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Posterior Vitreous Detachment: A Common Process with Potential for Ocular Morbidity

By Diana L. Shechtman, O.D., F.A.A.O. and Diane E. Calderon, O.D., F.A.A.O.

Release Date: November 2008
Expiration Date: November 30, 2011

Goal Statement:

Posterior vitreous detachment (PVD) is a frequent consequence of aging. Understanding the anatomical makeup and biochemical properties of the vitreous are critical in the diagnosis of PVD as well as associated vitreoretinal conditions.

Faculty/Editorial Board:

Diana L. Shechtman, O.D. and Diane E. Calderon, O.D.

Credit Statement:

This course is COPE approved for 1 hour of CE credit. COPE ID is 23658-PS. Please check your state licensing board to see if this approval counts toward your CE requirement for relicensure. There is a $30 fee to take this course.

Joint-Sponsorship Statement:

This continuing education course is joint-sponsored by the University of Alabama School of Optometry.

Disclosure Statement:

Dr. Shechtman is on the speakers’ bureau of VSP, MSS and Alcon.


POSTERIOR VITREOUS DETACHMENT (PVD) is a frequent consequence of aging. With age, the vitreous degenerates, leading to a PVD. A posterior vitreous detachment is described as a separation of the posterior cortex of the vitreous from the internal limiting membrane of the retina. Vitreopapillary separation is the most common location. (Figure 1)

fig1

This is described as an annular ring, known as a Weiss’ ring, attached to the posterior hyaloid and located anterior to the optic nerve. (Figure 2) This process is readily observed in the elderly population, affecting 65% of patients over the age of 65.1,2 Even though a PVD is usually detected in an older female both genders may be affected and it is believed that the process starts much earlier.3 Conditions, such as myopia, trauma, inherited vitreoretinal disease, surgery, and inflammation may accelerate the process.4 Floaters are the most common symptoms, described as “cobwebs, flies or hair-like-structures.” Flashes, or photopsias, may also be associated with an acute PVD. Flashes do not always specify the presence of a retinal break or retinal detachment. Flashes indicate traction upon the retina, resulting in stimulating of the photoreceptors.

fig2

Although we have recognized the vitreous as an important ocular structure for more than a century,5 we are only recently beginning to understand its pathogenic role in various vitreoretinal diseases. PVD is typically described as a benign process; however, the location of firm vitreo-retinal adhesions plays a critical role in various pathological vitreoretinal conditions.

There are a number of firm posterior vitreoretinal attachments, which include areas along retinal vessels, the vitreous base, macula and optic nerve. Depending on the site of firm vitreoretinal attachment, an incomplete PVD may lead to the development of a vitreous hemorrhage, retinal break (RB), rhegmatogenous retinal detachment (RRD), or vitreomacular traction syndrome (VMT). Understanding the anatomical makeup and biochemical properties of the vitreous are critical in the diagnosis of PVD as well as associated vitreoretinal conditions.

Vitreous Anatomy & Biochemistry

The vitreous is considered to be a transparent gel, primarily composed of water. A small but vital component of the vitreous consists of collagen and hyaluronic acid, which contributes to the “gel-like” consistency of the vitreous.6,7 Collagen is a structural protein, which is connected to hyaluronic acid.1 As we age, there is alteration between the hyaluronic-collagen complex, causing vitreous liquefaction and shrinkage. In addition, with age, the internal limiting membrane becomes thickened, causing a decrease in vitreoretinal adhesion throughout the fundus.7 This weakening further facilitates the migration of the liquid vitreous into the subhyaloid space. The vitreous volume displacement causes a forward collapsing of the vitreous and a complete separation of the vitreous cortex from the retina, a PVD. This entire process commonly runs a complete and benign course with no further complications.

During the PVD process, if vitreous liquefaction surpasses the extent of weakening of vitreoretinal adherence, tractional forces will ensue upon areas of firm attachments.7 Depending on the site of the firm vitreoretinal attachment, a number of pathological events can occur during the PVD process, invariably attributing to retinal disturbances, such as a vitreous hemorrhage, VMT or retinal break which potentially can lead to a RRD.4,7,8 (Table 1)

Table 1. Complications Associated with PVD

VR traction site Retinal condition
Retinal vasculature Retinal hemorrhage or VH
Avulse retinal vessel
Macula VMT
Periphery Retinal breaks
Retinal detachment

What Happens in the Vitreous?

