis 3 (1.5%) 49 (41-57) 0 1 (33%) Miscellaneous 8 (3.8%) 48.4 (26-66) 1 (12%) 0(0%)

a. Vitreous wick syndrome a. 2 (0.9%) a. 0 b. Radiation retinopathy b. 1 (0.5%) b. 1 c. Syphilitic vasculitis c. 1 (0.5%) c. 0 d. Choroidal melanoma d. 1 (0.5%) d. 0 e. Carotid-cavernous fistula,

operated e. 1 (0.5%) e. 0 f. Squamous cell carcinoma

of the conjunctiva f. 1 (0.5%) f. 0 g. Angiomatosis retinae g. 1 (0.5%) g. 0

Total 208 (100%) 61.5 (19-89) 96 (46%) 106 (51%)

vein obstruction occurred in 3 eyes. Bilateral NVG was not encountered in the retinal venous obstruction group of patients. Among all eyes in which clarity of the media permitted fluorescein angiography, evidence of retinal ischemia, as demonstrated by extensive zones of retinal capillary nonperfusion, could be seen. Although 12 (18%) of the 67 patients with CRVO also had diabetes mellitus, the companion eyes exhibited only background or no diabetic retinopathy; therefore, ischemic CRVO was thought to be the primary etiologic factor in these cases. Of the patients with venous obstructive disease, 57% (43/ 75) were women.

Among the eyes with hemispheric retinal venous ob­struction, three had a superior obstruction, while in two it occurred inferiorly. Two of the five patients in this group also had diabetes mellitus. Carotid arteriography was performed in one nondiabetic patient and was normal.

In each of the three cases ofNVG occurring secondary to branch retinal vein obstruction the obstructed vessel was located superotemporally and involved nearly a whole quadrant of the fundus. One patient was diabetic and none had clinical evidence suggestive of carotid obstruc­tive disease, although carotid angiography was not per­formed in this subgroup.

Systemic arterial hypertension was found in 53% (40/ 75) of subjects in the venous obstruction group. Three

316

of five patients (60%) with hemispheric obstructions were hypertensive, as was each of the three with a branch vein obstruction.

DIABETIC RETINOPATHY

Diabetic retinopathy was primarily responsible for the development ofNVG in 67 (32.2%) of208 cases. Overall, 96 (46.2%) of 208 patients in this series had diabetes mellitus, making it the most common primary systemic disease entity found in association with NVG. Women comprised 66% (44/67) of people in this group and men comprised 34%, nearly a 2: 1 ratio. Evidence of systemic arterial hypertension was noted in 60% (40/67) of these cases.

Within the total sample (n = 208), unilateral NVG was found in 88% (183/208) of the subjects and bilateral NVG was present in 12% (25/208). Among the 25 bilateral cases, 24 occurred secondary to diabetic retinopathy, while the remaining nondiabetic patient had bilateral 95% in­ternal carotid artery obstruction and the NVG was thought to be a component of the ocular ischemic syndrome.

Subdivision of the diabetic group into factions with and without posterior segment proliferative disease re­vealed that 53 (79%) of 67 patients also had either neo­vascularization of the optic disc or retina. In 3 (4%) no evidence of posterior segment neovascularization could

BROWN, et al • NEOVASCULAR GLAUCOMA

be seen, while in 11 (17%) an accurate determination could not be made ophthalmoscopically or angiograph­ically because of poor clarity of the media.

CAROTID ARTERY OBSTRUCTION

Of the 208 patients, 27 (12,9%) had NVG associated with atherosclerotic carotid arterial obstruction (ocular ischemic syndrome).6 In each case the obstruction was established by intra-arterial or digital subtraction carotid angiography, was 90% or greater, and involved at least the ipsilateral internal carotid or common carotid artery. Eight (30%) of the 27 patients were also diabetic and twenty (74%) were men. One additional patient (included under Miscellaneous, below) developed NVG 15 years after ligation of the external carotid and clipping of the internal carotid to successfully close a carotid-cavernous fistula.

UNKNOWN

In 9 patients (4.4% of total) no underlying etiology was found for the NVG. None of these people were diabetic, and each had a vitreous hemorrhage sufficiently dense so as to obscure the fundus view. Follow-up in this group was poor, and most patients were seen on only one oc­casion.

CENTRAL RETINAL ARTERY OBSTRUCTION

The eight patients with NVG following central retinal artery obstruction comprised 3.8% of the whole group. Of these patients two also had diabetes mellitus. However, no person in this subgroup underwent carotid angiography since each was seen prior to the advent of the digital subtraction technique and none were thought to be can­didates for intra-arterial angiography.

