Proliferative vitreoretinopathy (PVR) is the most common cause of failure in retinal detachment surgery.[1, 2, 3, 4, 5, 6, 7, 8, 9] It can occur in untreated eyes or occur after pneumatic retinopexy, cryotherapy, laser retinopexy, scleral buckling, or vitrectomy.[4, 7, 8] Because excessive retinopexy and operating on inflamed eyes can cause proliferative vitreoretinopathy, some cases should be considered iatrogenic. Epimacular membranes occurring after retinal detachment surgery can be thought of as limited proliferative vitreoretinopathy. Proliferative vitreoretinopathy can occur from glial or retinal pigment epithelium (RPE) proliferation.[1, 2, 3, 10, 11, 12, 13] PVR can also occur in diabetic traction retinal detachment cases if there are associated retinal breaks. Penetrating or blunt trauma may also result in proliferative vitreoretinopathy.
Also see the clinical guideline summary from the American Academy of Ophthalmology, Posterior vitreous detachment, retinal breaks, and lattice degeneration.
Proliferative vitreoretinopathy is a reparative process, similar to a keloid, initiated by full- or partial-thickness retinal breaks, retinopexy, and other types of retinal damage. Loss of contact inhibition causes the surrounding glial or RPE cells to migrate to one or both surfaces of the retina.[1] Although the cells exhibit modest mitotic activity, it is largely a hypocellular process. Glial or RPE cells migrate further and cover the posterior surface of the detached posterior hyaloid face.[9, 10, 13, 14] Fibronectin-lined coated pits serve as attachments of RPE or glial cells to collagen fibers and other components of the extracellular matrix. The migration/contraction mechanism causes tangential force on the retina via multiple star folds and fixed folds.[13, 15, 14] The collagen fibers of anterior and posterior vitreous cortex contract because of a similar hypocellular contraction process.
Of all retinal detachment surgery cases, 5-10% develop proliferative vitreoretinopathy.[8]
International
Worldwide incidence is the same as that in the United States.
Mortality/Morbidity
Proliferative vitreoretinopathy has no associated mortality. Morbidity is limited to blindness in the affected eye if not treated successfully. If several operations are required to repair proliferative vitreoretinopathy, poor vision may result even with a successfully attached retina.
Race
No known racial predilection exists for proliferative retinal detachment.
Sex
No known sexual predilection exists for proliferative retinal detachment.
Age
Although proliferative vitreoretinopathy can occur at all ages, some observers believe that proliferative tissue may develop more rapidly in children.
Retinal examination using binocular indirect ophthalmoscopy reveals the following:
Retinal detachment
Combination of star folds, fixed folds, subretinal proliferation, and vitreous contraction[16] - In some patients, the vitreous contraction component predominates, whereas in other patients, the periretinal proliferation is more apparent. Subretinal proliferation can be annular (napkin ring), placoid, or dendritic (bands, strands). Hypocellular vitreous contraction can involve circumferential fibers, radial pre-equatorial fibers, and contracted anterior and posterior vitreous cortex.[2, 3]
Retinal breaks directly or indirectly cause most cases of proliferative vitreoretinopathy. Direct causation is a result of the loss of contact inhibition of retinal glial cells and RPE cells. Proliferative vitreoretinopathy may also result from cryopexy, diathermy, and laser retinopexy, especially if excessive. Repeated retinal surgery increases the risk for development or worsening of proliferative vitreoretinopathy.
Gas and silicone may contribute to proliferative vitreoretinopathy by sequestrating RPE, inflammatory, and glial cells; fibronectin; various cytokines; and fibrin at the retinal surface.
Diagnostic ultrasonography is only necessary if opacities of the cornea, the anterior chamber, or the lens; pupillary membranes; retro–intraocular lens (IOL) membranes; or vitreous opacities prevent optical visualization of the retina.
Binocular indirect ophthalmoscopy is performed for diagnostic purposes. Contact lens examination can be used with slit lamp biomicroscopy for higher magnification and better resolution.
B-scan diagnostic ultrasonography is performed if the retina cannot be seen because of corneal disease, cataract, posterior capsular opacification, vitreitis, or vitreous hemorrhage.
Biopsy is never indicated, and histologic samples should not be obtained during surgery. Minimal mitotic activity with significant interaction between retinal pigment epithelium (RPE) and glial cells and extracellular matrix has been reported in pathologic specimens.[13, 17, 18]
Topical and subconjunctival or retrobulbar repository steroids should be used at the time of surgery for all patients who are not steroid glaucoma responders. Using topical and subconjunctival steroids may avoid the adverse effects associated with oral corticosteroids.