Vitreous Hemorrhage (VH)
A VH is characterized by the presence of blood posterior to the crystalline lens and anterior to the internal limiting membrane. (Figure 3) Since the vitreous is an avascular structure, blood found within the vitreous must come from the superficial retinal vasculature. The main causes of a vitreous hemorrhage include superficial retinal neovascularization, trauma and a PVD (with or without associated retinal breaks). A firm vitreoretinal attachment is maintained along the retinal vessels. During the PVD process sufficient traction along a vessel can lead to a vessel tear, resulting in a vitreous hemorrhage.

fig3

A VH can present as a large, dense, diffusely disperse hemorrhage within the vitreous cavity or a localized hemorrhage without characteristic borders or as a single streak of blood. Vitreous hemorrhages tend to clot quickly while resolving slowly. Patients may present with a history of multiple floaters or smoky vision, typically described as a “red” haze. Decrease in visual acuity is dependent upon the density and location of the VH. Since the VH is situated in a gel within a cavity, it will shift with head movements. Thus, patients may experience intermittent visual obstruction with head movement.

PVD without retinal breaks account for less than 10% of VH cases.9,10 Although PVD may be associated with a VH in the absence of a retinal break, the presence of a vitreous hemorrhage is considered a risk factor for the presence of a coexisting retinal break.11 Vitreous hemorrhages are indicative of vitreoretinal traction and potential impending retinal break. Since many VHs settle inferiorly due to gravity, location of VH does not aid in detecting the possible site of an accompanying RB. In the presence of a VH, it is imperative to scrutinize the retina for any evidence of retinal breaks. In cases of dense VH, ultrasonography (B-scan) may aid in ascertaining the presence of retinal detachment, retinal tear, or any other associated etiologies. In the absence of a retinal break, VH should be followed until complete resolution has occurred.

What Happens in the Periphery?

Retinal Break (RB)
Retinal breaks commonly result from the vitreous pulling on the retina, causing a full-thickness retinal defect. This is common following the evolution of a partial PVD with associated continuous localized traction onto the retina. Up to 15% of all patients who present with acute symptomatic PVD have at least one retinal break.9,10,12 Since the strongest vitreoretinal attachment is at the vitreous base, most retinal breaks are located between the equator and the ora.12,13 There is a downward gravitational force exerted on the remaining attached vitreous base, causing a greater prevalence for superior retinal breaks. Vitreoretinal traction induced by a PVD increases the risk for a RRD. Ominous accompanying signs include symptomatic breaks, as well as the presence of vitreoretinal traction, a vitreal or preretinal hemorrhage, pigmented vitreal cells (Schaffer’s sign) and a large retinal cuff of fluid. It is not uncommon for patients to present with an asymptomatic retinal break, which is only discovered during a routine eye exam.

The most common types of retinal breaks include atrophic retinal holes, operculated retinal holes and flap tears. Pathogenesis of each is associated with distinct mechanisms, contributing to variable propensity toward the progression to a RRD. Since atrophic retinal holes are not typically associated with vitreoretinal traction, this entity will not be discussed in this article. A retinal break provides a passage for the vitreous into the retina, thus the potential for a RRD. Management depends on the type of RB, associated findings, and risk factors (Table 2). For example, myopia (>6.00D) and aphakia are considered risk factors for retinal breaks to progress to RRD.14,15

Table 2. Predisposing Risk Factors

  • High myope
  • History of previous RD
  • Trauma
  • Cataract surgery

Categorizing the type of retinal break, in addition to identifying associated signs and symptoms, is imperative. Not all retinal breaks progress to a RRD. Proper management relies on determining which RB may progress to RRD: in other words, which retinal breaks would benefit from prophylactic treatment.

Operculated Retinal Hole
An operculated retinal hole represents a round, red full-thickness retinal defect with an associated avulsed piece of retinal tissue in the vitreous cortex. Operculated retinal holes are thought to be a sudden occurrence rather than a progressive change and most often occur at the same time as a PVD and or associated with retinal tufts.16 Due to their close association with PVD, operculated retinal holes are found more commonly in older people.16 Operculated retinal holes are a result of increased focal vitreoretinal adhesion in the periphery, pulling a plug of retinal tissue onto the cortex of the vitreous. This avulsed retinal tissue (operculum) is often found directly overlying the retinal break, but can be found elsewhere depending on the direction of the force of the vitreous traction at the time of the separation. The operculum is noted to be smaller than its associated retinal break due to degeneration that has occurred over time from vascular insufficiency previously supplied by the underlying retinal layers. An operculum can be distinguished from a vitreous floater due to its disc-shaped appearance as compared to the spherical appearance of a vitreous floater.16 Operculated retinal holes may be symptomatic in the initial stages, but symptoms subside once the traction is released and the operculum is finally formed. Since they are not associated with continuous vitreoretinal traction, most are followed on an annual basis.

