What is posterior vitreous degeneration (PVD)?

Posterior Vitreous Detachment (PVD)

Posterior vitreous detachment (PVD) is a separation of the posterior vitreous cortex from the internal limiting membrane of the retina, which typically occurs between ages 45-65 as part of the normal aging process. 1, 2

Definition and Pathophysiology

PVD occurs when the vitreous humor, a gel-like substance filling the eye, undergoes age-related changes:

• The vitreous undergoes liquefaction (synchysis) where liquid pockets form within the gel network 3
• Concurrent weakening of vitreoretinal adhesion occurs at the interface between the vitreous and retina
• When liquefaction exceeds the degree of vitreoretinal dehiscence, it results in anomalous PVD (APVD) 4

The separation can be:

• Complete (C-PVD) - full separation from the retina
• Partial (P-PVD) - incomplete separation with areas of persistent adhesion 5

Clinical Presentation

Patients with PVD commonly present with:

• Light flashes (photopsias) - most noticeable in dark environments, caused by vitreous traction on the retina
• Floaters (myodesopias) - may be due to:
  • Blood from torn retinal vessels
  • Condensations of vitreous collagen
  • Epipapillary glial tissue (Weiss ring) torn from the optic nerve head 1, 2

Diagnosis

PVD is primarily diagnosed through:

• Slit-lamp biomicroscopy - shows a prominent plane defining the posterior vitreous face
• Presence of a Weiss ring (glial annulus in the vitreous cavity) - strong evidence of PVD
• Optical coherence tomography (OCT) - provides high-resolution imaging of the vitreoretinal interface, allowing for detailed classification of PVD types 1, 5

Complications

PVD can lead to several complications:

• Retinal tears and breaks - 8-22% of patients with acute PVD symptoms have retinal tears at initial examination
• Rhegmatogenous retinal detachment (RRD) - most serious complication
• Vitreous hemorrhage - from torn retinal vessels
• Vitreomacular traction syndrome (VMT) - when partial vitreous separation causes mechanical distortion of the macula
• Macular holes - especially with small vitreofoveolar adhesions (≤500 μm) 1, 2, 6

Risk Factors

Factors that increase risk or accelerate PVD development:

• Age - peak incidence between 55-59 years
• Myopia - earlier onset, with low myopia (1-3 diopters) having fourfold risk
• Previous eye surgery - particularly cataract surgery
• Trauma
• Genetic disorders (e.g., Stickler syndrome) 1, 2

Management

For uncomplicated PVD:

• Patient education about symptoms of retinal tears/detachment
• Follow-up examination within 6 weeks if new symptoms develop

For PVD with retinal breaks:

• Prophylactic treatment of symptomatic retinal breaks to prevent retinal detachment
• Treatment of peripheral horseshoe tears should extend to the ora serrata 1

Important Clinical Considerations

• Patients with acute PVD symptoms but no retinal breaks initially have a 2-5% chance of developing breaks in subsequent weeks
• 5-14% of patients with an initial retinal break will develop additional breaks during long-term follow-up
• Cataract surgery is a risk factor for new retinal breaks
• The most common cause of treatment failure is inadequate treatment, particularly along the anterior border where visualization is more difficult 1

Evolution of PVD

Recent studies have shown that:

• PVD begins in the perifoveal macula
• Early PVD stages can persist chronically and progress slowly over months to years
• The size and strength of residual vitreoretinal adhesion determines the type of macular pathology that may develop 6

Understanding the natural progression and potential complications of PVD is essential for appropriate management and prevention of vision-threatening sequelae.