corona of red blood cells that encircle not only an extrafoveal choroidal neovascular membrane, but also a subfoveal portion of the membrane as well. One can confidently conclude, even without the assistance of indocyanine green angiography, that laser coagula-tion of the prominently fluorescent extrafoveal site for such an eye would, in the long run, be doomed to failure.

W. REX HAWKINS, M.D.

Houston, Texas

AUTHOR REPLY I THANK DR. HAWKINS FOR HIS INTEREST IN MY ARTICLE.

Submacular hemorrhage is associated with a poor visual prognosis caused by multiple factors, which were listed in the third paragraph of the discussion of my article. One of these factors is indeed fibrin-mediated retinal damage as it was elegantly demon-strated by Toth and associates.1 Dr. Hawkins states that an underlying choroidal neovascular membrane and retinal pigment epithelial destruction, rather than the hemorrhage itself, is the cause for the poor visual outcome, and that it is not possible to deter-mine postoperatively if the visual improvement is the result of the removal of the hemorrhage or the disappearance of the choroidal neovascular mem-brane, or both.

Rather than the choroidal neovascular membrane itself, it is the leaky substances such as blood, lipid, plasma, fibrin, and the like, that damage the sensory retina and lead to a poor visual outcome. Not all patients with subfoveal choroidal neovascularization have a poor prognosis. These patients can sometimes enjoy good visual function, particularly when the choroidal neovascular membrane is not leaking or when it is located under the retinal pigment epitheli-um and there is apposition of the retinal pigment epithelium to the sensory retina.2,3 Clinicopathologic studies of laser-treated choroidal neovascularization have demonstrated that choroidal neovascularization can still be present despite that we cannot visualize it clinically or angiographically (involuted or obliterated choroidal neovascularization).4 Dr. Hawkins also states that the degree to which the hemorrhagic component contributes to the mechanical injury sustained by the macula has not received adequate study. Although we all would like more studies to be

available, I would point to the existing literature on this topic listed as references 1 to 4 of the original article.1,5'7

Dr. Hawkins questions "whether or not the hemor-rhagic component markedly decreases the visual prognosis beyond that which results from the develop-ment of the choroidal neovascular membrane alone." According to the Macular Photocoagulation Study, patients with classic subfoveal choroidal neovascular-ization in age-related macular degeneration without treatment had an average visual acuity of 20/400 after two years.8 Eyes with occult subfoveal choroidal neovascularization have a better visual prognosis.2,3 In a study by Soubrane and associates,2 60% of the eyes had an initial visual acuity of 20/50 or better and 36% of the eyes had a final ( 12 to 95 months) visual acuity of 20/50 or better. In another study of occult sub-foveal choroidal neovascularization, 25% of the eyes had a visual acuity of 20/40 or better, and the average final (six to 53 months) visual acuity was 20/250.3 In contrast, a study of eyes with submacular hemorrhage secondary to age-related macular degeneration dem-onstrated a markedly worse visual prognosis with patients having an average final visual acuity of 20/1700.7

I do not have a better explanation than the one I gave in paragraph 12 of the discussion regarding the failure to visualize choroidal neovascularization angi-ographically after removal of the submacular hemor-rhage. I have been able to review the fluorescein angiograms of five patients before the development of the submacular hemorrhage, and they all demonstrate occult choroidal neovascularization caused by leakage of an undetermined source. To date, we do not have much information of the histopathologic factors or behavior of occult choroidal neovascularization be-cause of leakage of the undetermined source, and we could only speculate on the mechanisms that lead to involution of these membranes. Glaser and associates9

have suggested that factors and substances released by stimulated retinal pigment epithelium or other cells may play a role in containment and resolution of choroidal neovascularization. Experimental studies by Miller, Miller, and Ryan10 suggest that involution of choroidal neovascularization with cessation of visible fluorescein leakage is the result of retinal pigment epithelium proliferation that envelopes the choroidal neovascular membrane and probably resorbs the

VOL.UO, No. 4 CORRESPONDENCE 551

accumulated subretinal fluid, as well as prevent its further accumulation. It could be possible that either the hemorrhage or the surgery could stimulate one of these mechanisms and lead to involution of the choroidal neovascular membrane.

I do not agree that "a contracted or inactive submacular choroidal neovascular membrane contin-ues to exhibit a prominent degree of hyperfluores-cence." Angiographically, an active choroidal neo-vascular membrane will leak, a scar will stain, and a laser-treated, well-defined choroidal neovascular membrane will be hypofluorescent. As Miller, Miller, and Ryan10 have shown, involution of choroidal neovascularization is accompanied by cessation of visible fluorescein leakage.

Indeed, Figure 7, top right shows an area of hyperfluorescence superior and superonasal to the fovea, which I interpreted as occult choroidal neovas-cularization caused by blocked fluorescence. I realize that without stereoscopic pairs it is difficult to inter-pret the postoperative fluorescein angiogram. The hypofluorescence seen in the postoperative angio-gram is because of residual subsensory blood and not because of subretinal pigment epithelial blood, and my interpretation after mapping the fovea was that the choroidal neovascular membrane did not extend under its center.

Although Dr. Hawkins might be correct in point-ing out that "laser photocoagulation of the promi-nently fluorescent extrafoveal site for such an eye would, in the long run, be doomed to failure," the

patient's visual acuity has improved to 20/100 at 42 months postoperatively.

HILEL LEWIS, M.D. Cleveland, Ohio

REFERENCES

1. Toth CA, Morse LS, Hjelmeland LM, Landers MB III. Fibrin directs early retinal damage after experimental subretinal hemorrhage. Arch Ophthalmol 1991;109:723-9.

2. Soubrane G, Coscas G, Français C, Koenig F. Occult subretinal new vessels in age-related macular degeneration: natural history and early laser treatment. Ophthalmology 1990;97:649-57.

3. Bressler NM, Frost LA, Bressler SB, Murphy RP, Fine SL. Natural course of poorly defined choroidal neovascularization associated with macular degeneration. Arch Ophthalmol 1988;106:1537-42.

4. Green WR. Clinicopathologic studies of treated choroidal neovascular membranes. Retina 1991;11:328-56.

5. Glatt H, Machemer R. Experimental subretinal hemorrhage in rabbits. Am J Ophthalmol 1982;94:762-73.

6. Lewis H, Resnick SC, Flannery JG, Straatsma BR. Tissue plasminogen activator treatment of experimental subretinal hemorrhage. Am J Ophthalmol 1991;111:197-204·

7. Bennett SR, Folk JC, Blodi CF, Klugman M. Factors prognostic of visual outcome in patients with subretinal hemorrhage. Am J Ophthalmol 1990;109:33-7.

8. Macular Photocoagulation Study Group. Laser photocoagu-lation of subfoveal neovascular lesions in age-related macular degeneration: results of a randomized clinical trial. Arch Ophthalmol 1991;109:1220-31.

9. Glaser BM, Campochiaro PA, Davis JL Jr, Sato M. Retinal pigment epithelial cells release an inhibitor of neovasculariza-tion. Arch Ophthalmol 1985;103:1870-5.

10. Miller H, Miller B, Ryan SJ. The role of retinal pigment epithelium in the involution of subretinal neovascularization. Invest Ophthalmol Vis Sei 1986;27:1644-52.

552 AMERICAN JOURNAL OF OPHTHALMOLOGY OCTOBER 1995