Signs and Symptoms
Posterior vitreous detachment (PVD) refers to the separation of the cortical vitreous from the internal limiting membrane (ILM) of the retina anywhere posterior to the vitreous base.1-14 It may be localized, partial or complete.3,5 Symptoms include the appearance of floating spots in the visual field, particularly noticeable against the bright blue sky or light colored surfaces such as reading words on a white page or looking at a white wall. The floating spots are the result of shadows cast by collagen fibrils suspended and drifting through the liquefied portions of the vitreous gel. The result is the characteristic entoptic phenomenon known as “floaters.” The phenomenon is often accentuated in environments having fluorescent illumination.7
In cases where floaters are the result of acute PVD with accompanying vitreous hemorrhage, the floating spots may be large or may be numerous. In the event the vitreous hemorrhage is on the visual axis, a reduction of acuity may be present.13,14 In cases where there is an incomplete detachment and retinal traction, the symptom of flashing lights (photopsia) may occur.7-9 PVD has no racial or gender predilection and is common, occurring in approximately 50% of patients over the age of 50, increasing to approximately 75% by age 65.8,11,12 There is an increased risk of PVD in aphakic or pseudophakic eyes, myopes and eyes with a history of trauma or intraocular inflammation.9,12 Women may be prone to PVD at a younger age secondary to reduced hyaluronic acid synthesis associated with decreasing postmenopausal estrogen levels.2,8,11
Biomicroscopic examination reveals an optically clear space filled with liquefied vitreous between the detached posterior hyaloid and the retina.1,5,10 The pathognomonic sign of a PVD is the presence of a clinically observable fibrous annulus of tissue (Weiss or Vogt ring) in the vicinity of the optic disc.9 This ring represents the remnants of the circular attachment of the posterior, primary cortical vitreous to the site encircling the nerve (Area of Martegiani).10 The presence of a Weiss ring does not indicate total separation of the posterior hyaloid membrane from the ILM, nor does its absence confirm that the posterior hyaloid membrane remains attached.4 While patients on anticoagulation therapy may have a larger incidence of vitreous hemorrhage following acute PVD, their risk for retinal tears and detachments does not seem to be any higher.13,14
In cases where the detachment is incomplete, traction is produced by tangential mechanical forces caused by focal condensations and shrinkage of the vitreous.15,16 This causes vitreomacular traction (VMT) syndrome.15,16 These patients may experience variable changes in visual acuity and metamorphopsia which has the potential to worsen as the tissue distorts.15,16
The vitreous is comprised of water, inorganic salts, ascorbic acid and two major macromolecules: collagen and glycosaminoglycans (GAGs), particularly hyaluronic acid.17-21 The vitreous “gel” is formed by a dilute meshwork of collagen fibrils that provides a scaffold-like structure that is supported by hyaluronic acid.17 Attachments of the vitreous to the retina occur in areas where the ILM is the thinnest, including the vitreous base, the margins of the optic disc, the back of the crystalline lens in contact with the hyloidocapsular ligament of Wieger, the foveola, along large retinal vessels and sites of abnormal vitreoretinal adhesion such as lattice margins or areas of chorioretinal scar formation.1,5,7 It was previously thought that the posterior vitreous collagen fibrils directly inserted into the ILM but recent findings suggest that an extracellular matrix composed of laminin, fibronectin and sulfated proteoglycans interface and act as a “molecular glue.”6,8 The balance of the posterior vitreous adherence is more diffuse.8
As aging occurs, progressive reorganization of the hyaluronic acid and collagen molecules induces two major vitreous changes: liquefaction and aggregation of collagen fibrils.11,21 Synchysis refers to liquefaction of the vitreous and is typically an aging process accelerated by myopia, inflammation, trauma, hereditary vitreoretinal syndromes such as Stickler’s and Marfan’s syndromes, retinal vascular diseases, aphakia and vitreous hemorrhage.1,11,19-23 Synchysis is the most common degenerative change in the vitreous and has been found to be present as early as four years of age. Liquefied vitreous may account for approximately 20% of the vitreous volume by ages 14-18.1,3 The degeneration continues steadily after age 40 with more than half of the vitreous body becoming liquid by the age of 80.2,11,18
