Letter by Lee et al Regarding Article, “Spontaneous Resolution of Central Serous Chorioretinopathy in a Patient With Congenital Retinal Macrovessel”
To the Editor:
We read the article by Ascaso entitled, “Spontaneous Resolution of Central Serous Chorioretinopathy in a Patient with Congenital Retinal Macrovessel” published in Volume 124 of Circulation with great interest.1
In our opinion, the images provided in the article do not seem to show what we can see in typical central serous chorioretinopathy (CSCR). In the images provided, the leakage seen on fundus fluorescein angiography definitely appears to be originating from an anastomotic site at the congenital retinal macrovessels (CRMs). The retinal vessels are visible below the leakage point, which means that the leakage point cannot be at the level of the retinal pigment epithelium (RPE). In general, acute CSCR findings on fundus fluorescein angiography have been described as leakage from the RPE level, but not from the associated retinal vessels. CSCR is characterized by the development of serous detachment at the central sensory retina. Malfunction of the RPE is part of the presumed pathophysiology. The buildup of fluid seems to occur because of small breaks in the RPE. However, the leakage of the retinal macrovessels originates at the retinal level.
From our perspective, the findings from the optical coherence tomography (OCT) images in this article seem more like intraretinal cyst instead of serous retinal detachment (SRD). There were uncertain elevated SRD-like lesions, but these findings are more typical of macular edema originating from the retinal level. SRD in forms of acute CSCR is usually characterized by a dome-shaped accumulation of subretinal fluid on OCT located below the sensory retina.2
Consequently, in our view, the image findings shown in the article might have resulted from the leakages of altered vessels associated with the CRM. Microalteration of the inner blood-retina barrier may result in fluorescein leakage on fundus fluorescein angiography that may cause intraretinal cystic changes shown on OCT. A few microaneurysms in the capillary network of the juxtafoveal area are accordance with our assumption that the leakage might be the result of microalteration of the retinal vessels. There are a few more similar cases of CRM combined with macular edema that have been reported previously.3,4
Nevertheless, this case report is valuable because this is the first well-documented report of what may be a spontaneously resolved CSCR with CRM, and this could provide information about a possible etiologic relationship between CSCR and CRM. Currently, spectral domain OCT techniques have been developed to produce more detailed cross-sectional retinal images and RPE changes in CSCR. In our opinion, serial fundus fluorescein angiography images or 3-dimensional images with spectral domain OCT could be helpful in convincing the reader that the findings of this article are associated with CSCR.
Won June Lee, MD
Byung Ro Lee, MD
Hee Yoon Cho, MD
Department of Ophthalmology
Hanyang University College of Medicine
- © 2012 American Heart Association, Inc.