Proliferative Vitreoretinopathy

Chapter 107 Proliferative Vitreoretinopathy



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Introduction


Proliferative vitreoretinopathy (PVR) is the clinical syndrome associated with retinal traction and detachment in which cells with proliferative potential multiply and contract on retinal surfaces and in the vitreous compartment.14 PVR presents with a spectrum of severity ranging from subtle retinal wrinkling, to fixed folds and tears with rolled edges and to total rigid retinal detachment, retinal shortening and advanced periretinal proliferation (Figs 107.1, 107.2). PVR is the most common cause of failure in retinal detachment surgery. It can occur in untreated eyes with retinal detachment, especially with vitreous hemorrhage, or after cryotherapy or even laser retinopexy, pneumatic retinopexy, scleral buckling or vitrectomy and after a variety of surgical complications. It is common after penetrating injuries and a variety of conditions associated with prolonged inflammation. Although surgical reattachment of retinas associated with PVR can now be achieved in most cases, visual results remain disappointing. Therefore, prevention through early recognition of risk factors and subtle signs of PVR and appropriate modification of standard surgical techniques for retinal detachment remain all-important. Some degree of PVR is found in up to 10% of retinal detachments.57 If PVR is progressive and macula reattachment delayed, then despite complex surgery, low vision is the result in the majority of eyes.





Pathophysiology


The pathophysiology of PVR is discussed in detail in Chapter 97, Pathogenesis of proliferative vitreoretinopathy.


PVR is characterized by proliferation of cells derived from retinal pigment epithelium, glia, or inflammatory recruitment on the retinal surfaces and within the vitreous gel.8,9 These metaplastic cells transdifferentiate and assume contractile properties through internal cellular contractile proteins and by laying down extracellular collagen.10 They multiply and grow along available scaffolding, either the retinal surfaces or elements of residual vitreous gel. Mass contraction leads to retinal wrinkles, folds, tears, and traction retinal detachment. The vitreous compartment is normally almost devoid of cellular content with just a few hyalocytes. It is protected from outside invasion by the internal limiting membrane of the retina and from cytokines and other chemoattractants by the blood–retinal barrier. The process of PVR can start when there is an interruption to the surface lining such as can occur with a posterior vitreous detachment and local preretinal membrane formation or retinal tears in the periphery. Retinal tears with surrounding detachment may encourage inflow of freed-up pigment epithelial cells through the break into the vitreous and onto the retinal surface or onto residual contracted vitreous strands and the vitreous base. Simultaneous breakdown of the blood–retinal barrier with retinal detachment or any cause of intraocular inflammation, including cryotherapy, laser and the trauma associated with scleral buckling, can all lead to the influx of circulating inflammatory cells and a whole range of proteins associated with inflammation.11 The process is more likely to be triggered in patients with posterior segment trauma, uveitis, choroidal detachment or severe diabetic retinopathy in the presence of retinal tears. The PVR process is self-propagating and can be considered an inappropriate excess wound-healing response. Cellular proliferation and contraction increases the breakdown of the blood–ocular barrier, in turn causing more traction and more influx of inflammatory cytokines and inflammatory cells. Macular pucker after retinal detachment repair can be considered a mild form of PVR. PVR most frequently develops in the inferior retinal quadrants, probably because the retinal pigment epithelial and inflammatory cells liberated into the vitreous cavity through retinal tears or those associated with vitreous hemorrhage, settle inferiorly with gravity.12 The PVR process usually takes 4–12 weeks to develop a critical mass of cells and significant retinal traction after retinal detachment surgery or other ocular interference such as trauma. As in normal wound healing, the proliferating cells go through a life cycle and as they progressively lay down collagen, the membranes become hypocellular leaving contracted collagen sheets, membranes, and cords in the vitreous cavity, or on the retinal surfaces and sometimes under the retina. Contraction of equatorial membranes may lead to a funnel-shaped retinal detachment while shortening of the inferior retina may lead to large, inoperable posterior retinal breaks. Severe PVR may also be superimposed on diabetic tractional retinal detachment when associated with retinal tears. PVR also may occur in other vascular retinopathies such as Eales disease in the presence of retinal breaks and especially in penetrating ocular trauma. The proliferative/inflammatory process underlying PVR complicating retinal detachment is typically associated with loss of central vision even after successful surgery and this may be due to inflammation-induced apoptosis of the receptor cells at the macula13 or degeneration of the receptors associated with prolonged retinal detachment.14 The cellular and biochemical processes underlying PVR are complex and are explored in detail in Chapter 97, Pathogenesis of proliferative vitreoretinopathy.