Intraocular steroids, 5-fluorouracil (5-FU), daunomycin, and low-dose radiation are not effective in this disorder.[19, 20, 21, 22]
The surgical objective is to enable retinal conformation to the retinal pigment epithelium (RPE). In cases of moderate star folds without static vitreous traction, scleral buckling without vitreous surgery is indicated. Minimal retinopexy to the breaks should be used to avoid both inflammation and further proliferation. To reduce the incidence of recurrent proliferative vitreoretinopathy (PVR) and inflammation, retreatment of the RPE and excessive retinopexy should be avoided. Post-reattachment retinopexy made possible by fluid-air exchange or liquid perfluorocarbon-assisted drainage of subretinal fluid helps reduce proliferation and overtreatment of the RPE, but it is applicable only to vitrectomy. Laser probably causes less proliferative vitreoretinopathy than cryotherapy, but it is impractical during scleral buckling surgery.[4, 5, 6, 7]
A broad, moderately high, encircling buckle with a smooth contour is an option for mild proliferative vitreoretinopathy, although the author of this article and an increasing number of surgeons use a vitrectomy- approach, preferably with a combined scleral buckle. If a buckle approach is chosen, the following is a simplified, effective approach to scleral buckling:
Scleral buckling is best achieved with a silicone exoplant and 2-3 mattress sutures per quadrant. The broad buckle extends back to the thicker, stronger, untreated retina and to the ora to prevent anterior leakage. Extrusion and infection rates are higher with sponges.
Posterior scleral bites should be single, long, and circumferential, and as posterior as possible without damaging the vortex veins.
The anterior bites should be parallel to the limbus and placed in the scleral condensations at the muscle ring, representing the external landmark of the ora and thickest sclera.
Because they tie without an assistant and do not slip, 5-0 monofilament nylon sutures are preferred to Mersilene. The ends must be cut flush with the knot to avoid protrusion through the conjunctiva.
To achieve reattachment and to create space for the large buckle, complete or near complete drainage of the subretinal fluid (SRF), preferably with the direct needle drainage method, is required.
Air, or preferably expandable gas injection, seals the retinal breaks via a surface tension effect and allows restoration of a pressure gradient and better drainage of the SRF.
Air (gas) injection causes lateral displacement of the retina. To avoid retinal incarceration in the drainage site, perform transscleral drainage of the SRF posteriorly, after injection.
Perform vitreous surgery[14, 23, 24] when it is anticipated that scleral buckling cannot sufficiently compensate for vitreous traction and periretinal membrane contraction to reattach the retina.[8, 24, 25, 26] Scleral buckling is not minimally invasive or sutureless and induces on average of 2.74 D of myopia, which is unacceptable to patients who have undergone Lasik or refractive cataract surgery. In addition, scleral buckling is associated with a significant incidence of strabismus, extruded/infected buckles, and conjunctival/Tenon capsule damage, which negatively affects subsequent glaucoma filtration surgery. Combining a scleral buckle with vitrectomy (ie, vit-buckle) is unnecessary for the same reasons and does not improve outcomes but is still in common use. Note the following:
The anterior and posterior vitreous cortices are usually in contact, resulting in a frontal plane configuration.[14, 23, 24]
First, remove the frontal plane component with the vitreous cutter, highest cutting rate, and minimal linear suction.
Resect the radial component (anterior loop traction) of anterior proliferative vitreoretinopathy with the suction cutter if sufficient distance exists between the anterior attachment at the pars plana and the posterior attachment of this former peripheral cortical vitreous to the retina at the equator. In rare instances, fine curved scissors (23G or preferably 25G) are required to resect this anterior loop component. The circumferential component can be removed with the 23/25G vitreous cutter or fine, curved scissors.[14, 23, 24]
Epiretinal membranes should be peeled using end-grasping forceps (preferably 25G or 27G Alcon DSP disposable forceps) for inside-out peeling of epiretinal membranes; picks, bent needles, microvitreoretinal (MVR) blades, and over/under or side-opening forceps probably cause more trauma to the retina and are not recommended.[14, 23, 24]
If the membrane is dense and well developed and highly adherent, it can be delaminated from the retinal surface using curved scissors with both scissor blades between the retina and the membrane.
Use segmentation and/or delamination with a fine curved scissors with blades parallel to the retina.