COMBINED RETINAL ARTERIAL/VENOUS OBSTRUCTION

This subgroup accounted for 3.8% of the total. Each of the eight patients within this subgroup had an acute retinal arterial obstruction in association with the nu­merous intraretinal hemorrhages seen with central retinal venous obstruction. Four of these patients had a central retinal artery obstruction and four presented with a branch or cilioretinal artery obstruction. In one case, combined central arterial and venous obstructions occurred follow­ing a retrobulbar injection, and NVG ensued within two weeks. Two of the patients with combined central retinal arterial and central retinal venous obstructions underwent carotid angiography, and in each instance it was normal.

RETINAL DETACHMENT

Rhegmatogenous retinal detachment accounted for NVG in 3 (1.5%) of the cases. In two patients the NVG developed after unsuccessful detachment repair, while in the third patient it occurred in a diabetic with a history compatible with a detachment of six months' duration.

Two nonrhegmatogenous serous retinal detachments were seen in the series, and these are listed under Miscellaneous, below.

ANTERIOR UVEITIS

Three people (1.5%) had anterior uveitis and NVG. However, two also had mature cataracts that obscured a fundus view and none underwent carotid angiography.

MISCELLANEOUS

Eight patients (3.8% of the total) were included in this group. Two had vitreous to the wound in association with a mild anterior uveitis (vitreous wick syndrome) after cataract surgery, but neither underwent a carotid artery evaluation. One patient developed NVG after 3500 rads of external beam irradiation for an orbital lymphoma, and another had retinal vascular compromise secondary to presumed syphilitic vasculitis. Two patients had a non­rhegmatogenous retinal detachment; the first occurred in conjunction with a choroidal melanoma, and the second was associated with angiomatosis retinae. Squamous cell carcinoma of the conjunctiva invading the anterior chamber was thought to produce NVG in one case, and the final patient in this group developed NVG 15 years after carotid ligation surgery for treatment of an ipsilateral carotid-cavernous fistula.

DISCUSSION

Our series agrees with the clinical study of Hoskins (100 cases),2 in which diabetic retinopathy and central retinal vein obstruction were found to be the leading etiologic diagnoses in eyes with NVG. Both are diseases that compromise the retinal vasculature, thus producing retinal ischemia, and perhaps the elaboration of an "an­giogenic factor."7 Although diabetic retinopathy was not the leading primary cause ofNVG in our series, diabetes was overall the most commonly associated primary sys­temic disease entity (46.2%). However, the diagnosis of diabetes was made by history, suggesting that even a higher incidence might be found if each patient was tested with a glucose tolerance test.

If one considers systemic arterial hypertension to be a primary predisposing disease entity, then it must be con­sidered to be the most frequently noted abnormality seen in conjunction with NVG. By history it was found in 51 % of our subjects, as compared to the 27% to 34% incidence that is present in an age-matched general pop­ulation.8 Systemic hypertension most likely exacerbates other vascular diseases (ie, diabetic retinopathy), or pre­disposes to the development of etiologic entities (ie, retinal venous obstruction) that lead to NVG, rather than pri­marily inducing NVG. For this reason we have chosen not to list it as the leading primary cause of NVG.

In contrast to previous series in which retinal detach­ment1,4 and uveitis2 were also common causes of NVG, the present study noted that chronic arterial obstructive

317

OPHTHALMOLOGY • APRIL 1984 • VOLUME 91 • NUMBER 4

disease, usually of the large neck vessels, was the third most frequent cause. When one considers that essentially only the patients in our series in whom the ocular ischemic syndrome was suspected received an angiographic carotid artery evaluation, it becomes apparent that an incidence of 12.9% for associated severe carotid artery obstructive disease may be falsely low among the total group. As has been reported recently, the association of central retinal artery obstruction with NVG is strongly suggestive of severe, atherosclerotic carotid artery disease.6 Eyes with NVG following a central retinal artery obstruction should be more appropriately characterized as having the ocular ischemic syndrome if a concomitant severe carotid artery obstruction is present. Since not all of our patients with NVG after a central retinal artery obstruction underwent carotid angiography, the likelihood is high that cases of marked carotid atherosclerosis remained undetected. Some cases of atherosclerotic carotid obstruction were most probably also overlooked in the diabetic retinopathy and venous obstruction groups, since an obvious precip­itating fundus abnormality was present and carotid an­giography was therefore rarely performed.