Risk factors for development of PVR


The most common clinical setting is the development of clinically significant PVR a few weeks after previous retinal detachment repair, whether by scleral buckling, primary vitrectomy, or both (Fig. 107.3). A few eyes develop PVR spontaneously with retinal detachment prior to surgery.6 Previous trauma, prolonged inflammation of the posterior segment, viral infections of the posterior segment and prolonged chorioretinitis are also associated with spontaneous PVR. The risks in the presence of retinal detachment are increased with large retinal breaks or giant tears, vitreous hemorrhage associated with retinal tears, multiple previous eye surgery, previous trauma to the posterior segment and pre-existing signs of localized PVR such as fixed folds.1517 The risk is increased in retinal detachments with more than two quadrants involved and those with coexisting choroidal detachment. The risk is also increased in retinal detachments associated with a variety of systemic conditions such as Wagner disease, Stickler syndrome, Marfan syndrome, and familial exudative vitreoretinopathy. A high rate of PVR is reported following a range of novel complex surgical procedures, including macular translocation, retinal prosthesis implantation and endoresection of ocular tumors. Surgical problems that increase the risk of PVR include vitreous and subretinal bleeding, choroidal detachment,18 failure to close retinal breaks resulting in prolonged retinal detachment, incarceration of retina in an external subretinal fluid drainage site, and heavy or excessive cryotherapy.1921 Seeding of pigment epithelial cells onto the retinal surface at the time of drainage of subretinal fluid through an internal retinotomy or retinal break may increase the risk. Prolonged inflammation after retinal detachment surgery increases the risk of PVR, especially if associated with postoperative uveitis, residual intraocular blood or failure to remove all traction off the retina and failure to support it with a scleral buckle. The greatest risk period is 4–12 weeks after detachment surgery. A patient with any of the above predisposing risk factors, either preoperatively, or as a result of surgery should be followed more frequently in the postoperative period to ensure early detection of PVR and recurrence of retinal detachment.




Clinical signs and diagnosis of PVR


The early signs of PVR are subtle and include cellular dispersion in the vitreous and on the retinal surface and localized fibrocellular membranes, which appear as a white opacification of the retinal surface and small wrinkles or fixed folds (Figs 107.4, 107.5). Cellular proliferation at the edge of a retinal tear can lead to local contraction and a rolled posterior edge (Fig. 107.6). More extensive PVR has fixed folds with retinal detachment especially inferiorly and fine membranes bridging the valleys between folds, as well as decreased mobility of the detached retina. Advanced PVR with posterior vitreous detachment results in the eventual formation of a funnel-shaped detachment with a contracted equatorial membrane (Figs 107.1, 107.2). In some cases, anterior traction at the vitreous base draws retina forward towards the ciliary body or detaches the ora serrata (Fig. 107.7). Diagnosis of established PVR in the presence of rhegmatogenous retinal detachment is made by indirect ophthalmoscopy and slit-lamp biomicroscopy with a +78 or +90 diopter lens or corneal contact lens. In eyes with opaque media, B-scan ultrasonography outlines immobile retinal folds of detachment and prominent vitreous membranes (Fig. 107.8). Early and subtle signs of PVR should always be looked for and noted in the preoperative assessment of retinal detachment as it may result in modification of the choice of surgical techniques outlined below during primary repair. Early recognition of signs of impending PVR following reattachment of a retina in the 1–3-month period following surgery, allows more timely intervention. In many cases of early PVR, timely intervention can avoid the substantial visual loss that almost invariably occurs with macula detachment in patients with delayed diagnosis and reoperation.








