What is the cause and treatment of posterior vitreous detachment (PVD), especially in older adults (above 60 years) with a history of myopia or recent cataract surgery?

Posterior Vitreous Detachment: Causes and Treatment

What Causes Posterior Vitreous Detachment

Posterior vitreous detachment is caused by age-related vitreous syneresis (liquefaction) and weakening of vitreoretinal adhesions, leading to separation of the posterior vitreous cortex from the internal limiting membrane of the retina. 1

Primary Mechanisms

• Age-related degeneration is the fundamental cause, with vitreous collagen condensation and liquefaction occurring naturally as the vitreous gel structure breaks down 1, 2
• PVD typically occurs between ages 45-65 in the general population, with earlier onset in men than women 1
• The process represents the culmination of para-physiological age-related vitreous modifications 3

Accelerating Risk Factors

• Myopia causes earlier PVD onset due to increased axial length and altered vitreoretinal interface 1, 4
• Cataract surgery precipitates PVD in approximately 34% of cases, making it a significant iatrogenic trigger 1, 3
• Ocular trauma (both blunt and penetrating) can induce PVD at any age, with symptoms appearing immediately or up to 6 weeks post-injury 1, 5
• Other surgical procedures including Nd:YAG laser capsulotomy and intraocular injections can trigger vitreous separation 5

How to Treat Posterior Vitreous Detachment

Immediate Management: Rule Out Sight-Threatening Complications

All patients with new PVD symptoms require urgent examination by an ophthalmologist skilled in binocular indirect ophthalmoscopy with scleral depression, as 8-22% have retinal tears at initial presentation. 1, 6, 4

Essential Examination Components

• Measure visual acuity to establish baseline and detect subtle vision loss 6
• Examine vitreous for hemorrhage, pigmented cells (Shafer's sign), or detachment 6, 7
• Perform thorough peripheral fundus examination with scleral depression—this is mandatory as 15% of retinal tears are only visible with indentation and not on slit-lamp biomicroscopy alone 4
• Use B-scan ultrasonography when media opacity prevents direct visualization 1, 6

Treatment Algorithm Based on Findings

1. Uncomplicated PVD (No Retinal Breaks)

• Observation with reassurance is the appropriate management, as symptoms typically diminish over several months 1, 6
• Educate patients about warning signs: sudden increase in floaters, peripheral visual field loss, or decreased visual acuity requiring immediate return 1, 6
• Schedule follow-up within 6 weeks for patients with vitreous pigment, hemorrhage, or visible vitreoretinal traction, as 2-5% will develop retinal breaks during this period 1, 6, 7

2. Symptomatic Retinal Tears (Horseshoe or Flap Tears)

Treat immediately with laser photocoagulation or cryotherapy to create chorioretinal adhesion surrounding the tear, reducing retinal detachment risk from >50% to <5%. 1

• Extend treatment to the ora serrata if the tear cannot be completely surrounded 1
• The most common treatment failure is inadequate coverage of the anterior border where visualization is difficult 1
• At least half of untreated symptomatic horseshoe tears with persistent vitreoretinal traction will progress to retinal detachment 1

3. Asymptomatic Retinal Breaks

• Operculated holes and atrophic round holes rarely require treatment, as they have minimal progression risk without vitreoretinal traction 1
• Asymptomatic horseshoe tears have approximately 5% progression risk and may be observed with close follow-up, though treatment decisions must weigh individual risk factors 1
• Lattice degeneration with round holes and minimal subretinal fluid generally does not require prophylactic treatment 1

4. Dense Vitreous Hemorrhage Obscuring Retinal View

• Perform B-scan ultrasonography immediately to detect retinal tears (sensitivity 44-100%) 1
• Follow weekly until hemorrhage clears enough for complete peripheral examination 1
• Consider early vitrectomy (within 7 days) if retinal tear is suspected on ultrasound and view remains obscured, to reduce risk of macula-involving retinal detachment 1

Management of Persistent Symptomatic Floaters

For debilitating floaters persisting after several months that significantly impair quality of life, pars plana vitrectomy is the definitive treatment option. 1, 6

• Studies document significant reduction in contrast sensitivity function with PVD, validating the impact on quality of life 1
• Pars plana vitrectomy demonstrates greater patient satisfaction and documented improvement in contrast sensitivity compared to YAG laser vitreolysis 1, 6
• YAG vitreolysis provides only moderate symptom resolution but is less invasive 1, 6
• Pharmacologic agents (ocriplasmin) and pneumatic vitreolysis lack sufficient evidence for simple floaters and carry risks including retinal tear, retinal detachment, and macular hole formation 1

Critical Follow-Up Protocol

• All patients require re-examination within 6 weeks of PVD onset, as this is when new retinal breaks most commonly develop 1, 6, 7
• Approximately 80% of patients who develop delayed retinal breaks had pigmented cells, hemorrhage, or new symptoms prompting return 1, 7
• Between 5-14% of patients with an initial retinal break will develop additional breaks during long-term follow-up 1, 6
• Cataract surgery is a specific risk factor for developing new retinal breaks after initial PVD 1

Common Pitfalls to Avoid

• Never assume minimal floaters are benign—even 1-2 floaters with flashes can indicate retinal tears requiring treatment, as 29% of phakic eyes with retinal tears present with only this minimal symptomatology 8
• Do not rely solely on slit-lamp examination, as 15% of retinal tears are visible only with indentation indirect ophthalmoscopy 4
• Absence of Weiss ring does not exclude retinal tear—32% of eyes with retinal tears lack this finding 4
• Failing to examine the fellow eye misses 0.7% of asymptomatic retinal tears 4