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Branch retinal vein occlusion and vitreovascular traction: a preliminary spectral domain OCT case-control study

Francisco J Ascaso, Esteban Padgett, Esther Núñez, Laura Villén, Andrzej Grzybowski, José A Cristóbal
Graefe's Archive for Clinical and Experimental Ophthalmology 2014, 252 (3): 375-81

OBJECTIVE: Branch retinal vein occlusion (BRVO) typically occurs at an arteriovenous (AV) crossing site. Although the pathogenesis is unclear, vitreovascular traction might have a significant role in some BRVO cases. The purpose of present study was to determine the incidence of vitreoretinal traction at the obstruction site in patients diagnosed with BRVO.

METHODS: In this prospective observational case–control study, 32 consecutive BRVO patients were studied with spectral-domain optical coherence tomography (SD-OCT) to detect the presence of vitreovascular traction or vitreous adherence at the occlusion site.

RESULTS: SD-OCT directed to the occlusion site revealed a vitreovascular traction at this point in eight eyes (25 %). Fourteen eyes (43.75 %) were associated with an adherence of posterior hyaloids without signs of retinal traction, whereas ten eyes (31.25 %) had neither vitreoretinal adherence nor vitreous traction. Regarding either the same vessel segment of the fellow eye, none of the cases revealed vitreovascular traction in the correspondent AV crossing site; 12 cases (37.5 %) presented vitreoretinal adherence; and the remaining 20 cases (62.5 %) showed neither traction nor adhesion. Thus, vitreovascular traction in the occlusion site was significantly associated with BRVO (p = 0.024, chi-squared test). B-scan ultrasonography showed that the posterior vitreous cortex remains more frequently attached in eyes with BRVO compared to unaffected fellow eyes (p = 0.041, chi-squared test).

CONCLUSIONS: A common firm vitreous adhesion at the obstruction site is reported herein, pointing out the possible role of vitreovascular traction in the etiology of some cases of BRVO. Likewise, although not all BRVO cases can be explained by this pathogenic mechanism, an attached posterior vitreous cortex might be a cofactor in the origin of this entity.

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