Classification of PVR


There is benefit in classifying and recording the extent of PVR in all eyes with retinal detachment. This active process prompts a thorough search for the signs in all patients before surgery and in the postoperative period. It allows cross-comparison of severity of disease in any clinical series that may be audited or published and is the basis for assessing the effect of various therapies through clinical trials. The most commonly used classification system remains that published by the Retina Society Terminology Committee in 1983.3 It classifies the appearance of PVR on the basis of clinical signs and geographic distribution into four grades (Table 107.1). A major drawback is that it ignores antero-posterior epiretinal proliferation and hence the importance of anterior traction in PVR. It is also a static classification that says nothing about the degree of cellular proliferative activity at the time of the grading. An inactive Grade D PVR affecting all quadrants may have a better prognosis with surgery than a very cellular, active, proliferating PVR affecting only two or three quadrants as in Grade C. The revised classification of PVR of 1991,4 took into account more detailed information about the location, extent and severity of PVR in an individual eye and hence is more useful especially for clinical trials (Tables 107.2, 107.3). Further modifications of the classification of PVR were proposed as part of the multicenter controlled trial of silicone oil (SO) as an adjunct treatment for PVR,22 but the added complexity was found to be less reproducible between different examiners than the more simplified classifications. Nevertheless, the description of PVR and accompanying preoperative retinal drawing should always be sufficiently detailed to allow any eye to be graded for clinical research and auditing of results of surgery.


Table 107.1 Retina Society PVR Classification (1983)




































Grade (stage) Characteristics
A Vitreous haze, vitreous pigment clumps
B Wrinkling of the inner retinal surface, rolled edge of retinal break, retinal stiffness, vessel tortuosity
C Full-thickness retinal folds in
 C-1  One quadrant
 C-2  Two quadrants
 C-3  Three quadrants
D Fixed retinal folds in four quadrants
 D-1  Wide funnel shape
 D-2  Narrow funnel shape (anterior end of funnel visible by indirect ophthalmoscopy with 20 diopter lens)
 D-3  Closed funnel (optic nerve not visible)

(Reprinted from: Retina Society Terminology Committee. The classification of retinal detachment with proliferative vitreoretinopathy. Ophthalmology 1983;90:121–5. ©1983, with permission from the American Academy of Ophthalmology.)


Table 107.2 Updated Proliferative Vitreoretinopathy Grade Classification (1991)


















Grade Features
A Vitreous haze, vitreous pigment clumps, pigment clusters on inferior retina
B Wrinkling of the inner retinal surface, retinal stiffness, vessel tortuosity, rolled and irregular edge of retinal break, decreased mobility of vitreous
CP 1–12 Posterior to equator, focal, diffuse or circumferential full-thickness folds, *subretinal strands
CA 1–12 Anterior to equator, focal, diffuse, or circumferential full-thickness folds, *subretinal strands, *anterior displacement, *condensed vitreous strands

* Expressed in the total number of clock-hours involved. (Reproduced with permission from Machemer R, Aaberg TM, Freeman HM, et al. Am J Ophthalmol 1991;112:159–65.)


Table 107.3 Updated Proliferative Vitreoretinopathy Contraction Type Classification (1991)



























Type Location (in relation to equator) Features
Focal Posterior Star fold posterior to vitreous base
Diffuse Posterior Confluent star folds posterior to vitreous base; optic disc may not be visible
Subretinal Posterior/anterior Proliferation under the retina; annular strand near disc; linear strands; motheaten-appearing sheets
Circumferential Anterior Contraction along posterior edge of vitreous base with central displacement of the retina; peripheral retina stretched; posterior retina in radial folds
Anterior Anterior Vitreous base pulled anteriorly by proliferative tissue; peripheral retinal trough; displacement ciliary processes may be stretched, may be covered by membrane; iris may be retracted

(Reproduced with permission from Machemer R, Aaberg TM, Freeman HM, et al. Am J Ophthalmol 1991;112:159–65.)



