Chapter (1) terminology, diagnosis and classification of proliferative vitreoretinopathy definition

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Chapter (1)



Proliferative vitreoretinopathy (PVR) is a clinical condition characterized by proliferation and contraction of nonvascular cellular membranes on both retinal surfaces, vitreous base and vitreous gel after rhegmatogenous retinal detachment (Lewis, 1994).

This process is extremely important as these membranes exert tractionand may cause recurrent detachment by reopening otherwise successfully tretinal breaks, create new breaks, distort or obscure the macula and produce ocular hypotony (Lean, 2000).

The fact that recurrent retinal detachment following a primary repair procedure might be due to proliferation was first suspected by Taylor Smith who, in 1960, described the histology of preretinal membranes which he thought might be responsible for recurrent retinal detachment. At that time it was widely believed that it was vitreous itself which retracted and had led to term "massive vireous retraction" (MVR) (Smith 1960).

As the recognition of the importance of retinal surface membranes became accepted, the disease description was changed to "massive preretinal retraction" (MPR). However, the terminology "massive periretinal proliferation" (MPP) was suggested by Machemer, and it became widely used after he demonstrated the cellular basis of the condition and emphasized that both surface of the retina as well as the posterior vitreous surface were involved Laqua and Machemer, (1975).

In 1983, the Retina Society Terminology Committee (RSTC) proposed new terminology and a clinical classification. The suggested name proliferative vitreoretinopathy (PVR), was chosen to emphasize the proliferative nature of the process and to indicate that both the vitreous gel and the retina are involved (RSTC, 1983).


Rhegmatogenous retinal detachment occurs in 1 per 10000 persons annually. Treatment consists of reattaching the retina to prevent severe visual loss. Although surgical repair of the retina is usually successful PVR is the leading cause of failure of retinal reattachment (Michaelson and Stein, 1969).

PVR complicates approximately 5-10% of treated rhegmatogenous retinal detachment and typically occurs 6-8 weeks postoperatively (Rachal and Burton, 1979). PVR usually occurs after surgical repair, but can develop in some untreated detachments particularly those with large breakd and long standing cases. Quite rarely it occurs after massive choroidal detachments or in eyes with large, treated retinal tears but no previous retinal detachment (Ayelward, 1999).

Proliferative vitreoretinopathy is most strongly associated with the following risk factors; preoperative presence of PVR, uveitis, giant, large or multiple tears, RD greater than two quadrants, vitreous hemorrhage, aphakia (either true aphakia or pseudophakia with capsular dehiscence during cataract surgery as the posterior capsule has an important role in the blood-retinal barrier (BRB) irrespective of the presence of an intraocular lens "IOL"), choroidal detachment Girard et al., (1994); Kon et al., (2000), intraoperative vitreous hemorrhage, excessive cryotherapy, diathermy or photocoagulation, loss of vitreous during drainage of subretinal fluid, undetected breaks, use of air or sulfur hexafluoride (SF6) gas, repeated surgical procedures, and postoperative choroidal detachment or vitreous hemorrhage (Glaser et al., 1993; Kim and Arroyo, 2002).

Two additional situations that predispose to PVR and have not received sufficient emphasis in the literature: RRD or TRD produced after vitreous hemorrhage secondary to branch vein occlusion and RD in an eye with chronic and recurrent posterior uveitis. In a report on 136 cases of PVR that developed after a variety of vitreoretinal disease and surgery, nine (6.6%) were associated with these two conditions (Mietz and Heimann, 1995).

The following equation was suggested by by Asaria and Coworkers to predict the risk of developing PVR: risk of developing PVR= 2.88 x (grade C PVR) + 1.85 x (grade B PVR) + 2.92 x (aphakia) + 1.77 x (anterior uveitis)+ 1.23 x (quadrants of detachment) + 0.83 x(vitreous hemorrhage)+ 1.23 x (previous cryotherapy). If a risk factor is present, then 1 is added to the equation; if a risk factor is absent, then 0 is added to the equation. For quadrants detached, a figure of 1-4 should be added. If the risk factor score is greater than 6.33, then the patient is at high risk (Asaria et al., 2001 a).

Thus, despite successful treatment, PVR can recur due to the above mentioned risk factors exerting traction on the retina resulting in formation of new breaks, reopening the treated breaks, or directly detaching the retina. The tendency of PVR to recur has generated much interest in the use of pharmacological agents for adjuvant therapy to surgery (Ayelward, 2004).

Diagnosis and classification:

The clinical spectrum of proliferative vitreoretinopathy (PVR) varies according to the extent and location of membranes, and the presence and position of retinal breaks. Macular pucker after successful retinal detachment surgery can be considered a mild form of PVR. PVR most frequently develops in the inferior retina or is at least most severe in the inferior retina. In its most severe form, contraction produces a total funnel shaped detachment with retina adherent anteiorly to ciliary body and even to the iris, which can result in hypotony and perhaps phthisis bulbi (Ayelward, 1999).

Prodromal stage

The earliest sign of PVR include marked vitreous flare and clumps of pigment in the vitreous. Increased stiffness of the detached retina often occurs, which can be detected with indirect ophthalmoscopy while the patients eye is making saccades. A fresh retinal detachment without PVR appears to undulate under these conditions, an undulation that is reduced if significant surface membranes are present (Aylward, 1999).

Early stage

Retinal Shagreen :

Retinal shagreen is an appearance of the retina that resembles Moroccan leather or a somewhat shriveled orange skin that contains a partly dried fruit. The affected retina shows short retinal folds running at angles to one another. They never affect visible retinal vessels because they are located in the outer layers of the retina. Shagreen is always located posterior to the equator. Near the equator this appearance stops, sometimes abruptly, and anterior to it the detached retina is smooth and transparent. This transparency indicates that the retina is adherent to the vitreous. It is thought that shagreen is produced by small folds in the outer limiting lamina of the retina. They occur either because this layer is somewhat elastic and may retract when the retina detaches or because a thin, newly formed membrane has grown over the retinal surface and retracted (Schepens et al., 2000).

Fig.1-1. Proliferative vitreoretinopathy grade A. schematic drawing of pigmented clumps and Tyndall effect visible in vitreous with the slitlamp. The posterior vitreous surface appears condensed (Retina Society Terminology Committee, 1983).
Breaks with Rolled Edges

Breaks with rolled edges are generally signs of early PVR. When present, they often affect horseshoe-shaped tears located at the equator or slightly anterior to it. The vitreous is often extensively detached and partially collapsed. Vitreous cortex that remains attached to the break's posterior edge may be responsible for its rolled edge. Occasionally, there are several tears of this type in a row. A fixed equatorial retinal fold is often found on the anterior border of a row of such tears (Schepens et al., 2000).

Established stage

Circular Folds

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