Letters to the Editor Chang et al have developed and appreciate the many contributions they have made, including perfluorocarbon liquids and wide-angle viewing systems. We do not, however, as they state, recommend routine use of inferior retinectomy in all cases of PVR and clarify emphatically any misunderstanding that might have arisen. Careful reading of our “Patients and Methods” reveals that of the 281 eyes operated on for a diagnosis of retinal detachment (RD) with PVR during the period in question, only 104 (37%) required a retinectomy. These selected 104 eyes were the subject of our report. Furthermore, as stated in “Patients and Methods” the decision to do an inferior retinectomy was reached only if persistent RD or retinal traction were noted after membrane peeling. In our view, such persistent traction is almost always the result of anterior PVR. It has been our experience that with PVR surgery, failure of the retina to reattach, recurrence of RD, and hypotony are almost always due to persistent or recurrent anterior PVR. 2. We address their comments concerning our technique of lens removal in radical anterior base dissection. Although we agree that removal of the crystalline lens or intraocular lens (IOL) is not necessary in all cases of PVR, we strongly feel that such removal is necessary in cases of well-established anterior PVR and that our reported results support this view. The concept of eliminating the entire structure of the basal vitreous inferiorly, or radical base dissection, evolved after bitter experience with the failure of lesser measures. Radical base dissection includes the removal of the basal vitreous as well as its connections to anterior structures. Therefore, because the retina and vitreous are not separable within the vitreous base, retinectomy is required. Just as important, in our view, is eliminating the connection of the anterior vitreous to the ciliary body, ciliary processes, zonules, lens, or IOL, all of which are often significantly involved in the scarring that defines anterior PVR. As discussed in the article, removal of these structures, which are not only the sources of traction but also the structures on which reproliferation can occur, is possible only with excellent exposure of the surgical field. This is not physically possible with the crystalline lens in place nor is it possible with an IOL in place without severely injuring the zonule and destabilizing the lens. Furthermore, residual capsule and scar within the anterior vitreous make viewing the surgical field suboptimal. Although retinectomy is usually necessary inferiorly, where intrabasal scarring is most prominent, anterior vitreous removal is best done for 360° to rid the eye of the scaffold for further anterior proliferation and traction. Clearly, aphakic eyes do not present the above difficulties, and aphakia facilitates radical base dissection.
3. Our results clearly show that removal of the IOL in cases of severe anterior PVR improves outcomes, likely due to the improved exposure to the anterior base and inclusion of the anterior hyloid in the dissection. Although we agree that confounding variables may have influenced the results, given the large difference observed and anatomic realities stated above, we feel that removal of the IOL is the superior method in cases where anterior PVR is the problem and has a high likelihood of recurrence. In the Tseng et al study,2 they reported an increased risk of anterior PVR after retinectomy, which is likely due to inadequate removal of perilenticular vitreous. 4. We agree that physiological outcomes of vision and intraocular pressure are relevant. Sadly, however, these are most often determined by the preoperative health of the retina and severity of the PVR. In our series, the average number of previous operations was 1.8. Undoubtedly, repairing the RD the first time or correcting eyes with PVR definitively the first time would lead to superior visual results. Finally, we agree with the comments of Tennant et al in their letter regarding intravitreal triamcinolone as a surgical adjunct for identifying residual vitreous. Often, in cases of severe anterior PVR, despite meticulous vitreous removal and membrane peeling posteriorly, normal retinal architecture cannot be restored due to intrinsic foreshortening of the retina, contraction within the vitreous base, and fibrosis to anterior structures. In these cases, retinectomy may be required to flatten the retina completely and permanently. POLLY A. QUIRAM, MD, PHD Royal Oak, Michigan STEVEN D. SCHWARTZ, MD CHRISTINE R. GONZALES, MD ALLAN E. KREIGER, MD Los Angeles, California References 1. Quiram PA, Gonzales CR, Hu W, et al. Outcomes of vitrectomy with inferior retinectomy in patients with recurrent rhegmatogenous retinal detachments and proliferative vitreoretinopathy. Ophthalmology 2006;113:2041–7. 2. Tseng JJ, Barile GR, Schiff WM, et al. Influence of relaxing retinotomy on surgical outcomes in proliferative vitreoretinopathy. Am J Ophthalmol 2005;140:628 –36.