Prevention of PVR


Prevention of PVR relies mainly on an understanding of which eyes with or without retinal detachment are at greater risk of development of PVR, and a recognition of the early signs of the condition. Increased awareness allows the surgeon to modify the treatment plan and in most cases, prevent this devastating complication. Eyes with large or multiple retinal breaks or giant tears are more likely to develop PVR as mobilized pigment epithelial cells spill into the vitreous and onto the retinal surface in increased numbers. Likewise, eyes with previous or current penetrating trauma with or without retinal detachment may present with increased cellular content in the vitreous and an enhanced inflammatory response. Eyes with chronic retinal detachment, choroidal detachment, uveitis, viral retinitis, and chorioretinitis associated with detachment, all have an increased risk of PVR, particularly if associated with a retinal break. Retinal detachment following cataract surgery with retained lens fragments in the vitreous or following multiple anterior segment surgeries where there may be an enhanced inflammatory response, are at higher risk of PVR. Most eyes with PVR however, have undergone a repair of rhegmatogenous retinal detachment in the last 1–3 months and many of these eyes may have developed PVR regardless of the technique used for initial repair. Intraoperative complications including choroidal hemorrhage, retained vitreous hemorrhage and intense photocoagulation or especially heavy cryotherapy increase the risks. Laser probably causes less breakdown of the blood–retinal barrier than cryopexy and mobilizes less pigment epithelial cells because of the size of each application and the fact that it is only applied to attached retina. Any eyes with the more subtle early stages of PVR including pigment particles in the vitreous, localized fixed folds, retinal breaks with rolled edges, visible vitreous membranes, detached segment of the pars plana ciliaris and ora serrata, and decreased mobility of retinal detachment folds on eye movement during examination usually require vitrectomy to decrease the chance of progression to the full syndrome. The signs of early PVR may indicate the need for combined vitrectomy and scleral buckling rather than one or the other and also vitreous substitution with long-acting gas or SO.



Surgery for PVR


There has been substantial improvement in the success rate of surgery for PVR progressively over the past four decades.23,24 The clinical severity of PVR is very variable and therefore the extent of surgery is planned accordingly. PVR varies from a single inactive fixed star fold on the retinal surface to a rigid total retinal detachment with a funnel shape and dense equatorial fixed membranes. There may be fixed folds involving only the posterior retina or fibrotic organization of the vitreous base with both circumferential and anterior loop traction dragging the retina forward or detaching the pars plana ciliaris. Fixed folds may tent the retina and be relatively easily divided or peeled to relieve traction, or there may be extensive surface retinal fibrosis and consequent shortening of the retina in the anterior/posterior plane requiring a relaxing retinotomy. The severity of PVR may also differ markedly in terms of current inflammation and cellular proliferative activity or take the form of fixed, quiescent acellular membranes which are unlikely to recur if divided or peeled. These factors may affect the timing of repeat vitreoretinal surgery. It is urgent if the macula is still attached or salvageable. It may sometimes be better to wait a few days and quiet the eye down with corticosteroids if the macular vision is not salvageable until the inflammatory activity is less intense. On the other hand, leaving an eye with a retinal detachment and early PVR almost always will lead to further progression and eventual inoperability, so that most eyes deemed to be operable should be operated on as soon as possible. The objects of vitreoretinal surgery for PVR are to permanently support the retina from any ongoing traction and to close any open retinal breaks. These goals are achieved by an encircling scleral buckle, meticulous relief of all retinal traction with vitrectomy and temporary or long-term tamponade of the retina with long-acting gas or SO. These steps must be achieved without causing prolonged ocular inflammation or further cellular access to the retinal surface, or else recurrence is frequent.




Vitrectomy and PVR


A comprehensive vitrectomy is essential in the management of PVR. Some surgeons rely on a meticulous vitrectomy and SO tamponade without scleral buckling and report comparable results with a combined proceedure.25 In any event, almost all eyes with retinal detachment and PVR also require a vitrectomy to remove all vitreous gel, cellular and inflammatory material, blood, and fibroblastic membranes. It is necessary to relieve all traction by division and peeling or delamination of fixed membranes and to remove as much as possible of the vitreous base. It is also important to divide any membranes causing anterior loop traction and to release the tractional effect on scarred shortened retina. This surgery is greatly facilitated by the extraordinary advances in the technology now available. Wide-angle viewing systems are either indirect and attached to the operating microscope, or consist of an operating corneal contact lens and a microscope image inverter. Contact lenses provide a crisper image and easier visual access to the far inferior periphery but need frequent repositioning and replenishing with viscoelastic. Indirect viewing systems provide a less panoramic view and the view is dependent on precise eye positioning, making angulation more difficult. Wide-field illumination is achieved with a range of fiberoptic light sources or a chandelier arrangement inserted into the eye through a separate pars plana entry site. Vitreous cutting and suction probes (vitrectors) have vastly improved and the surgeon has a choice of 25G, 23G, and the traditional 20G instruments. Air-driven vitrectors can cycle at up to 5000 cycles per minute and have a variable duty cycle controlled by electronic sensors. This allows faster removal of core vitreous and opacities, but also safer cutting and aspiration close to the retinal surface. Another major advance has been the intraoperative use of heavier-than-water perfluorocarbon fluid which displaces subretinal fluid anteriorly and flattens the bullous posterior retina. This highlights tractional membranes and facilitates peeling and dissection by stabilizing the posterior retina. Sometimes relaxing retinotomy is required to fully relieve traction caused by densely adherent fixed folds or shortened fibrosed retina. Rarely subretinal membranes need to be removed or divided through a small deliberate retinotomy. Internal drainage of subretinal fluid and fluid–air exchange of the vitreous compartment allows the testing of release of all retinal traction. Any persistent retinal elevation after fluid–air exchange means that complete release of traction or retinal shortening has not been achieved. Reattached retina and open retinal breaks are sealed with endolaser photocoagulation or cryotherapy and a decision made as to whether temporary tamponade with perfluoropropane (C3F8) gas will be sufficient or SO–air exchange is necessary. Although a controlled trial showed the eventual outcomes to be similar, many surgeons prefer SO to gas because it results in less postoperative inflammation, quicker rehabilitation and fewer reoperations. The use of heavier-than-water SO can also improve inferior retinal tamponade in severe cases of PVR, and is being increasingly used.



