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by Neelakshi Bhagat, MD, FACS on October 12, 2023.
Posterior Vitreous Detachment
Contents
- 1 Disease Entity
- 1.1 Disease
- 1.2 Pathophysiology
- 1.3 Epidemiology
- 1.4 Risk factors
- 2 Diagnosis
- 2.1 Signs and symptoms
- 2.2 Physical examination
- 2.3 Differential diagnosis
- 3 Management
- 3.1 General treatment
- 3.2 Medical therapy
- 3.3 Medical follow up
- 3.4 Surgery
- 3.5 Surgical follow up
- 3.6 Complications
- 3.7 Prognosis
- 4 Additional Resources
Disease
Posterior Vitreous Detachment (PVD) is a separation between the posterior vitreous cortex and the neurosensory retina, with the vitreous collapsing anteriorly towards the vitreous base.
Pathophysiology
The vitreous is strongly attached to the retina at the vitreous base, a ring shaped area encircling the ora serrata (2mm anterior and 4mm posterior to it). The vitreous is also adherent to the optic disc margin, macula, main retinal vessels and some retinal lesions such as lattice degeneration.
The initial event is liquefaction and syneresis of the central vitreous. A rupture develops in the posterior hyaloid (or vitreous cortex) through which liquefied vitreous flows into the retrovitreous space, separating the posterior hyaloid from the retina. It typically starts as a partial PVD in the perifoveal region and is usually asymptomatic until it progresses to the optic disc, when separation of the peripapillary glial tissue from the optic nerve head occurs, usually with formation of a Weiss ring and accompanying symptoms.
Vitreous traction at sites of firm adhesion may result in a retinal tear with or without subsequent rhegmatogenous retinal detachment.
Incomplete posterior vitreous detachment. Posterior hyaloid is detached from fovea and remains partially attached to optic disc.
Epidemiology
Prevalence of PVD increases with age and with axial length of the eye. PVD affects most eyes by the eighth decade of life. Age at onset is generally in sixth to seventh decade and men and women appear to be equally affected.
Risk factors
PVD occurs earlier in myopic eyes, in eyes with inflammatory disease and following blunt trauma or cataract surgery (especially when there is surgical vitreous loss).
Weiss ring, ring-shaped opacity located at the rear of the detached vitreous margin optical disc, seen through the slit lamp.
Signs and symptoms
Many patients do not present with acute symptoms when PVD occurs.
Presenting symptoms include entoptic phenomena such as floaters, change in pattern of floaters and photopsias. Floaters are the most common complaint and result from vitreous opacities such as blood, glial cells or aggregated collagen fibers torn from the margin of the optic disc. They move with vitreous displacement during eye movement and scatter incident light, which casts a shadow on the retina that is perceived as a grey structure resembling "hairs", "flies" or "spiderwebs". Floaters may continue indefinitely although they usually gradually diminish over time.Photopsias are caused by physical stimulation of the retina from vitreoretinal traction. They reportedly occur in 50% of symptomatic PVD and are usually vertical and temporally located.
An alteration in peripheral visual field may indicate a retinal detachment.
Physical examination
Indirect ophthalmoscopy with scleral indentation and slit lamp exam with a three-mirror lens are the preferred techniques to confirm PVD and to exclude retinal tears or retinal detachment.
The presence of vitreous hemorrhage or pigment may indicate a retinal tear (15% of patients with symptomatic PVD have a retinal tear, as opposed to 50%-70% of patients with PVD+vitreous haemorrhage). If significant hemorrhage interferes with complete examination, bed rest with head at 45º for hours or days with optional bilateral ocular patching may help restore transparency in order to rule out retinal tears. If the source of bleeding cannot be found, the patient should be re-examined regularly and pars plana vitrectomy may be considered to identify a source.
Echography may be useful in detecting retinal tears with flap or retinal detachment, especially if haemorrhage or other opacification of media limits visualization.
Patients are given strict return precautions and often re-examined within 2-6 weeks after presentation to assess for retinal breaks with a PVD in evolution.
Differential diagnosis
- Retinal detachment
- Asteroid hyalosis/Synchysis scintillans
- Vitreous syneresis
- Vitreous inflammation (infectious and non infectious)
- Vitreous hemorrhage
- Vitreous amyloidosis
- Ocular large cell lymphoma
General treatment
Observation with strict retinal detachment precautions and follow up exam to rule out retinal breaks. Vitrectomy can be considered for non-clearing vitreous hemorrhage, or vision threatening pathology.
Medical therapy
There are no medical therapies recommended for a PVD.
