IPosterior vitreous detachment (PVD) is one of the most prevalent age-related occurrences in the posterior segment. PVD is defined as the separation of the posterior vitreous cortex (posterior hyaloid) from the internal limiting membrane of the retina and the neurosensory layer of the retina. PVD was first described histopathologically by Müller in 1856 and clinically by Brière in 1875, but the condition was not thoroughly explored until 1914. Vitreous humor is a gel-like substance that is present between the lens and the retina. The composition of vitreous humor includes water (98%), type II collagen, and hyaluronic acid. The vitreous humor is surrounded by a translucent membrane known as the hyaloid membrane. The vitreous is completely attached to the retina in the early period of life. Vitreoretinal adhesion is heterogeneous; the attachment is physiologically stronger at the vitreous base, surrounding retinal arteries, at the optic disc margin, and at the macula. Adhesion gradients are significant because PVD-related traction is concentrated at focal anchoring points. PVD is typically a gradual process that begins with partial paramacular and peripheral separation and may require years to achieve complete detachment, with perifoveal and finally peripapillary release occurring later. Acute PVD may involve horseshoe tears (due to prolonged traction), operculated breaks, rhegmatogenous retinal detachment (RRD), and bleeding when arteries are implicated. The natural history of PVD is typically asymptomatic and uncomplicated; however, a clinically significant minority of patients exhibit acute symptoms, including floaters (myodesopsia) and flashes (photopsia), indicative of vitreous opacities and tractional stimulation of the retina. Floaters are small, cobweb-shaped particles emerging from a compact collagen matrix of the posterior vitreous cortex. A rapid increase in floaters with sudden-onset photopsia (flashes) requires immediate ophthalmic care. In exam preparation, clinicians should note that a Weiss ring signifies peripapillary detachment, but the finding does not necessarily confirm that the entire posterior hyaloid is detached from the retina. Acute symptomatic PVD represents one of the most common causes of urgent ophthalmic consultation for flashes and floaters in older adults. Although most cases are uncomplicated, the possibility of retinal tear or RRD necessitates prompt recognition and timely retinal examination. Failure to identify early retinal breaks may result in irreversible vision loss, emphasizing the importance of appropriate triage and interprofessional coordination in emergency and outpatient ophthalmic settings. PVD is increasingly recognized as part of a dynamic spectrum of vitreomacular interface disorders rather than an isolated age-related event. Incomplete or anomalous separation of the posterior hyaloid may generate persistent traction at the macula or optic nerve head, contributing to vitreomacular traction (VMT) syndrome, epiretinal membrane formation, full-thickness macular hole development, and traction-related vascular complications. Advances in spectral-domain and swept-source optical coherence tomography (OCT) have substantially improved understanding of the sequential stages of vitreous separation and their relationship to retinal pathology. OCT permits high-resolution visualization of the vitreoretinal interface and can identify partial PVD, persistent vitreomacular adhesion, shallow perifoveal detachment, and tractional macular abnormalities that may not be evident on routine biomicroscopy. These imaging advances have refined diagnostic classification systems and improved understanding of the natural history of vitreous separation. Wide-angle OCT montage imaging has further shown that vitreous separation is a decades-long process that may begin as early as the third decade of life, starting in the paramacular and peripheral retina rather than at the perifovea, and progressing to perifoveal, peripapillary, and finally complete separation with advancing age. Vitreoschisis, a split within the posterior vitreous cortex, is present at the initiation of PVD in more than 40% of otherwise healthy eyes, which explains why a layer of residual cortical vitreous may remain on the retinal surface even when the separation appears clinically complete. This residual cortex is the substrate for later epiretinal membrane formation and for the persistence of vitreoretinal traction after an apparently uncomplicated PVD. Extensive real-world datasets indicate that complications frequently occur in eyes exhibiting acute PVD, warranting thorough follow-up techniques. In a multicenter analysis of a retina-specialist database, roughly 25% of eyes experienced at least 1 complication (vitreous hemorrhage, retinal break, or retinal detachment) during the early clinical course, with a significant proportion of retinal breaks or detachments identified after the initial visit rather than at presentation. Complementary evidence from a comprehensive care setting indicates clinically significant rates of retinal tears and RRD in acute symptomatic presentations, with risk substantially influenced by patient history and examination characteristics, including vitreous pigment, vitreous hemorrhage, high myopia, lattice degeneration, and diminished presenting acuity. Partial PVD and persistent vitreomacular adhesion can lead to VMT, epiretinal membrane formation, and macular holes. In contrast, more complete separation may alleviate traction but may still result in symptomatic floaters due to collagen aggregation and vitreous opacities. These findings support guideline-based recommendations that prioritize immediate dilated examination and risk-adjusted re-examination over mere reassurance.