Retinal Flap Tear (Horseshoe tear)
A retinal flap tear, also known as a horseshoe tear, commonly occurs in association with an incomplete PVD. During the PVD process, traction at this site may lead to the development of a flap tear. The cardinal feature of a retinal flap tear in a “U” or “Horseshoe” shape, representing an incomplete full thickness retinal tear associated with partial vitreoretinal adherence. As the vitreous is displaced forward, the flap assumes a triangular shape, with the apex oriented toward the posterior pole and the attached base parallel with the peripheral retina. (Figure 4)

fig4

Horseshoe tears are the leading cause of rhegmatogenous retinal detachments (RRD). Even an asymptomatic horseshoe tear can result in RRD, making the timely diagnosis of this condition extremely important. Symptomatic retinal flap tears are prophylactically treated, creating retinal scars (chorioretinal adhesions) in order to seal down the detached retina.

Management of Retinal Breaks
The decision to refer for a treatment is anecdotal, depending on variable factors, such as the type of retinal break, risk factors, and accompanying symptoms and signs.17 Various studies have confirmed that symptoms are the single most likely predictor that a retinal break will progress to a RRD.18,19 A retinal consult is typically considered for acute symptomatic retinal breaks. An acute symptomatic PVD can co-exist with a longstanding retinal break. Clinical trials have not aided in determining whether these retinal breaks would benefit from prophylactic treatment.18 The presence of a retinal or vitreal hemorrhage, along with Schaffer’s sign can further help determine the acute nature of a retinal break.

Retinal break with accompanying subclinical retinal detachment (associated fluid cuff <2.00DD) should also be referred for a retinal consult. While fluid cuff surrounding a retinal break is an inauspicious sign, retinal pigment epithelial changes are considered a sign of chronicity and decrease the likelihood that the retinal break will progress to a RRD.

Most retinal holes only require a yearly dilated fundus exam. Asymptomatic retinal holes are routinely monitored. On the other hand, a symptomatic operculated hole with persistent vitreoretinal traction may benefit from a retinal consult, although most have not been reported to progress to a RRD.10

Retinal flap tears carry the highest risk for progression, but there is some controversy as to whether a non-symptomatic retinal flap tear should be treated.18 Only 5% of asymptomatic retinal breaks progress to RRD.20,21 At the site of a retinal flap tear, the retina is incompletely pulled away and vitreoretinal traction exerts tractional forces upon the edge of the tear. Since retinal tears have a predisposition to evolve to a RRD, one may consider that all flap tears, at the very least, deserve a retinal consult. This is especially true in the presence of other risk factors such as aphakia, myopia, or history of RD in the fellow eye.

What Happens in the Macula?

Vitreomacular Tractional Syndrome (VMT)
Vitreomacular traction is described an incomplete posterior vitreous detachment with continuous adherence as the macula.22-24 (Figure 5) This continuous vitreomacular adherence induces tractional forces upon the macula. VMT is commonly described as a taut posterior hyaloid in a “dumbbell” configuration. The clinical picture is variable with symptoms ranging from mild blurred vision and metamorphopsia to severe decrease in visual acuity and accompanying photopsias. The typical patient is older with no history of cataract surgery. The nature of the vitreomacular attachment has been associated with a number of maculopathies, including cystoid macular edema, macular hole formation and epiretinal membranes.24-26 The dynamic nature of the traction, strength of remaining attachment and extent of vitreoretinal separation may all contribute to the distinct type of associated maculopathy.27 The clinical course is unpredictable with a few cases remaining stable for years or associated with spontaneous posterior vitreous detachment. A spontaneous PVD is typically associated with alleviation of both the associated symptoms and maculopathies, but the occurrence is low.28 The classic course is one of progression associated with further deterioration. Thus, in many cases, pars plana vitrectomy is a necessity.28

fig5

Conclusion

Many PVDs result in a complete detachment from the retina without any further complication. Yet, depending on the site of firm vitreoretinal attachment, the PVD process may lead to the development of vitreoretinal traction resulting in a vitreous hemorrhage, retinal break, which may be associated with a retinal detachment, or vitreomacular traction syndrome (VMT). The vitreoretinal conditions reaffirm the importance of further evaluation of every patient presenting with an acute PVD. A dilated fundus exam should be performed in all patients who present with signs and/or symptoms of a PVD. Scleral depression should also be considered, in order to rule out the presences of a retinal break or retinal detachment. The vitreous should be carefully scrutinized for the presences of hemorrhages or pigment.

