Ophthalmology Volume 105, Number 12, December 1998 feeder vessels, identified with these angiograms, are frequently large in size and hard to occlude. Our study was the first to attain not only anatomical success but functional success in a large series of patients with primary subfoveal CNV secondary to AMD, by using a 20° field size of a scanning laser ophthalmoscope to identify small-sized feeder vessels. I apologize for missing Dr. Bloom’s article. However, this prospective study started in 1993 and was presented at the Annual Meeting of the American Academy of Ophthalmology in Chicago, in October of 1996. In addition, a preliminary study on feeder vessel photocoagulation was reported by me.1 Recently, we also experienced a tear of the retinal pigment epithelium (RPE) after this treatment in a patient with large pigment epithelial detachment. A tear of the RPE is a severe complication after standard laser treatment of CNV and may occur, though rarely, after this treatment. We used sequential dye red-yellow photocoagulation for the majority of the patients in the study. However, dye yellow was mainly used in the area of the RPE and choroid with little pigment, and dye red was only applied to the feeder vessel if overlaid by blood. The dye red may be more effective for Japanese patients, who have more pigment, than for white patients. As you mentioned, however, the use of a wavelength selectively absorbed by hemoglobin may be ideal and more suitable for white patients. At present, we suppose that the dye yellow laser alone may suffice to attain the permanent occlusion of feeder vessels. FUMIO SHIRAGA, MD Okayama, Japan Reference 1. Shiraga F. Identification of feeder vessels in subfoveal choroidal neovascularization. Jpn J Clin Ophthalmol 1995; 49:63–71.
Dear Editor: For many years, ophthalmologists have been attempting to treat subfoveal primary and recurrent CNV in AMD by treating only a portion of the neovascular membrane. One such partial treatment is a “feeder vessel” technique. The rationale is quite obvious: preservation of the fovea by obliteration of extrafoveal vessels that perfuse the membrane. Most who have tried this approach have eventually abandoned it because no more than a temporary closure or spasm of the feeding vessels can be accomplished. Subsequent reperfusion and further proliferation of the CNV invariably occur. With refinements in indocyanine green angiography (ICG), many clinicians have revisited the concept of partial treatment and feeder vessel photocoagulation based on enhanced imaging of the choroidal circulation and the involved abnormal vessels. In their article on this subject, Shiraga et al (Ophthalmology 1998; 105:662–9) studied a series of patients treated in this fashion with promising results. This has not been our experience with AMD, but we have seen partial treatment succeed in a similar disorder, idiopathic polypoidal choroidal vasculopathy (IPCV).
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In their article, Shiraga et al did not state their definition of AMD. Most practitioners would consider soft or exudative drusen and pigment epithelial atrophic and granular abnormalities necessary parts of this diagnosis. In fact, the clinical photographs included in this article do not clearly show any evidence of these manifestations. Rather, their clinical and angiographic illustrations reveal an abnormal choroidal vasculature composed of two elements that are quite characteristic for IPCV: dilated inner choroidal vessels and aneurysmal vascular changes. We have reported that this vascular abnormality occurs more frequently in pigmented races, including black and Asian patients, but it can also occur in white patients.1–3 We have also reported that these patients tend to have a more favorable clinical course and that photocoagulation of the leaking or bleeding aneurysms can result in resolution of the serosanguineous complications. Thus, we wonder whether a number of the 37 patients reported in the series by Shiraga et al actually have IPCV. If the population treated by Shiraga et al in fact includes patients with IPCV, conclusions regarding the efficacy of using the feeder vessel technique to treat subfoveal CNV in AMD cannot be drawn from their data. Accordingly, based on our clinical experience, we would suggest that the feeder vessel technique is not likely to be of benefit to the latter group of patients, even with the advantages of ICG. For future studies, it is important to distinguish between typical AMD and IPCV, both of which have distinct demographic, morphologic, and prognostic features. K. BAILEY FREUND, MD LAWRENCE A. YANNUZZI, MD RICHARD F. SPAIDE, MD New York, New York References 1. Yannuzzi LA, Sorenson J, Spaide RF, Lipson B. Idiopathic polypoidal choroidAL vasculopathy (IPCV). Retina 1990; 10: 1– 8. 2. Spaide RF, Yannuzzi LA, Slakter JS, et al. Indocyanine green videoangiography of idiopathic polypoidal choroidal vasculopathy. Retina 1995; 15:100 –10. 3. Yannuzzi LA, Ciardella A, Spaide RF, et al. The expanding clinical spectrum of idiopathic polypoidal choroidal vasculopathy. Arch Ophthalmol 1997; 115:478 – 85.
Author’s reply Dear Editor: I apologize that we did not state the definition of AMD. Our eligibility criteria included the presence of drusen and/or retinal pigment epithelial atrophy in the studied eyes and/or fellow eyes. As Freund et al pointed out, there may be fewer age-related changes of the retinal pigment epithelium in our clinical photographs. Japanese patients with AMD seem to have fewer age-related changes, such as soft or exudative drusen and pigment epithelial atrophy, than white patients. However, the majority of these patients have the typical natural course of AMD in that choroidal neovascular membranes have enlarged over a period of weeks to months, resulting in large fibrous scars, accompanied by significant loss of central vision.