Segmentation of the epiretinal membrane in the center of a star fold and between each fold releases the tangential traction. The goal is to release sufficient tangential traction to allow retinal conformation to the RPE with minimal damage to the retina, rather than removing all membranes.[14, 23, 24]
If they are creating sufficient contour change in the retina to prevent reattachment, subretinal membranes can be segmented with scissors or removed with forceps. This can be accomplished through a preexisting retinal break, or closed forceps can be used to create a punch-thru retinotomy. Subretinal surgery does not require a large retinotomy, which creates unnecessary damage to the retina and exposure of the RPE.
Internal drainage of the SRF should precede fluid-air exchange to enable removal of all posterior SRF through preexisting peripheral retinal breaks.[14, 23, 24] Note the following:
Drainage retinotomy is often helpful.
Liquid perfluorocarbons can stabilize the retina during membrane peeling, as well as help remove all subretinal fluid, but are rarely needed in PVR cases.
Use of a soft-tip cannula placed through a convenient retinal break or a posterior drainage retinotomy and held near the RPE allows a feasibility test for intraoperative retinal attachment.
Appearance of subretinal air indicates the failure to release all tangential forces on the retina and the need for further segmentation, delamination, retinectomy, or scleral buckling. It may also indicate inoperability.
Retinectomy is as follows:
If internal drainage of the SRF and fluid-air exchange with continued internal drainage of the SRF results in subretinal air, incremental retinectomy with the vitreous cutter should be used to release tangential forces on the retina.
Retinectomy is indicated when the retina is incarcerated in a wound or previous drain site and when dense membranes are strongly adherent to broad areas of atrophic retina.
Perform air-gas exchange or air-silicone exchange after internal drainage of the SRF, fluid-air exchange, and laser endophotocoagulation.
Perform confluent moderate intensity endolaser around breaks.
Avoid excessive retinopexy and panretinal photocoagulation to reduce tissue damage and recurrence of proliferation.
Laser indirect ophthalmoscope is not necessary in vitreous surgery and may cause corneal damage and light scatter-mediated macular damage.
Gas or silicone oil surface tension management is required in all cases requiring vitrectomy.[14, 23, 24] Note the following:
Internal drainage of subretinal fluid should precede fluid-air exchange and continue as the exchange is completed.
Subsequent air-gas exchange allows creation of a complete fill of the vitreous space without hypotony or multiple small bubbles.
Using an 18% concentration of C3 F8 has been shown to produce better outcomes than a 25% concentration of SF6 because the bubble lasts longer (ie, 3 wk instead of 1 wk). Do not use concentrations greater than these because expansion causes an elevation of IOP with a total fill.
The gas mixture is injected through the infusion cannula.
Fluid egress is accomplished through a soft-tip cannula positioned through the retinal break, near the RPE, and managed by a foot-controlled linear (proportional) suction system.
Surface tension management with highly purified silicone oil (1000 centistokes)[27, 28, 29, 30, 31, 32] is preferable to gas for most advanced or recurrent proliferative vitreoretinopathy cases. Note the following:
If a posterior chamber lens is in place, it maintains the silicone posteriorly, avoiding corneal contact and subacute angle-closure glaucoma without an inferior peripheral iridectomy.
If the eye is phakic, use phacoemulsification and a posterior chamber lens because cataract formation universally follows intravitreal use of silicone oil.
Use an inferior iridectomy in all aphakic eyes to prevent silicone pupillary block.
Remove any capsule present with the end-opening forceps to avoid fibrosis at the iridectomy site.
If possible, avoid viscoelastics, blood, and inflammation, all of which may increase emulsification of silicone oil.
Patients who are aphakic and have silicone oil are instructed to avoid prolonged supine positioning to reduce subacute angle-closure glaucoma and corneal contact.
In most cases, silicone oil is not removed. Performing many procedures just to enable silicone removal is not indicated in older patients, especially if the patients is pseudophakic.
Silicone is used for rhegmatogenous confinement and facilitates stabilization of recurrent inferior and peripheral retinal detachments.[27, 28, 29, 30, 31, 32] Remove silicone only if all breaks are sealed by retinopexy.
The ultimate strength of retinopexy lesions is reached 7-10 days after application.
Gas and silicone bubbles float in aqueous humor; therefore, head positioning is crucial to developing adherence in the 10-day period after surgery.