In series of histopathologic specimens studied with ru­beosis iridis, the incidence of carotid artery atherosclerotic disease as an etiologic factor has been low. Schulze4 found this in one of 105 eyes and Anderson and associates! noted it in none of 70 eyes, although in one eye rubeosis was thought to occur on the basis of proximal giant cell arteritis. However, carotid artery atherosclerosis producing NVG would not be detected by histopathology of the globe alone.

It is recognized that ocular ischemia secondary to ca­rotid artery disease can masquerade as anterior uveitis.9

Hoskins2 found iritis to be the third most common eti­ologic factor associated with NVG (11 % of cases) in his group, although we have been unable to confirm this association in our series. Possibly, some previously re­ported cases of iritis in conjunction with NVG were in actuality manifesting the ocular ischemic syndrome. In­deed, most cases of NVG have prominent flare in the anterior chamber, probably on the basis of leakage of serum products from the new iris vessels, and on occasion this response may be confused with iritis. Additionally, the high intraocular pressures seen with acute NVG can cause ocular inflammation and an anterior chamber cel­lular response. Although NVG was attributed to chronic arterial segment uveitis in three of our cases, no fundus view was possible in two, and in none was a carotid artery evaluation undertaken. Iridocyclitis as a primary cause of NVG should be a diagnosis of exclusion until other etiologies are ruled out, although rubeosis iridis in as­sociation with a mildly increased intraocular pressure has been shown to occur in conjunction with Fuchs' hetero­chromic cyclitis. 10

The data in this study strongly suggest that the presence of bilateral NVG indicates diabetic retinopathy as the primary underlying cause. Since diabetic retinopathy is usually bilateral and relatively symmetrical as compared to central retinal venous obstruction (14% incidence of bilaterality)!! and retinopathy with the ocular ischemic syndrome (8% incidence ofbilaterality),6 it is readily ap-318

parent that the incidence of bilateral NVG should be higher with the former disease.

The differences in ages between groups with different etiologic factors for NVG has been noted by Madsen.5

As with his series, we found that the age at the time of development of NVG was younger in patients with di­abetes (54.7 years) than in those with retinal venous ob­struction (69.1 years), or in people with carotid artery obstruction (64.2 years). Although these age differences were not statistically significant (X2 = 1.71, df = 2, p < .50), they parallel those seen in the three groups at the time of development of posterior segment neovascular changes also.6.!!.12

Among the three major causes of NVG, the sex dis­tribution appears to differ and is dependent upon the etiology. Whereas women comprised 65.7% of the group with NVG occurring primary secondary to diabetes (z = -2, p < .02), and 57% of the venous group (z = -0.7, p < .24), men were more commonly seen in the carotid artery disease group by a factor of approximately 3: 1 (z = 2.92, p < .002). However, when one considers that 61 % of diabetics in the United States are female 13 and 75% of those previously reported with severe carotid artery atherosclerosis and ocular sequelae were male,6 the reasons for the sex differences are closely correlated with the prev­alence of the underlying disease. Madsen5 also noted that NVG secondary to diabetes was more common in women than men by a ratio of 3:2, but did not quantify specifically retinal venous obstruction or carotid artery disease.

Among the 199 patients in this study with an identified etiologic factor as a presumed cause ofNVG, 193 (97.0%) had associated posterior segment disease producing retinal ischemia by either vaso-occlusive phenomena or structural alterations (ie, retinal detachment separating the retina from the underlying choroid). Those not manifesting pos­terior segment disease included three cases that we at­tributed to anterior uveitis, two with the vitreous wick syndrome and one with squamous cell carcinoma in­vading the anterior chamber. In two of the uveitis patients no fundus view was possible, and none of the uveitis or vitreous wick syndrome patients had a carotid artery evaluation. From the data presented here, the vast ma­jority of patients with NVG have it occurring in asso­ciation with, and possibly on the basis of, retinal ischemia.

One entity not encountered in this series as a sole precipitating factor for NVG was primary open-angle glaucoma. Hoskins believed that chronic open-angle glaucoma was an etiologic factor for NVG in two of his 100 clinical cases, while Schulze noted "chronic glau­coma" as the principal diagnosis in six of 105 pathology specimens with rubeosis iridis. The present study suggests that attributing the development of NVG to open-angle glaucoma should be suspect. Most probably such cases actually occur on the basis of occult carotid artery ob­structive disease or unrecognized central retinal venous obstruction.

