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Prevalence of vitreomacular adhesion: an optical coherence tomography analysis in the retina clinic setting

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      The aims of this study were to determine the prevalence of vitreomacular adhesion (VMA) in a random sample of clinical patients at three US retina clinics and to assess comorbid retinal conditions, ocular diseases, prior treatment history, and other medical histories.

      Patients and methods

      This observational, retrospective cohort study was based on patients from the Doheny Eye Centers, Duke Eye Center, and Tufts Medical Center who received a bilateral spectral domain optical coherence tomography (SD-OCT) scan (one scan/eye) for clinical evaluation with available medical records. The study had three phases: 1) collection of retrospective patient data; 2) review of OCT scans at a reading center to assess VMA and associated conditions; and 3) analyses and reporting of data on the prevalence of VMA, patient demographics, and comorbid conditions. Data were obtained from electronic health records and OCT grading forms. Outcome measures from bilateral SD-OCT scans and medical records included OCT evaluation of VMA and retinal comorbid conditions.


      In 719 patients with 1,483 reviewable OCT scans, the prevalence of VMA was estimated at 14.74% (90% CI, 12.58%–16.92%). The prevalence of unilateral VMA was estimated at 12.39%, while bilateral VMA was 2.36%. In patients with VMA, 34 out of 123 eyes with VMA (27.64%) also had fovea deformed by vitreomacular traction. Macular hole (MH) was significantly more prevalent in VMA-diagnosed eyes versus non-VMA-diagnosed eyes (6.5% versus 1.9%; P=0.02). There was a significantly higher incidence of full-thickness MH ( P=0.008), operculum/flaps ( P<0.0001), and lamellar or pseudo-holes ( P=0.048) in VMA-diagnosed versus non-VMA-diagnosed eyes. Age, MH as a comorbid condition, full-thickness MH, lamellar or pseudo-holes, and operculum were predictive of a VMA diagnosis.


      The prevalence of VMA was estimated at 14.74% in a random sample of patients from three retina clinics. VMA diagnosis can be predicted by factors, including age, MH as a comorbid condition, and lamellar or pseudo-holes.

      Related collections

      Most cited references 21

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      The International Vitreomacular Traction Study Group classification of vitreomacular adhesion, traction, and macular hole.

      The International Vitreomacular Traction Study (IVTS) Group was convened to develop an optical coherence tomography (OCT)-based anatomic classification system for diseases of the vitreomacular interface (VMI).
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        Posterior vitreous detachment: evolution and complications of its early stages.

         Mark Johnson (2010)
        To summarize emerging concepts regarding the onset and progression, traction effects, and complications of the early stages of age-related posterior vitreous detachment (PVD). Interpretive essay. Review and synthesis of selected literature, with clinical illustrations, interpretation, and perspective. Imaging of the vitreoretinal interface with optical coherence tomography has shown that PVD begins in the perifoveal macula. Recent longitudinal studies have demonstrated conclusively that early PVD stages persist chronically and progress slowly over months to years. Vitreous traction forces resulting from perifoveal PVD with a small vitreofoveolar adhesion (500 microm or less) may cause localized cystoid foveal thickening or one of several macular hole conditions. Traction associated with larger adhesion zones may cause or exacerbate a separate group of macular disorders. Ultrastructural studies suggest that epiretinal membrane develops from cortical vitreous remnants left on the retinal surface after PVD and plays an important role in traction vitreomaculopathies. Age-related PVD is an insidious, chronic event that begins in the perifoveal macula and evolves over a prolonged period before vitreopapillary separation. Although asymptomatic in most individuals, its early stages may be complicated by a variety of macular and optic disc pathologic features, determined in part by the size and strength of the residual vitreoretinal adhesion. (c) 2010 Elsevier Inc. All rights reserved.
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          Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease.

           J. Sebag (2004)
          Posterior vitreous detachment (PVD) is the consequence of changes in the macromolecular structure of gel vitreous that result in liquefaction, concurrent with alterations in the extracellular matrix at the vitro-retinal interface that allow the posterior vitreous cortex to detach from the internal limiting lamina of the retina. Gel liquefaction that exceeds the degree of vitro-retinal dehiscence results in anomalous PVD (APVD). APVD varies in its clinical manifestations depending upon where in the fundus vitreo-retinal adhesion is strongest. At the periphery, APVD results in retinal tears and detachments. In the macula, APVD causes vitreo-macular traction syndrome, results in vitreoeschisis with macular pucker or macular holes, or contributes to some cases of diabetic macular edema. At the optic disc and retina, APVD causes vitreo-papillary traction and promotes retinal and optic disc neovascularization. Unifying the spectrum of vitreo-retinal diseases into the conceptual frame-work of APVD underscores that to more effectively treat, and ultimately prevent, these disorders it is necessary to replicate the two components of an innocuous PVD, i.e., gel liquefaction and vitreo-retinal dehiscence. Pharmacologic vitreolysis is designed to mitigate against APVD by chemically breaking down vitreous macromolecules and weakening vitro-retinal adhesion to safely detach the posterior vitreous cortex. This would not only facilitate surgery, but if performed early in the natural history of disease, it should prevent progressive disease.

            Author and article information

            [1 ]Department of Ophthalmology, New England Eye Center, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, USA
            [2 ]Duke Eye Center, Duke Reading Center, Durham, NC, USA
            [3 ]Department of Ophthalmology, Doheny Eye Centers, University of California, Los Angeles, CA, USA
            Author notes
            Correspondence: Elias Reichel, Department of Ophthalmology, New England Eye Center, Tufts Medical Center, Tufts University School of Medicine, 800 Washington Street, Box 450, Boston, MA 02111, USA, Tel +1 617 636 1648, Fax +1 617 636 4866, Email ereichel@
            Clin Ophthalmol
            Clin Ophthalmol
            Clinical Ophthalmology
            Clinical Ophthalmology (Auckland, N.Z.)
            Dove Medical Press
            06 April 2016
            : 10
            : 627-633
            27103782 4827918 10.2147/OPTH.S95524 opth-10-627
            © 2016 Reichel et al. This work is published and licensed by Dove Medical Press Limited

            The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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