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Ординатура / Офтальмология / Английские материалы / Retinal and Vitreoretinal Diseases and Surgery_Boyd, Cortez, Sabates_2010

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Surgical Management of ProliferativeVitreoretinopathy

563

Prevention

Although PVR cannot completely be prevented today, ophthalmic surgeons can take several steps to decrease the likelihood of its development.

Judicious Use of Cryotherapy

We as surgeons can judiciously use cryoretinopexy during repair of rhegmatogenous retinal detachment (Figure 3). The more cryotherapy used, the more likely is a breakdown of the blood ocular barrier as well as the dispersion of the retinal pigment epithelial cells into the vitreous cavity. Once these cells have entered the vitreous cavity, they are likely to proliferate and contract. Any treatment that minimizes the dispersion of retinal pigment epithelial cells into the vitreous cavity is likely to decrease the development of PVR. If cryotherapy is the selected treatment, only the minimum amount needed should be used, and the base of the retinal break should not be treated. Only the area surrounding the retinal break should be treated. This reduces the likelihood that pigment epithelium will migrate into the vitreous cavity.

Role of Laser Treatment

It is recommended that the surgeon minimize the breakdown of the blood ocular barrier. Some surgeons believe that laser

Figure 3: Judicious Use of Cryotherapy - Overall View. This internal/external conceptual illustration shows a cross section and corresponding surgeon’s view of the final configuration of proper cryotherapy to a retinal break (T). Only the minimum amount of cryotherapy needed should be used. Only the area surrounding the retinal break should be treated, and the base of the break should not be treated. This reduces the likelihood that pigment epithelial cells will migrate into the vitreous cavity. View through ophthalmoscope (O). Cryoprobe (C). Portion of sclera (S) removed to reveal internal configuration. (Art from Jaypee - Highlights Medical Publishers).

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treatment will create a chorioretinal adhesion decreasing the likelihood of breakdown of the blood ocular barrier. In order for the laser to take effect, the retinal break must already be closed. If subretinal fluid remains, it is more common to use initial cryotherapy.

Management of PVR

The current management of PVR primarily involves surgical remedy. Currently retinal detachments may be repaired using any of several techniques, including laser retinopexy, pneumatic retinopexy, encircling or segmental scleral buckling, or pars plana vitrectomy (PPV).

Laser retinopexy is a valuable technique that can be considered for limited detachments when there is no noticeable visual field loss. Benefits of laser retinopexy include patient convenience, no need for systemic anesthesia, and limited cost. Laser retinopexy may be effective treatment for retinal detachments with only grade A PVR, but is less likely to be successful when grade B or more PVR is present.

Pneumatic retinopexy likewise has the advantages of being an in-office procedure with less anesthesia-related morbidity. It can be utilized in patients with larger detachments but it is dependent on patient positioning and cooperation. Similarly, pneumatic retinopexy may be useful with detachments associated with grade A PVR, but it is less effective in the setting of grades B and C PVR.

Scleral buckling is frequently utilized when treating PVR detachments. Scleral buckles relieve both anterior-posterior traction and circumferential traction. This acts as an opposing force against which proliferative membranes must pull to redetach the retina. In the setting of PVR, encircling bands that support the entire vitreous base are more useful than segmental elements and are frequently used in conjunction with PPV. With milder degrees of grade C PVR, such as PVR limited to 1 quadrant, scleral buckling alone may be a viable option.8 This was similarly shown by Yao et al., who achieved high rates of anatomic success using scleral buckling alone in chronic detachments with PVR.9

Pars plana vitrectomy with or without scleral buckling remains the mainstay of surgical repair when PVR is present. One major advantage of vitrectomy over other surgical modalities is that it allows for removal of the inciting proliferative nidus. During surgical repair, vitreous cells can be removed, which may prevent these cells from progressing to further stages of PVR. Another obvious advantage of PPV over other treatment modalities is that PPV allows direct access to the proliferating membranes, which can be peeled during surgery. One disadvantage of PPV over other treatment modalities is that it may increase permeability of the blood retina/aqueous barrier more than other techniques.

Surgical Techniques

The goal of PVR detachment surgery is similar to traditional retinal detachment

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surgery: treat all tears and relieve all traction. Several surgical techniques may enable more permanent anatomic success. After performing a core vitrectomy and meticulous peripheral dissectionwith360°ofscleraldepression,attention is directed to the proliferative membranes. Intravitrealtriamcinoloneacetonidesuspension may highlight these membranes.10,11

The main surgical goals in managing PVR include closing the retinal breaks, sealing the retinal breaks, and completely releasing all periretinal traction. The technique used should minimize iatrogenic ocular complications and the recurrence of traction and achieve long-term stabilization of the attached retina. Mild cases of PVR should be treated with scleral buckling alone. Severe cases, however, require vitreoretinal surgery in addition to scleral buckling. The timing of surgery is controversial.