It should be noted that the patients included in this study were seen on a referred basis, thereby perhaps cre­ating bias toward selection of cases of NVG with retinal etiologies. For this reason it is likely that certain uncom­mon causes of NVG, such as advanced retinopathy of

BROWN, et al • NEOVASCULAR GLAUCOMA

prematurity and retinoblastoma, were referred to other subspecialty services. However, in many instances patients with NVG were referred to us for evaluation and treatment because of our interest in NVG regardless of the under­lying condition. Therefore this study is probably a rela­tively accurate representation of the prevalences of eti­ologic entities that would be seen if a similar cross-sec­tional analysis of every patient with NVG could be undertaken.

One final point deserves mention. It has been the au­thors' impression that NVG is quite uncommon in as­sociation with sickling hemoglobinopathies. Although at least two cases of NVG in patients with flat retinas and sickling hemoglobinopathy have been reported, both also had diabetes mellitus. 14 In a review of 47 patients with proliferative sickling hemoglobinopathies seen on the Retina Vascular Unit over the past four years, none pre­sented with or developed NVG, with a mean follow-up of over one year. The reason for this probably lies in the fact that the peripheral retinal nonperfusion seen with sickling hemoglobinopathies does not involve as much retinal area as the extensive nonperfusion and/or hypo­perfusion associated with most of the other etiologic en­tities listed in this series. 15

,16 Theoretically, a lesser area of retinal ischemia may not elicit sufficient production of an "angiogenic factor" to cause rubeosis iridis.

ACKNOWLEDGMENT

The authors would like to thank Gary Cassel, MD, for his assistance with the statistical analyses.

REFERENCES

1. Anderson OM, Morin JD, Hunter WS. Rubeosis iridis. Can J Ophthalmol 1971; 6:183-8.

2. Hoskins HD Jr. Neovascular glaucoma: current concepts. Tr Am Acad Ophthalmol Otolaryngol 1974; 78:330-3.

3. Gartner S, Henkind P. Neovascularization of the iris (rubeosis iridis). Surv Ophthalmol 1978; 22:291-312.

4. Schulze RR. Rubeosis iridis. Am J Ophthalmol1967; 63:487-95.

5. Madsen PH. Haemorrhagic glaucoma; comparative study in diabetic and nondiabetic patients. Br J Ophthalmol 1971; 55:444-50.

6. Brown GC, Magargal LE, Simeone FA, et al. Arterial obstruction and ocular neovascularization. Ophthalmology 1982; 89:139-46.

7. Glaser BM, D'Amore PA, Michels RG, et al. The demonstration of angiogenic activity from ocular tissues: preliminary report. Ophthal­mology 1980; 87:440-6.

8. Leibowitz HM, Krueger DE, Maunder LR, et al. The Framingham Eye Study Monograph. An ophthalmological and epidemiological study of cataract, glaucoma, diabetic retinopathy, macular degeneration and visual acuity in a general population of 2631 adults 1973-1973. Surv Ophthalmol 1980; 24(suppl):349.

9. Knox DL. Ischemic ocular inflammation. Am J Ophthalmol 1965; 60:995-1002.

10. Perry HD, Yanoff M, Scheie HG. Rubeosis in Fuchs heterochromic cyclitis. Arch Ophthalmol 1975; 93:337-9.

11. Magargal LE, Brown GC, Augsburger JJ, Parrish RK. Neovascular glaucoma following central retinal vein obstruction. Ophthalmology 1981; 88:1095-101.

12. Aiello LM, Rand LI, Briones JC, et al. Diabetic retinopathy in Joslin Clinic patients with adult-onset diabetes. Ophthalmology 1981; 88:619-23.

13. West EM. Epidemiology of Diabetes and Its Vascular Lesions. New York: Elsevier-Dutton 1978; 138.

14. Boniuk M, Burton GL. Unilateral glaucoma associated with sickle-cell retinopathy. Trans Am Acad Ophthalmol OtolaryngoI1964; 68:316-28

15. Tasman W, Magargal LE, Augsburger JJ. Effects of argon laser pho­tocoagulation on rubeosis iridis and angle neovascularization. Oph· thalmology 1980; 87:400-2.

16. Magargal LE, Donoso LA, Sanbom GE. Retinal ischemia and risk of neovascularization following central retinal vein obstruction. Oph­thalmology 1982; 89:1241-5.