The process of synchysis leaves pockets of liquefaction known as lacunae. Biomicroscopically, they are regions that develop centrally, devoid of collagen fibrils. These lacunae typically enlarge and coalesce over time.3,11,21,23,25 Syneresis refers to the process of vitreous collapse where collagen fibrils aggregate into macroscopic bundles of parallel fibrils.1,11,18,21,26
When both synchysis and syneresis are present, the collagen aggregates become suspended and mobile within the lacunae.21 They create moving penumbra which, when large enough, can be detected by the patient. The aggregates can also be observed clinically as freely moving dark particles in the vitreous that scatter with ocular movement.1,5,21
The process of PVD begins with synchysis of the vitreous and weakening of the vitreoretinal adhesions.18-23 Enlargement of formed lacunae cause the posterior vitreal cortical wall overlying the involved area to become thinned.19 As the vitreoretinal adhesions dissolve, discontinuities form within the posterior hyaloid (either via fissure evolution or via a microbreak in the thin cortical vitreous layer).27 This allows synchytic vitreous to enter the subhyaloid space, dissecting the posterior hyaloid from the ILM of the retina.1-5,10-21
PVD typically begins in a single superior perifoveal quadrant. The vitreoretinal ILM attachments at the fovea and optic nerve head often remain attached.28 Over time, as the perifoveal detachment enlarges, it completely surrounds the attachments at the fovea.28 Finally, detachment of the vitreous from the foveal region produces a funnel-shaped configuration with attachments at the optic disc and vitreous base.26-28 When the PVD releases from the optic nerve, the process is complete.28-30 A complete PVD occurs when the posterior cortical vitreous is detached from the entire retina, including its attachment to the optic nerve up to the posterior border of the vitreous base.31 Even healthy young eyes may begin to form incomplete or partial PVD beginning as early as the fourth decade of life.30 These cases may remain asymptomatic but progress slowly for years before becoming a complete PVD.30
An anomalous PVD results when synchysis occurs without sufficient detachment from the ILM. Here, gel liquefaction exceeds the degree of vitroretinal dehiscence (separation).18 This results in tractional effects at the interface.18 Those with genetic collagen disease, such Marfan’s, Ehlers-Danlos and Stickler’s syndromes have a higher incidence of anomalous PVD.11,18,32 The physics of anomalous PVD has the potential to generate forces which split the posterior vitreous cortex causing vitreoschisis.18 When this phenomenon occurs in the periphery, tractional forces increase the risk of retinal tears and detachments.16,18 When it occurs in or adjacent to the macula, it has the potential to induce wrinkling of the neurosensory retina referred to as macular pucker. The pathology is also known as cellophane maculopathy, epiretinal membrane, vitreoretinal interface maculopathy and VMT syndrome.16,18,33
Vitreoschisis may contribute to the process of macular hole formation and increase the risk diabetic macular edema.16,33 When vitreoschisis occurs in the region of the optic disc, vitreo-papillary traction may increase the risk of neovascularization of the disc.18 In susceptible patients, the process can increase the risk of proliferative vitreoretinopathy.18
Uchino et al. have proposed a grading system for age-related PVD:
Stage 1—incomplete perifoveal PVD in up to three quadrants
Stage 2—incomplete perifoveal PVD in all quadrants, with residual attachment to the fovea and optic disc
Stage 3—incomplete PVD over the posterior pole with residual attachment to the optic disc
Stage 4—complete PVD.30
The management for acute PVD is thorough examination of the posterior segment to rule out the presence of retinal holes, tears and detachments. The vitreous should be evaluated for “tobacco dust,” sometimes referred to as Schaffer’s sign (retinal pigment epithelial cells or red blood cells that are passed into the vitreous following a retinal tear) and hemorrhage.34-36 Dilated biomicroscopy (with and without a contact or non-contact fundus lens), three-mirror lens and binocular indirect ophthalmoscopy with and without scleral indentation should all be considered to examine for retinal breaks requiring immediate treatment.