Surgical steps for established PVR


Modern surgery for PVR is greatly facilitated by a wide-angle microscopic viewing system, and a fully integrated, electronically controlled, surgical system. Vastly improved fluidics and a range of inbuilt modalities improve the efficiency, duration and predictability of vitreoretinal surgery. High-speed 23G or 25G cutters able to trim vitreous and membranes off the retinal surface at up to 5000 cuts/minute have greatly improved the ability to remove residual vitreous and membranes particularly around the vitreous base, while avoiding retinal incarceration with the cutter and the creation of iatrogenic retinal breaks (Video 7, available online). Illuminated picks or chandelier endoillumination allow bimanual dissection of intraocular tissue. Endodiathermy probes and small extrusion/suction needles allow the creation of a controlled microretinotomy for endodrainage of subretinal fluid. Flexible endolaser probes facilitate 360° peripheral laser photocoagulation and treatment of any retinal breaks. Laser is superior to cryotherapy in this situation, as it can seal flattened retinal breaks and allow 360° photocoagulation with less postoperative inflammation, and stimulation of repeat cellular proliferation. An integrated fluid–air exchange pump with self-monitoring of intraocular pressure facilitates fluid–air exchange and formal checking that the retina is totally mobilized and retinal breaks are completely flat. Difficult visualization still makes cryotherapy necessary in some cases. Soft silicone-tipped fluid extrusion needles (23G or 25G) facilitate complete drainage of subretinal fluid through a retinal break or intentional posterior retinotomy. The introduction of 23G and 25G vitreous forceps and scissors have improved the ability to peel, delaminate and relieve retinal traction in a controlled manner. An integrated pump for the delivery of SO to the vitreous and fluorinated heavy silicone to tamponade the inferior, flattened retina, are important additions. The use of these tools in a stepwise logical manner means that up to 90% of eyes with advanced PVR may be successfully reattached. Advances in instrumentation for phacoemulsification of the lens have also resulted in a shift by many surgeons from posterior lensectomy to formal anterior lens extraction and insertion of an intraocular lens. Planned extracapsular lens removal still enables surgery at the vitreous base, while retaining a barrier to the anterior segment for SO or gas. Eyes left aphakic after pars plana phacofragmentation that are filled with SO risk corneal endothelial damage and secondary glaucoma from emulsified SO bubbles in the anterior chamber or pupil block.