Discussion by

Jonathan Herschler, MD

In 1958, J. Lawton Smith first brought carotid disease to our attention as a cause for neovascular glaucoma.' In 1982, Dr. Brown and his associates reminded us of the possibility that carotid insufficiency could cause neovascular glaucoma.2 They emphasized considering this diagnosis if neovascular glaucoma followed central retinal artery occlusion.

In the present paper, the authors give us a statistical sampling of208 neovascular glaucoma patients who were referred to their consultative practices. They found 13% of these cases to have high-grade (90% or greater) carotid artery stenosis as a cause for their neovascular glaucoma. Is 13% too high a number? Is there a selection bias in that the authors are well-known retinal specialists? I feel the answers to these questions are probably "no" to the first and "yes" to the second. Let me address the latter first.

From the Department of Ophthalmology, University of Arizona Health Sciences Center, Tucson, Arizona.

Although it is impossible to know exactly the extent to which a referral bias has been introduced, it is clear that one must exist. The authors could find no neovascular glaucoma cases they could assign to a non-retinal etiology such as glaucoma or uveitis. It is probably not correct to assume that other published series were mistaken in diagnosing these as etiologies for some cases of neovascular glaucoma. This undoubtedly has induced an overestimation of retinal etiologies in this sense. Counter­balancing this is the stated fact that the authors only submitted patients to carotid angiography if they strongly suspected carotid insufficiency to be present. Thus, certain cases undoubtedly went undetected in which carotid insufficiency, with resultant ocular ischemia, did exist. Hopefully, the retinal selection bias and the undetection underestimation approximately counter­balance; thus, 15% of neovascular glaucomas due to carotid insufficiency is probably a reasonably accurate incidence.

The advent of intravenous digital subtraction angiography has made studying the carotids a procedure with much less morbidity than conventional arteriography. The technique of

319

OPHTHALMOLOGY • APRIL 1984 • VOLUME 91 • NUMBER 4

intravenous angiography is just the beginning in a revolution in imaging in medicine. The imaging revolution will affect oph­thalmology on many fronts. The study of the circulation of and to the globe, with new imaging methods, will have additional major diagnostic and therapeutic implications.

To this end I would like to address one additional point raised by the authors. Although it is possible that a vasogenic factor, produced by ischemic retina, is the only cause of rubeosis iridis and resulting neovascular glaucoma, I feel primary anterior seg­ment ischemia is an equally likely etiology.

Surely, as the authors stated, not only the retinal circulation but also the choroidal circulation is affected by diseases such as carotid insufficiency, diabetes, and systemic hypertension. The ophthalmic artery is the vascular supply to the posterior and anterior segments, and it seems likely that reduced flow is present in all branches of the ophthalmic circulation, including those to the anterior segment. The report of anterior segment ischemia following cycIocryotherapy for neovascular g1aucoma3

lends credence to the concept of poor blood supply to the anterior segment in patients who develop neovascular glaucoma.

The fact that panretinal photocoagulation may cause regres­sion of anterior segment neovascularization is not proof that the cause for the anterior segment neovascularization is in the posterior segment. Panretinal photocoagulation destroys much retinal and choroidal tissue and thus would be expected to de­crease demands in treated areas and to increase blood flow to all untreated areas, including the anterior segment. Prior to the common use of panretinal photocoagulation, neovascular g1au-

320

coma was often treated by cyclocryotherapy. It was not uncom­mon to see rubeosis regress following cyclocryotherapy. Does this mean that the ciliary body was the source of a vasogenic factor in those cases?

We need to develop noninvasive techniques to study blood flow to crucial ocular structures such as the choroid, retina, iris, ciliary body, and optic nerve. Only then will we begin to un­derstand the true cause-and-effect relationships between various diseases and neovascular glaucoma. When these techniques are perfected, new therapeutic avenues will open that will likely make our present concepts and treatments seem simplistic at best and superstitious at worse.

In summary, the authors are to be congratulated on amassing a very extensive series of cases with neovascular glaucoma and highlighting carotid insufficiency with resultant ocular ischemia as an important cause. The significance of making this etiologic diagnosis has implications for the patient's well-being that extend far beyond the eye affected.

References

1. Smith JL. Unilateral glaucoma in carotid occlusive disease, JAMA 1962, 182:683-4.

2. Brown GC, Magargal LE, Simeone FA, et al. Arterial obstruction and ocular neovascularization. Ophthalmology, 1982, 89: 139-46.

3. Krupin T, Mitchel KB, Becker B. Cycrocryotherapy in neovascular glaucoma. Am J Ophthalmol 1978,86:24-6.