Patients should be educated to the classic signs and symptoms of retinal detachment: repetitive flashing lights, sudden shower of additional new floating spots, cobwebs in the field of vision, visual acuity loss and missing visual field as if a curtain was blocking the view. Since patients initially diagnosed as having uncomplicated PVD have approximately a 3.4% chance of a retinal tear within the first six weeks following the event, they should be advised to limit their activity (no contact or competitive sports, no weight lifting, no jogging or running) over that period until they can be re-evaluated.7,11 Patients should be counseled that in most cases the symptoms disappear on their own. In the event symptoms remain and create a distracting annoyance, pars plana vitrectomy can be discussed as an option, although the procedure is not routinely recommended.37 Pharmacologic vitreolysis can be used for anomalous PVD leading to vitreomacular traction.
• The Weiss ring, which results from a PVD, may be complete (circular) or broken and often casts a shadow during indirect ophthalmoscopic examination.
• Patients with posterior vitreous detachment with vitreous pigment granules or hemorrhage are much more likely to have a retinal tear compared with those who have normal findings on qualitative vitreous examination.
• Patients should be educated about the potential long-term complications of the pars plana vitrectomy option for the removal of floaters (i.e., potential for cataractogenesis in phakic patients, potential for prolonged healing course, potential for macular edema).
• Patients who develop late-onset retinal breaks and/or detachment (following retinal examination) after acute PVD typically are patients who complained of increased symptoms following the acute PVD event. Patients not reporting increased symptoms despite having a PVD are unlikely to have late-onset retinal complications.
1. KhuKrana, AK. The Vitreous. In: KhuKrana, AK. Comprehensive Ophthalmology. Daryaganj, Delhi, India, New Age International 2007:243-248.
2. Sebag J. Development and aging of the vitreous. In: Sebag J. The vitreous: structure, function, and pathobiology. New York: Springer-Verlag; 1989:73-92.
3. Le Goff MM, Bishop PN. Adult vitreous structure and postnatal changes. Eye. 2008;22(10):1214–1222.
4. Snead MP, Snead DR, James S, Richards AJ. Clinicopathological changes at the vitreoretinal junction: posterior vitreous detachment. Eye (Lond). 2008;22(10):1257-62.
5. Johnson MW. Posterior vitreous detachment: evolution and complications of its early stages. Am J Ophthalmol. 2010;149(3):371-82.
6. Serpetopoulos CN, Korakitis RA. An optical explanation of the entoptic phenomenon of ‘clouds’ in posterior vitreous detachment. Ophthalmic Physiol Opt. 1998;18(5):446-51.
7. Hollands H, Johnson D, Brox AC, et al. Acute-onset floaters and flashes: is this patient at risk for retinal detachment? JAMA. 2009;302(20):2243-9.
8. Sharma S, Walker R, Brown GC, Cruess AF. The importance of qualitative vitreous examination in patients with acute posterior vitreous detachment. Arch Ophthalmol. 1999;117(3):343-6.
9. Margo CE, Harman LE. Posterior vitreous detachment. How to approach sudden-onset floaters and flashing lights. Postgrad Med. 2005;117(3):37-42.
10. Tiedeman J, Mittra R, Han D, et al. Vitreous and retinal detachments. In: Regillo C, Brown G, Flynn H. Vitreoretinal disease: the essentials. New York: Thieme; 1999: 65-86.
11. Majcher CE, Gurwood, A.S. The role of the vitreous in retinal disease. Review of Optometry Retinal Supplement 2012; 149(4): 6s-14s.
12. Smiddy WE, Michels RG, Glaser BM, deBustros S. Vitrectomy for macular traction caused by incomplete vitreous separation. Arch Ophthalmol. 1988;106(1)624-8.
13. El-Sanhouri AA, Foster RE, Petersen MR, et al. Retinal tears after posterior vitreous detachment and vitreous hemorrhage in patients on systemic anticoagulants. Eye (Lond). 2011;25(8):1016-9.