imageVIDEO 7




Operative technique


The surgery should begin with a well-prepared preoperative plan, which can be modified often during the operation, depending on the findings. Preoperative retinal and biomicroscopic diagrams aid this process by ensuring that all aspects of the pathological findings are, in fact, examined and taken into account. The conjunctiva is opened by limbal peritomy unless an encircling 360° buckle exists already or is not planned. Any preoperative scar tissue is gently dissected under and around the rectus muscles, which are looped with 4/0 black silk traction sutures. A 360° scleral band is then placed and sutured in position with permanent scleral sutures such as 5/0 polyester. The choice of scleral buckle width depends upon the extent of vitreous base contraction and size of any peripheral retinal tears. It may vary from a broad 7.0 mm, Style 277 or 276 encircling tire and 40 band through a solid encircling 5.0 mm wide scleral band down to a 2.5 mm wide style 240 encircling band. The trend is towards narrower bands to permanently support the vitreous base and any small peripheral retinal tears. Larger, more posterior tears can be supported by an extra meridional explant placed under the tear at the end of the operation, but in most cases after complete relief of traction, they are closed by an internal tamponade and sealed permanently with laser. The scleral sutures are placed at two-thirds scleral thickness, at least 1 mm anterior and posterior to the encircling buckle, one or sometimes two in each quadrant. The sutures are not tied and the buckle not tightened until the end of the procedure and after vitrectomy. If only an encircling band is employed, some surgeons prefer to anchor it with sclera “belt loops”. If an adequate encircling scleral buckle is already present from previous surgery then the above steps may be omitted and surgery proceeds with transconjunctival insertion of three 23G or 25G entry cannulas. Some surgeons still prefer a 20-gauge system, which requires intraoperative sutured ports. The three entry ports are placed in the inferotemporal, superotemporal, and superonasal quadrants with an angled entry to diminish the risk of leakage of air or fluid from the entry site postoperatively. The first port is placed near the horizontal in the inferotemporal quadrant so as not to impede rotation of the eye downwards during surgery to remove inferior vitreous base. The second and third ports are for the fiberoptic probe and vitrector or other instruments such as endodiathermy, endolaser, vitreous scissors, vitreous forceps, and extrusion needle. If a chandelier is to be used, it is inserted through a fourth port. The entry cannulas are placed 3.5 mm from the limbus above the midline almost opposite each other, again to facilitate superior and inferior rotation of the globe for peripheral visualization during surgery. Care must be taken to check that the pars plana ciliaris is not detached and that the indwelling ports have passed into the vitreous to avoid subretinal or suprachoroidal infusion during vitrectomy. At this point, a decision is made as to the adequacy of visualization of the retina, especially the periphery and vitreous base by switching microscopic illumination to an indirect, noncontact wide-angle viewing system, or by placement of a wide-angle corneal contact lens. If the pupil is small or the iris stuck down to the lens capsule, the anterior chamber is entered and aqueous replaced with viscoelastic sodium hyaluronate. Synechiae may be broken down by this injection and the pupil dilated, or else it is mechanically dilated using soft disposable iris hooks placed through clear cornea in each quadrant.




Core vitrectomy and removal of the vitreous base


During vitrectomy, the cornea is kept clear by a viscoelastic coating of methyl cellulose and the wide-angle view contact lens if used. The microscope is refocused for internal viewing and after insertion of a fiberoptic light probe and the vitrector. The three available probe sizes are all acceptable. The 25G has the smallest opening and is the safest. It is also the slowest. Because it is more flexible it can be difficult to rotate the eye superiorly enough to comfortably remove vitreous off a superior retinal break with a mobile detached retina. The 20G probe has the largest opening and most efficient fluidics but needs suturing. The 23G probe is the most popular compromise. Most eyes with established PVR already have a posterior vitreous detachment. Any remaining central gel is removed completely and then peripheral vitreous is removed meticulously and as completely as possible, particularly inferiorly where pigment and inflammatory cells tend to gravitate. This process is facilitated by the modern, high-speed, vitrectomy cutters with the port close to the tip. With these cutters, it is possible to shave the attached vitreous off the surface, without engaging the retina. A bimanual technique with an illuminated probe or pic held in the second hand can also be helpful in protecting the retina. Removal of the inferior vitreous base is also facilitated by having an assistant indent with a scleral depressor, squint hook, or cotton-tipped stick (Fig. 107.9). Formed vitreous attached to the peripheral retina is also very difficult to remove if the retina is detached and mobile, in which case it can be stabilized at this stage by partly filling the vitreous compartment with heavy fluorocarbon liquid (Fig. 107.10) (Video 7, available online). This has the dual effect of flattening the retina by displacing subretinal fluid anteriorly and breaking down invisible microscopic retinal bridges of scar tissue. In cases where vitreous remains attached to the retinal surface posteriorly as well as at the vitreous base, the process of removal may be facilitated by an intravitreal injection of triamcinolone. The white suspension sticks to vitreous membranes and residual vitreous gel, making them both more visible (Video 7, available online).2729


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Mar 21, 2017 | Posted by in OPHTHALMOLOGY | Comments Off on Proliferative Vitreoretinopathy
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