C3 F8 has been shown to be more effective than SF6 in management of proliferative vitreoretinopathy. Apparently, it is because the bubble duration is typically 3 weeks with C3 F8, while it is only 1 week with SF6.
Bed rest is not required as long as proper head positioning can be achieved in the postoperative period.
Patients with inferior retinal breaks must be prone for 7-10 days after surgery using either silicone or gas.
Subconjunctival dexamethasone is indicated at the end of surgery, unless the patient is a steroid glaucoma responder. Topical difluprednate and prednisolone acetate are the topical drugs of choice and should be used at 3-4 times per day.
Clinical Context:
For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Clinical Context:
Used to suppress inflammation. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Clinical Context:
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Longer duration creates additional steroid glaucoma risk in patients who are steroid responders.
Have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.
All patients must be examined on the first postoperative day to determine if increased IOP, flat chamber, incorrect patient positioning, or endophthalmitis (a rare finding) is present. Most patients are then examined in 1-3 weeks.
Outpatient surgery for vitreoretinal surgery is the criterion standard. Concomitant medical conditions should determine the need for an inpatient approach.
Topical fourth-generation fluoroquinolones (Vigamox) are used 4 times/day for approximately 1 week after surgery. All patients receive subconjunctival cefazolin (vancomycin if allergic to penicillins) and subconjunctival ceftriaxone at the end of surgery. Systemic antibiotics are not indicated.
Topical cycloplegics, such as Cyclogyl 1%, are used 2-3 times/day for 2-3 weeks after surgery.
Subconjunctival steroids, such as Kenalog (triamcinolone acetonide), are used in all patients except those who are steroid responders. The author never uses systemic steroids in these patients.
Topical steroids are used in all patients who are not steroid responders. The drops are administered 4 times/day. Prednisolone acetate 1% is the preferred agent.
Recurrent proliferative vitreoretinopathy is the most common complication, occurring at a frequency of 25-50%.[8, 14, 23, 24]
Cataracts may occur from prolonged gas or silicone oil contact with the lens.
Uveitis may occur from excessive retinopexy, lengthy surgery, iris trauma, or retained lens material.
Intravitreal, anterior chamber, subretinal, or suprachoroidal hemorrhage may occur.
Glaucoma secondary to uveitis, excessive gas bubbles, pupillary block, silicone oil emulsification and surgical trauma to vortex veins or aqueous veins may occur. Steroid-associated glaucoma due to injected or topical steroids may also occur.
Ocular or periocular manifestations are as follows:
Retina - Epiretinal membranes, fixed folds, star folds, and subretinal placoid or dendritic proliferation
The anatomical success rate is dependent on the patient mix, the technique used, unknown patient factors, and the surgeon's skill. The success rate of anatomical reattachment ranges from 50%-90%.[14, 23, 24] The success rate decreases with an increasing number of surgical procedures performed on the eye.
The visual prognosis is dependent on location, duration and height of the detachment, media clarity, epimacular membranes, and other unknown factors.
Inform the patients about positioning, activity, visual prognosis, complications, medications, anesthesia risk factors, and anatomical and visual success rates.
Steve Charles, MD, Founder and CEO of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine
Disclosure: Received royalty and consulting fees for: Alcon Laboratories.
Specialty Editors
Simon K Law, MD, PharmD, Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Andrew A Dahl, MD, FACS, Assistant Professor of Surgery (Ophthalmology), New York College of Medicine (NYCOM); Director of Residency Ophthalmology Training, The Institute for Family Health and Mid-Hudson Family Practice Residency Program; Staff Ophthalmologist, Telluride Medical Center
Disclosure: Nothing to disclose.
Additional Contributors
Russell P Jayne, MD, Vitreoretinal Surgeon, The Retina Center at Las Vegas
Freeman KD, Gregor ZJ. Electrophysiological responses after vitrectomy and intraocular tamponade. Trans Ophthalmol Soc UK. 1985. 104:129.
Glaser BM. A new method of treating giant tears without patient rotation with the use of intraocular gas and silicone oil. Presented at: Annual Meeting of American Academy of Ophthalmology: Atlanta, GA; Oct 2 1985.
Scott JD. The treatment of massive vitreous retraction by the separation of preretinal membranes using liquid silicone. Mod Probl Ophthalmol. 1975. 15:285.
Wiedemann P, Sorgente N, Kirmani M. Daunorubicin of experimental MPP-effective doses in vitro and in vivo. Invest Ophthalmol Vis Sci. 1983. 24 (Suppl):241.