Letters to the Editor Since Spaide et al published the article entitled, “Indocyanine Green Angiography (ICGA) of Idiopathic Polypoidal Choroidal Vasculopathy,”1 we have paid attention to distinguishing between idiopathic polypoidal choroidal vasculopathy (IPCV) and AMD, and we were surprised to discover more patients with IPCV than we expected. The patients with typical IPCV lesions and ICGA findings, as described previously,1,2 were excluded from our study on feeder vessel photocoagulation of subfoveal CNV secondary to AMD. The ICG angiograms presented in our article were taken using a 20° field size and enlarged, thus abnormal vessels on these angiograms seem to be dilated, as Freund et al mentioned. However, these did not show any tubular and polypoidal elements, and it also was not clear on two-dimensional images whether these vessels were located within the inner choroid or anterior to the choroid. In addition, the patients presented in the article had unilateral disease and did not have multiple and recurrent serosanguineous detachment of the RPE and neurosensory retina. Thus, these patients could be diagnosed as having AMD. However, the early stages of IPCV may show neither IPCV lesions nor typical ICGA findings. If it is true, a small number of the studied patients may be included in the expanding spectrum of IPCV that Yannuzzi et al stated.2 However, in the majority of the patients in our article, ICGA did not show polypoidal or aneurysmal vasculature but did show cartwheel or lacy patterns of CNV. Freund et al mentioned that feeder vessel photocoagulation is not likely to be of benefit in AMD. Large feeder vessels, identified by using fluorescein angiography or ICGA with digital video cameras, are indeed difficult to occlude permanently. A scanning laser ophthalmoscope using a 20° field size may be indispensable for the identification and effective treatment of them; otherwise, as we mentioned in the article, there may be a difference in the efficacy of this treatment when comparing white patients and pigmented patients. FUMIO SHIRAGA, MD Okayama, Japan References 1. Spaide RF, Yannuzzi LA, Slakter JS, et al. Indocyanine green videoangiography of idiopathic polypoidal choroidal vasculopathy. Retina 1995; 15:100 –10. 2. Yannuzzi LA, Ciardella A, Spaide RF, et al. The expanding clinical spectrum of idiopathic polypoidal choroidal vasculopathy. Arch Ophthalmol 1997; 115:478 – 85.
Traumatic Hyphema and Patient Outcomes— An Oversight Dear Editor: Since the publication of our article “Traumatic Hyphema: Outcomes of Outpatient Management,” (Ophthalmology 1998; 105:851–5) an important oversight has been brought to our attention. Our article did not acknowledge a previous study by Witteman et al1 published in 1985. This study was a retrospective analysis of 371 consecutive patients with traumatic hyphema treated in Wisconsin. The study included 109 patients with hyphema treated in the outpatient setting. The specific details of management of this subset of
patients were not completely specified; however, the authors reported a rebleeding rate of 1.8% without the use of antifibrinolytic agents. This work is particularly noteworthy given that it was published during a time when outpatient management of hyphema was still uncommon. It should have been referenced in our publication. YICHIEH SHIUEY, MD Boston, Massachusetts MARK J. LUCARELLI, MD Madison, Wisconsin Reference 1. Witteman GJ, Brubaker SJ, Johnson M, Marks RG. The incidence of rebleeding in traumatic hyphema. Ann Ophthalmol 1985; 17:525– 6.
Laser Thermal Keratoplasty for PRK Overcorrection Dear Editor: In his article “Laser Thermal Keratoplasty for the Treatment of Photorefractive Keratectomy Overcorrections: A 1-Year Follow-up,” (Ophthalmology 1998; 105:926 –31) Mihai Pop describes his work evaluating the efficacy of laser thermal keratoplasty (LTK) treatment for overcorrection of myopia after photorefractive keratectomy (PRK), implying in his conclusion that LTK is a potentially useful option for overtreatments limited to 2 diopters (D) or less. While I certainly concur that such work is important in assessing this technology, the results are more an example of how statistics can be deceiving than an example of convincing clinical benefit. Many complicated analyses are commonly performed to evaluate refractive surgical procedures. Yet simple inspection of the graphs illustrating “intended” versus “achieved” correction 12 months postoperatively provided by the author (replotted here as Figure 1) suggests that, at least under the protocols used in the study, LTK offers little in the way of precision, the preponderance of the points clearly representing notable undercorrections of varying degrees. In Table 6 of his article, the author reports percentages of eyes falling within ⫾0.5 D and ⫾1.0 D of emmetropia at various points in time from 1 month to 12 months postoperatively. Yet, if “success” is measured by coming within 0.5 D of the intended value, limiting ourselves to the 1-year postoperative results and considering the values that do not fall in this range, the technique fails miserably with 70% (21 of 30†) not meeting this standard for the PTK ⫹ LTK group, and 80% (20 of 25*) for the LTK group. Even if we confine ourselves to the cases in which only 1 to 2 D of hyperopia are treated as suggested by the author, these values improve only marginally to 69% (11 of 16) and 57% (4 of 7), respectively. * Because the raw data were not published, the graphs were manually plotted based on the figure in the article, and represent a best estimate. Apparently a few of the points were coincident and therefore not distinguishable; thus the “n” for each group is slightly lower than the published values for the graphs. This small data loss is not believed to make the logic any less valid.
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