Posterior Vitreous Detachment (PVD)
Posterior vitreous detachment (PVD) is a separation of the posterior vitreous cortex from the internal limiting membrane of the retina, typically occurring between ages 45-65, resulting from age-related changes in vitreous macromolecular structure that cause liquefaction and alterations at the vitreoretinal interface. 1, 2
Pathophysiology
PVD occurs due to two primary processes:
- Vitreous liquefaction: Age-related breakdown of vitreous macromolecules creates liquid pockets within the gel-like vitreous
- Vitreoretinal dehiscence: Weakening of adhesions between the vitreous cortex and internal limiting membrane 3
When liquefaction exceeds the degree of vitreoretinal dehiscence, this creates an anomalous PVD (APVD), which can lead to various complications 3.
Clinical Presentation
Patients with PVD commonly present with:
- Floaters (myodesopias): Due to condensations of vitreous collagen, blood from torn vessels, or epipapillary glial tissue (Weiss ring)
- Light flashes (photopsias): Most noticeable in the dark, caused by vitreous traction on the retina
- Visual field defects: Particularly if complications develop
- Blurred vision: Especially if the macula becomes involved 2
Diagnosis
PVD is primarily diagnosed through:
- Slit-lamp biomicroscopy: Shows a prominent plane defining the posterior vitreous face
- Presence of a Weiss ring: Strong evidence of PVD
- Optical coherence tomography (OCT): Provides high-resolution imaging of the vitreoretinal interface
- Indirect ophthalmoscopy with scleral depression: Particularly important for examining the peripheral retina 1, 2
Risk Factors
Factors that increase risk of PVD and its complications include:
- Age: Peak incidence between 55-59 years
- Myopia: Low myopia increases risk fourfold
- Previous eye surgery
- Trauma
- Genetic disorders: Such as Stickler syndrome
- Family history of retinal detachments 2
Complications
PVD can lead to several sight-threatening complications:
- Retinal tears and breaks: Occur in 8-22% of patients with acute PVD symptoms
- Rhegmatogenous retinal detachment: Most common type, occurring in approximately 10-18 per 100,000 persons annually
- Vitreous hemorrhage: Due to tearing of retinal vessels
- Vitreomacular traction syndrome
- Macular holes 2, 3
Management
Management of PVD focuses on:
- Thorough examination: Complete dilated fundus examination with scleral depression to identify retinal breaks
- Risk assessment: Patients with acute PVD and no retinal breaks have approximately 2% chance of developing breaks in subsequent weeks
- Treatment of complications:
- Patient education: All patients should be instructed to report promptly if they experience:
- Increased floaters
- Loss of visual field
- Decrease in visual acuity 1
Follow-up
- Patients with uncomplicated PVD should return for examination within 6 weeks if new symptoms develop
- Patients with risk factors should return promptly if new symptoms develop 2
Important Clinical Pearls
- The presence of both flashes and floaters significantly increases the risk of retinal tears (20% of cases) compared to isolated flashes (5.3%) 4
- Patients reporting more than 10 floaters or a "cloud" in their vision have a particularly high risk of developing retinal tears 4
- The presence of vitreous or retinal hemorrhage is strongly associated with retinal tears (30% of cases) 4
- PVD begins in the perifoveal macula and may persist chronically, progressing slowly over months to years before complete vitreopapillary separation 5
- Complete PVD is less common in elderly patients than previously thought, with one study showing only 15-19% of elderly patients having complete PVD 6
Prevention
At present, there are no effective methods of preventing the factors that lead to PVD. Research into pharmacologic vitreolysis aims to chemically break down vitreous macromolecules and weaken vitreoretinal adhesion to safely detach the posterior vitreous cortex, potentially preventing complications if performed early in the disease process 1, 3.