Vein Occlusion in Chinese Subjects Dear Editor: To determine the prevalence of retinal vein occlusions and the associated factors in the adult Chinese population, fundus photographs obtained in the Beijing Eye Study were examined. The Beijing Eye Study is a population-based cross-sectional cohort study that included 4439 of 5324 subjects invited to participate with an age of 40 years or older. The present investigation consisted of 8609 eyes (97.0%) of 4335 (97.7%) subjects for whom readable fundus photographs were available. The Medical Ethics Com-
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Ophthalmology Volume 114, Number 9, September 2007 mittee of the Beijing Tongren Hospital had approved the study protocol and all participants had given informed consent, according to the Declaration of Helsinki. The study has been described in detail recently.1 For our study, recent central retinal vein occlusion was characterized by the presence of retinal edema, optic disc hyperemia or edema, scattered superficial or deep hemorrhages, and venous dilatation. Old retinal vein occlusions were characterized by occluded and sheathed retinal veins. Branch retinal vein occlusion involved a more localized area of the retina in the sector of the obstructed venule and was characterized by scattered superficial and deep retinal hemorrhages, venous dilatation, intraretinal microvascular abnormalities, and occluded and sheathed retinal venules. An ischemic type of vein occlusion was characterized by retinal neovascularization that was distinguished from intraretinal collateral vessel formation between an occluded and nonoccluded region, in the case of branch retinal vein occlusions, or by very thin retinal vessels in the affected region.2 A retinal vein occlusion was detected in 60 (0.7%) eyes (95% confidence interval [CI], 0.5%– 0.9%) of 58 (1.3%; 95% CI, 1.0%–1.6%) subjects (33 women). The mean age of all patients with retinal vein occlusions was 63.0⫾8.9 years (range, 41– 82). The prevalence of branch retinal vein occlusion was 1.2% (53/4335; 95% CI, 0.9%–1.5%), and that of central retinal vein occlusion was 0.12% (5/4335; 95% CI, 0%– 0.2%). There were 7 subjects (7 eyes [12%]) with the ischemic type of retinal vein occlusion and 51 (53 eyes [88%]) with a nonischemic type. Bilateral involvement was observed in 2 subjects (3.3%). The prevalences of retinal vein occlusions for the age groups 40 to 49 years, 50 to 59, 60 to 69, and ⱖ70, respectively, were 0.3%, 1.3%, 2.1%, and 2.8%, respectively. The prevalence of retinal vein occlusions increased sharply after the age of 50 for women and after the age of 60 for men. The branch retinal vein occlusion originated at a arteriovenous crossing in 46 (85%) eyes, and in 8 (15%) eyes, the branch retinal vein occlusions originated from inside the optic disc. In a binary logistic analysis, branch retinal vein occlusion was significantly associated with age (P⬍0.001; 95% CI, 1.03–1.09), presence of glaucomatous optic nerve damage (P ⫽ 0.019; 95% CI, 1.32–24.4), and the known diagnosis of arterial hypertension (P ⫽ 0.002; 95% CI, 1.42– 4.6). The results suggest that in adult Chinese ⱖ40 years old retinal vein occlusions can be detected in about 0.7% of eyes, with branch retinal vein occlusions being about 12 times more common than central retinal vein occlusions, and with the nonischemic type being about 9 times more common than the ischemic type (neovascularization or very thin vessels). These prevalence figures are comparable with prevalence figures reported for Caucasian and Hispanic population groups.3,4 Branch retinal vein occlusions were associated with the presence of glaucomatous optic nerve damage, in agreement with other population-based studies.4 The prevalence of branch retinal vein occlusions was statistically independent of the optic disc size, confirming previous hospital-based and histomorphometric studies. Future studies may elucidate the clinical impact of the findings that retinal arterioles were found anterior to venules in 46
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(98%) of 47 eyes with gradable photographs and branch retinal vein occlusions and that the branch retinal vein occlusion originated at an arteriovenous crossing in 46 (85%) of the eyes. The association between retinal vein occlusions and glaucoma may be explained by glaucomatous changes in the lamina cribrosa such as compression and distortion of the lamina cribrosa plates, possibly leading to constriction of the aperture in the lamina cribrosa for the central retinal vein trunk.5 WEIWEI LIU, MD LIANG XU, MD Beijing, China JOST B. JONAS, MD Mannheim, Germany References 1. Xu L, Cui T, Zhang S, et al. Prevalence and risk factors of lens opacities in urban and rural Chinese in Beijing. Ophthalmology 2006;113:747–55. 2. Hayreh SS. Classification of central retinal vein occlusion. Ophthalmology 1983;90:458 –74. 3. Mitchell P, Smith W, Chang A. Prevalence and associations of retinal vein occlusion in Australia: the Blue Mountains Eye Study. Arch Ophthalmol 1996;114:1243–7. 4. Klein R, Klein BE, Moss SE, Meuer SM. The epidemiology of retinal vein occlusion: the Beaver Dam Eye Study. Ophthalmologica 2000;98:133– 41, discussion 141–3. 5. Jonas JB, Berenshtein E, Holbach L. Anatomic relationship between lamina cribrosa, intraocular space, and cerebrospinal fluid space. Invest Ophthalmol Vis Sci 2003;44:5189 –95.
Prognosis and Retinal Vessel Features Dear Editor: I read with interest the Alibrahim et al article.1 They found in a prospective study that wide retinal arterioles at baseline were associated with an increased incidence of diabetic retinopathy. The amount of pressure attenuation occurring in retinal arterioles can be described as a simple ratio of vessel length divided by vessel diameter.2 In other words, everything else being equal, dilated retinal arterioles increase the pressure seen in the capillaries compared with less dilated ones. According to the Starling principle and the Laplace law, a high pressure delivered to the retinal capillaries increases the processes of capillary leakage (edema) and rupture (hemorrhage). Hence, clinical diabetic retinopathy with its edema and hemorrhage can be seen to be accelerated by these dilated retinal arterioles. The flipside of this concept is that clinical conditions that result in a low pressure being experienced in the retinal capillaries will be associated with less retinopathy. Miller and D’Amico summarized some of these conditions to include chorioretinal scarring, optic atrophy, retinitis pigmentosa, and high myopia.3 In addition, Moss et al4 have demonstrated the protective effect of low ocular perfusion pressure on the appearance and progression of diabetic retinopathy. By delivering a low pressure to the retinal capillaries either through the retinal arteriolar geometry (e.g., narrow and/or long retinal arterioles) or by low ocular perfusion pressure,5 diabetic retinopathy can be minimized