Abstract

The anatomical proximity of anterior and posterior segment structures and the familiar microcirculatory milieu make both susceptible to arduous complications when either is surgically handled. Because of the complex haemodynamic reciprocity between vitreous, retina, choroid, and aqueous humour, any trivial alteration in one can present a catastrophic consequence in the other. A good number of evidence.based studies have already substantiated that postoperative rise in intraocular pressure (IOP) is a well-recognised complication after vitreoretinal surgeries like scleral buckling, pars plana vitrectomy (PPV), intravitreal gas and silicon oil injection as well as intravitreal steroid and antivascular endothelial growth factor (VEGF) injection. The cause is multifactorial. Determining the cardinal pathophysiological mechanism is very decisive as it provides the ultimate guide to opting for the suitable treatment modality. The superimposing clinical features mystify the diagnosis, and pre.existing conjunctival scars and episcleral explants make any further surgical management very tough. In many cases, anti-glaucoma medications are beneficial for managing the temporary rise in IOP. However, the options of laser treatment and filtration surgeries can be considered in resistant cases, and glaucoma drainage devices are the last resort for refractory patients where filtration surgeries fail. In this review, we provide fundamental insight into the possible pathogenic mechanisms, specifically focusing on how to discriminate among them and strategically approach the management with secondary elevation in IOP following vitreoretinal surgeries.

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