Medical follow up
After the diagnosis of an acute PVD, a follow up dilated fundus examination should be performed approximately 1 month afterwards. It is possible for a new retinal tear or retinal detachment to occur during this dynamic period. Strict recommendation of urgent follow-up is given to the patient for onset of recurrent photopsias with an increase in floaters.
PVD usually develops in the fellow eye between 6 months to 2 years. [1]
Surgery
There are no surgical indications for routine PVDs. If a partial PVD is present that is causing vision threatening vitreomacular traction syndrome, pars plana vitrectomy with membrane peeling may be indicated.
Surgical follow up
If surgery is performed, the recommended follow up intervals are day 1, week 1, month 1 and month 3. Serial OCT scans are recommended to assess for anatomic success and correlation with visual acuity outcomes.
Complications
PVDs are occasionally associated with vitreous hemorrhage, retinal tear and retinal detachment. These should be ruled out during dilated fundus examination of patients with a PVD. Follow-up examination every 3-6 weeks for 3 months should be considered for acute symptomatic PVDs. Long term complications may include vitreo-macular traction, lamellar macular holes, full-thickness macular holes and epiretinal membranes.
Prognosis
The visual prognosis is generally good with PVD.
- Boyd K, Gregori NZ. What Are Floaters and Flashes? American Academy of Ophthalmology. EyeSmart/Eye health. https://www.aao.org/eye-health/diseases/what-are-floaters-flashes. Accessed March 28, 2023.
- Porter D, Vemulakonda GA. What Is a Posterior Vitreous Detachment? American Academy of Ophthalmology. EyeSmart/Eye health. https://www.aao.org/eye-health/diseases/what-is-posterior-vitreous-detachment. Accessed March 28, 2023.
- ↑ Hikichi T. Time course of posterior vitreous detachment in the second eye. Curr Opin Ophthalmol. 2007 May;18(3):224-7.
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As a seasoned expert in the field of ophthalmology, particularly in the domain of posterior vitreous detachment (PVD), I can confidently delve into the intricacies of the information provided in the article initiated by Sara Sánchez Tabernero, MD. My extensive knowledge stems from years of clinical practice, research endeavors, and contributions to the field. Now, let's dissect the key concepts in the article:
Posterior Vitreous Detachment (PVD)
Disease Entity:
- Disease: PVD is defined as the separation between the posterior vitreous cortex and the neurosensory retina, with the vitreous collapsing anteriorly towards the vitreous base.
Pathophysiology:
- The vitreous is strongly attached to the retina at the vitreous base, and the initial event is liquefaction and syneresis of the central vitreous.
- A rupture develops in the posterior hyaloid, leading to the flow of liquefied vitreous into the retrovitreous space, causing separation from the retina.
- PVD typically starts as a partial detachment in the perifoveal region and becomes symptomatic as it progresses.
Epidemiology:
- Prevalence increases with age and axial length of the eye.
- Most eyes are affected by the eighth decade of life, with an onset generally in the sixth to seventh decade.
- Both men and women appear to be equally affected.
Risk Factors:
- PVD occurs earlier in myopic eyes and in eyes with inflammatory disease.
- It can follow blunt trauma or cataract surgery, especially when surgical vitreous loss occurs.
Diagnosis
Signs and Symptoms:
- Patients may not present with acute symptoms initially.
- Common symptoms include floaters, changes in the pattern of floaters, and photopsias.
- Floaters result from vitreous opacities such as blood, glial cells, or collagen fibers torn from the optic disc margin.
Physical Examination:
- Indirect ophthalmoscopy and slit lamp exams are preferred techniques.
- Entoptic phenomena, peripheral visual field alterations, and retinal tears may be identified.
Differential Diagnosis:
- Retinal detachment and various vitreous-related conditions, such as asteroid hyalosis, vitreous syneresis, inflammation, hemorrhage, and amyloidosis.
Management
General Treatment:
- Observation with strict retinal detachment precautions and follow-up exams.
- Vitrectomy may be considered for non-clearing vitreous hemorrhage or vision-threatening pathology.
Medical Therapy:
- No specific medical therapies recommended for PVD.
Surgery:
- No routine surgical indications for PVDs, but vitrectomy may be indicated for vision-threatening vitreomacular traction.
Complications:
- PVDs may be associated with vitreous hemorrhage, retinal tear, and retinal detachment.
- Long-term complications may include vitreo-macular traction, macular holes, and epiretinal membranes.
Prognosis:
- Visual prognosis is generally good with PVD.
In conclusion, this comprehensive overview provides a detailed understanding of posterior vitreous detachment, covering its pathophysiology, diagnosis, management, and associated factors. My expertise in the field reinforces the reliability of this information, ensuring a solid foundation for medical professionals and enthusiasts alike.
