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VITREOMACULAR ADHESION AND THE DEFECT IN POSTERIOR VITREOUS CORTEX VISUALIZED BY TRIAMCINOLONE-ASSISTED VITRECTOMY

Norihito Doi, Akinori Uemura, Kumiko Nakao, Taiji Sakamoto

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Abstract

In Brief Purpose: To study the vitreomacular adhesion and the contractile force of posterior hyaloid, which are shown in triamcinolone acetonide (TA)-assisted pars plana vitrectomy (PPV). Design: Interventional case series. Methods: Twenty-eight eyes with diabetic macular edema (DME) without posterior vitreous detachment (PVD) received TA-assisted PPV. Surgical PVD was performed by an aspiration of vitrectomy probe, and the dynamic changes of posterior vitreous cortex and residual vitreous cortex were evaluated. Results: A premacular defect was formed in the detached posterior vitreous cortex during surgical PVD in 27 of 28 eyes. Immediately thereafter, the small defect expanded into a large hole in the detached posterior vitreous cortex in all cases. A residual vitreous cortex was left on the macula in 22 eyes. Conclusions: These observations demonstrate a firm vitreoretinal adhesion in the central macula and suggest that the enlargement of the defect of posterior vitreous cortex may be extrusion of vitreous out through the premacular dehiscence into the preretinal space, or a tangentially contractile force may exist in the posterior vitreous cortex. Both macular adhesion and the traction of vitreous cortex might contribute to the pathogenesis of DME and other vitreomacular disease. We observed vitreous which was visualized in triamcinolone acetonide-assisted vitrectomy for 28 diabetic macular edema eyes. In most cases, a small defect in the posterior vitreous cortex was formed and immediately expanded to premacular round defect. This finding suggests that traction might be present in the premacular vitreous.

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What this paper is about

In Brief Purpose: To study the vitreomacular adhesion and the contractile force of posterior hyaloid, which are shown in triamcinolone acetonide (TA)-assisted pars plana vitrectomy (PPV). Design: Interventional case series. Methods: Twenty-eight eyes with diabetic macular edema (DME) without posterior vitreous detachment (PVD) received TA-assisted PPV. Surgical PVD was performed by an aspiration of vitrectomy probe, and the dynamic changes of posterior vitreous cortex and residual vitreous cortex were evaluated. Results: A premacular defect was formed in the detached posterior vitreous cortex during surgical PVD in 27 of 28 eyes. Immediately thereafter, the small defect expanded into a large hole in the detached posterior vitreous cortex in all cases. A residual vitreous cortex was left on the macula in 22 eyes. Conclusions: These observations demonstrate a firm vitreoretinal adhesion in the central macula and suggest that the enlargement of the defect of posterior vitreous cortex may be extrusion of vitreous out through the premacular dehiscence into the preretinal space, or a tangentially contractile force may exist in the posterior vitreous cortex. Both macular adhesion and the traction of vitreous cortex might contribute to the pathogenesis of DME and other vitreomacular disease. We observed vitreous which was visualized in triamcinolone acetonide-assisted vitrectomy for 28 diabetic macular edema eyes. In most cases, a small defect in the posterior vitreous cortex was formed and immediately expanded to premacular round defect. This finding suggests that traction might be present in the premacular vitreous.

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Available abstract

In Brief Purpose: To study the vitreomacular adhesion and the contractile force of posterior hyaloid, which are shown in triamcinolone acetonide (TA)-assisted pars plana vitrectomy (PPV). Design: Interventional case series. Methods: Twenty-eight eyes with diabetic macular edema (DME) without posterior vitreous detachment (PVD) received TA-assisted PPV. Surgical PVD was performed by an aspiration of vitrectomy probe, and the dynamic changes of posterior vitreous cortex and residual vitreous cortex were evaluated. Results: A premacular defect was formed in the detached posterior vitreous cortex during surgical PVD in 27 of 28 eyes. Immediately thereafter, the small defect expanded into a large hole in the detached posterior vitreous cortex in all cases. A residual vitreous cortex was left on the macula in 22 eyes. Conclusions: These observations demonstrate a firm vitreoretinal adhesion in the central macula and suggest that the enlargement of the defect of posterior vitreous cortex may be extrusion of vitreous out through the premacular dehiscence into the preretinal space, or a tangentially contractile force may exist in the posterior vitreous cortex. Both macular adhesion and the traction of vitreous cortex might contribute to the pathogenesis of DME and other vitreomacular disease. We observed vitreous which was visualized in triamcinolone acetonide-assisted vitrectomy for 28 diabetic macular edema eyes. In most cases, a small defect in the posterior vitreous cortex was formed and immediately expanded to premacular round defect. This finding suggests that traction might be present in the premacular vitreous.

Key concepts: Vitreous membrane, Vitrectomy, Posterior vitreous detachment, Pars plana, Triamcinolone acetonide, Ophthalmology, Medicine, Cortex (anatomy)

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