Posterior Vitreous Detachment — Floaters, Flashes, and Differentiation from Retinal Tear

The vitreous body is a gel-like structure occupying 80% of the ocular volume, composed of 99% water, hyaluronic acid, and a network of type II collagen fibrils. With aging, the vitreous undergoes progressive liquefaction (synchysis) and aggregation of collagen fibers (syneresis). When liquefied vitreous accesses the retrohyaloid space through a defect in the posterior hyaloid face, it separates the posterior vitreous cortex from the internal limiting membrane of the retina—a process termed posterior vitreous detachment. PVD typically begins peripherally and progresses centripetally over weeks to months, eventually completing with detachment of the vitreous from the optic nerve head.

PVD is highly age-related: 25% of individuals 50-65 years and 65% of those over 65 have completed PVD. Risk factors include myopia (especially axial length >26 mm), prior cataract surgery, intraocular inflammation, ocular trauma, and certain hereditary vitreoretinopathies. The symptoms result from mechanical traction on the retina before complete separation: photopsia (flashes of light) reflects mechanical or electrical stimulation of photoreceptors, while floaters represent shadows cast on the retina by mobile vitreous opacities, including the Weiss ring (annular condensation around the optic nerve), pigment cells, hemorrhage, or condensed collagen.

The critical clinical concern is differentiation of uncomplicated PVD from PVD with associated retinal tear. Approximately 10-15% of acute symptomatic PVDs have associated retinal breaks, which can progress to rhegmatogenous retinal detachment in 30-50% if untreated. Risk factors for retinal breaks include myopia, lattice degeneration, prior retinal detachment in the fellow eye, family history, and pseudophakia. Comprehensive dilated fundus examination with scleral depression by an ophthalmologist is essential, ideally within 24-72 hours of new symptoms. Patients with vitreous hemorrhage or pigment in the anterior vitreous (Shafer sign) have particularly high risk and require urgent evaluation. When detected promptly, retinal breaks are highly treatable with laser photocoagulation or cryopexy, preventing progression to retinal detachment.