In the absence of any complications, patients should be followed-up on a one–two week basis (depending on risk factors and associated signs or symptoms), until complete detachment of the posterior vitreous is noted. This commonly occurs within six weeks and is typically associated with resolution of photopsias. Any changes or progression in signs or symptoms, warrants prompt re-examination. Accompany risk factors, signs and symptoms, in addition to a complete clinical evaluation can aid in the appropriate management of a patient presenting with a PVD.

References

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  2. Farve M, Goldmann H: Zur Genese der hinteren Glaskorperabhebung. Ophthalmologica 1956;132: 87-97.
  3. Uchino E, Uemura A, Ohba N. Initial Stages of PVD in healthy eyes of older person evaluated by OCT. Arch ophthalmol 2001;119: 1475-79.
  4. Hikichi T, Trempe CL. Relationship between floaters, light flashes, or both and complications of PVD. AJO 1994;117: 593-8.
  5. Hayreh SS. Jonas JB. PVD: Clinical correlations. Ophthalmologica 2004; 218: 333-343.
  6. Berdahl JP, Mruthyunjaya P. Vitreous Hemmorhage: Diagnosis and Treatment. American Academy of Ophthalmology. http://www.aao.org/publications/eyenet/200703/pearls.cfm. (Last accessed April 10, 2008).
  7. Seabag J. Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease. Graef Arch Clin Exp Ophthalmol 2004;242: 690-8.
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  9. Tasman WS. PVD and peripheral breaks. Tran Am Acad Ophthalmol & Otol 1967; 72: 217-23.
  10. American Academy of Ophthalmology, Preferred Practice Pattern. Posterior Vitreous Detachment, Retinal Breaks, and Lattice Degeneration. Preferred Practice Pattern Guideline 2003. http://www.aao.org/education/guidelines/ppp/pvd_new.cfm. (Last accesses April 10, 2008).
  11. Novak MA. Welch RB. Complications of acute symptomatic PVD. AJO 1984;97:308-14.
  12. Brodley WW. Risk of retinal tears in patients with vitreous floaters. AJO 1983: 96: 783-7.
  13. Jaffe NS. Complications of acute PVD. Arch Ophthal 1968; 79: 568-71.
  14. Austin KL. Palmer JR. Seddon JM, et al. Case-control study of idiopathic RD. Int J Epi 1990; 19: 1045-50.
  15. National guidelines clearinghouse. RD and related peripheral vitreoretinal diseases. http://www.guideline.gov/summary/ summary.aspx?ss=15&doc_id=1996&string=. (Last accessed April 14, 2008.)
  16. Jones W. Reidy RW. Atlas of peripheral ocular fundus. MA: Butterworth Publ 1985.
  17. Colyear BH. Pischel D. Preventive treatment of RD by means of light coagulation. Trans Pac Coast Oto-Ophthalmol Soc 1960; 41: 1934-217.
  18. Wilkinson CP. Evidence-based analysis of phrophylactic treatment of asymptomatic RD and LD. Ophthalmol 2000; 107: 12-18.
  19. Tanner V. Harle D, Tan J. Acute PVD: the predictive value of vitreous pigment & symptomology. BJO 2000;84: 1264-68.
  20. Neumann E, Hyams S. Conservative management of RB. BIO 1972; 56: 482-6.
  21. Byer NE. What happens to untreated asymptomatic RD, and are they affected by PVD? Ophthalmol 1008; 105: 1045-50.
  22. Reese AB, Jones IR, Cooper WC. VMT syndrome confirmed histologically. AJO 1970; 69:975-977.
  23. Jaffe. NS. Vitreous traction at the posterior pole of the fundus due to alterations in the vitreous posterior. Trans Am Acad Ophthalmol Otolaryngol 1967; 71: 642-52.
  24. Smiddy WE, Michels RG, Green WR. Morphology, pathology, and surgery of idiopathic vitreo-retinal macular disorders. Retina 1990; 10:288-296.
  25. Hotta K, Hotta J. Retinoschisis with macular retinal detachment associated with VMTS. Retina 2004; 24: 307-09.
  26. Gass JDM. Idiopathic senile macular hole: its early stages and pathogenesis. Arch Ophthalmol 1988; 106: 629-39.
  27. Johnson MW. Tractional CME: variant of VMT syndrome. AJO 2005; 140: 184-192.
  28. Smiddy WE, Michels RG, Glaser BM, et al. Vitrectomy for macular traction caused by incomplete vitreous separation. Arch Ophthalmol 1988;106: 624-628.

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