14. Witmer MT, Cohen SM. Oral anticoagulation and the risk of vitreous hemorrhage and retinal tears in eyes with acute posterior vitreous detachment. Retina. 2012 Oct 26. [Epub ahead of print]
15. Kampik A. Pathology of epiretinal membrane, idiopathic macular hole, and vitreomacular traction syndrome. Retina. 2012;32 Suppl 2:S194-8.
16. Wylegała E, Woyna-Orlewicz A, Piłat J, et al. Traction maculopathies–pathogenesis and diagnostics. Klin Oczna. 2006;108(10-12):457-63.
17. Schubert H, Kincaid M, Green R, et al. Anatomy and physiology. In: Regillo C, Brown G, Flynn H. Vitreoretinal disease: the essentials. New York, Thieme, 1999: 3-25.
18. Sebag J. Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease.Graefes Arch Clin Exp Ophthalmol. 2004;242(8):690–8.
19. Johnson MW. Posterior vitreous detachment: evolution and complications of its early stages. Am J Ophthalmol. 2010;149(3):371–382.
20. Skeie JM, Mahaian VB. Dissection of the human vitreous body elements for proteomic analysis. J Vis Exp. 2011:23(47)2455-64.
21. Sebag J. Age-related changes in human vitreous structure. Graefes Arch Clin Exp Ophthalmol. 1987;225(2):89-93.
22. Maumenee IH. Vitreoretinal degeneration as a sign of generalized connective tissue diseases. Am J Ophthalmol 1979;88(9):432– 49.
23. Sebag J. Pathology of the vitreous. In: Sebag J. The vitreous: structure, function, and pathobiology. New York, Springer-Verlag,1989: 97–147.
24. Bishop PN. Structural macromolecules and supramolecular organization of the vitreous gel. Prog Retin Eye Res. 2000;19(3):323-44.
25. Bishop PN, Holmes DF, Kadler KE, et al. Age-related changes on the surface of vitreous collagen fibrils. Invest Ophthalmol Vis Sci 2004;45(4):1041–1046.
26. Bos KJ, Holmes DF, Kadler KE, et al. Axial structure of the heterotypic collagen fibrils of vitreous humour and cartilage. J Mol Biol 2001;306(5):1011–22.
27. Smiddy WE, Michels RG, Greene WR. Morphology, pathology, and surgery for idiopathic macular disorders. Retina. 1990;10(1):288–96.
28. MacDonald HR, Johnson RN, Schatz H. Surgical results in the vitreomacular traction syndrome. Ophthalmology. 1994;101(1)1397–1403.
29. Gandorfer A, Rohleder M, Kampik A. Epiretinal pathology of vitreomacular traction syndrome. Br J Ophthalmol. 2002;86(8):902-9.
30. Uchino E, Uemura A, Ohba N. Initial stages of posterior vitreous detachment in healthy eyes of older persons evaluated byoptical coherence tomography. Arch Ophthalmol. 2001;119(10):1475-9.
31. Halfter W, Winzen U, Bishop PN, et al. Regulation of eye size by the retinal basement membrane and vitreous body. Invest Ophthalmol Vis Sci. 2006;47(8):3586-94.
32. Maumenee IH. Vitreoretinal degeneration as a sign of generalized connective tissue diseases. Am J Ophthalmol 1979;88:432– 49.
33. Bottós J, Elizalde J, Arevalo JF, et al. Vitreomacular traction syndrome. J Ophthalmic Vis Res. 2012;7(2):148-61.
34. Machemer R. Pathogenesis and classification of massive periretinal proliferation. Br J Ophthalmol. 1978;62(11):737-47.
35. Khan Utman SA, Mahomed I, Baig HM. A case of atypical idiopathic choroidal effusion syndrome. J Coll Physicians Surg Pak. 2012;22(6):406-8.
36. Gupta M, Prasad S. Acute posterior vitreous detachment. Br J Ophthalmol 2001;85(4):504.
37. Stoffelns BM, Vetter J, Keicher A, Mirshahi A. Pars plana vitrectomy for visually disturbing vitreous floaters in pseudophacic eyes. Klin Monbl Augenheilkd. 2011;228(4):293-7.