Although waiting for the periretinal membranes to mature makes the surgery technically easier, waiting has not been determined to improve the anatomic success rate. Since delaying surgery is likely to be associated with a worse visual result because the retina has been detached for a long period of time, earlier surgical intervention is indicated in cases of severe PVR. In these cases it is better to remove posterior membranes before anterior membranes whenever possible, stripping from the posterior pole toward the periphery in order to avoid disinserting peripheral retina. After membrane stripping is performed, perfluorocarbon liquid (PFCL) can be used to flatten the retina and to help identify areas of residual traction.

Surgery begins in the same way in all cases but changes depending upon whether the surgeon uses perfluorocarbon liquids. Initially, the surgeon places a scleral buckle. If the patient already has a scleral buckle, the scleral buckle is rarely revised. Then the pupil is managed with sutures, iris hooks or an expander pupil ring, which are only required if the pupil is small, miotic, or if the fundus cannot be well visualized anteriorly at the vitreous base. At this stage the lens must be managed. It is removed when it is opacified or when an anterior component is present even when the lens is clear. The posterior and anterior vitreous is removed with the help of scleral depression. If perfluorocarbon liquids are not used, anterior membrane dissection is followed by posterior epiretinal membrane dissection.Any subretinal membranes that exert significant traction and prevent the retina from re-attaching must be dissected (Figure 4).

Many surgeons believe that in cases of severe PVR, meticulous vitreous base dissection, removal of membranes, and, when necessary, a retinectomy are critical. Quiram et al reported functional and anatomic outcomes in patients with recurrent rhegmatogenous retinal detachments secondary to PVR.12 In their series, patients who underwent radical anterior vitreous base dissection and lensectomy and patients who underwent inferior retinectomy had the highest success rates. Similarly, Tseng et al evaluated the utility of relaxing retinectomies in PVR detachments. They found that retinectomies were most useful when used in conjunction with silicone oil tamponade but added little additional benefit when combined with gas tamponade.13

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Figure 4: Surgical Treatment of PVR - Stage 2. Perfluorocarbon liquid (L) is injected. This will reveal any persistent traction from epiretinal membranes (P) which must be removed. A vitreoretinal pic or Grieshaber mini-diamond forceps (F) is used to remove such a membrane (P). Note subretinal membrane (S). Endoilluminator (E) and infusion terminal (I). (Art from Jaypee - Highlights Medical Publishers).

An important surgical factor that may determine the likelihood of success is the type of tamponade. The Silicone Study compared silicone oil with either sulfur hexafluoride (SF6), or perfluoropropane (C3F8) in eyes with severe PVR.14-16 The Silicone Study suggested that silicone oil was more effective than SF6 but approximately equivalent to C3F8 in cases of severe PVR. Conversely, Quiram et al

noted that patients who received silicone oil had better attachment rates than did patients who received gas tamponade.

If the use of silicone oil is planned, an inferior iridectomy is made prior to performing a fluid/air exchange. The vitreous base is again inspected with additional anterior dissection if required. Endophotocoagulation

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is used to treat preexisting and iatrogenic retinal breaks (Figure 5). The procedure is concluded with placement of an intraocular tamponade, either perfluoropropane gas or silicone oil.

One major drawback of conventional tamponades, ie, SF6, C3F8, and silicone oil, is that they have limited exposure to the inferior retina over time. Because gravity causes most of the proliferative mediatiators

to settle in the inferior retina, PVR is most common inferiorly. Ability to more effectively tamponade the inferior retina may prevent these recurrences. Recently some investigators have sought to more adequately tamponade the inferior retina using agents that are heavier than water. Berker et al used a heavy silicone oil, Oxane HD (Bausch & Lomb, Rochester, NY), and they found that doing so increased their anatomic success with an acceptable complication profile.17

Figure 5: Surgical Treatment of PVR - Endophotocoagulation of Retinal Breaks. Endophotocoagulation is used to treat pre-existing and iatrogenic retinal breaks in eyes with PVR. The edges of the tear are treated (L) with the endolaser probe (X). Endoilluminator (E). Infusion terminal (I). (Art from Jaypee - Highlights Medical Publishers).

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Posterior PVR

When all anterior traction has been released, the posterior retina is mobilized by dissecting the posterior membranes currently with endodrainage of subretinal fluid. The posterior epiretinal dissection is very important in order to release the posterior traction and allow the posterior retina not only to reattach intraoperatively but also to remain re-attached after the intraocular tamponade is either reabsorbed or removed from the eye.

According to Hilel Lewis, he prefers to use a bimanual technique with small-tip diamond forceps in one hand and a bent light pick in the other hand. Membrane dissection is started posteriorly at the optic nerve head, and epiretinal membranes are also engaged in the center of the star folds and gently stripped anteriorly. If the epiretinal membranes cannot be removed with a small-tip diamond forceps, he may use a bent myringotomy blade to engage the fine epiretinal.

Equatorial epiretinal membranes are frequently difficult to visualize. In cases in which equatorial traction is still present, perfluorocarbon liquids may identify residual epiretinal membranes that can be removed. Perfluorocarbon liquids should not be injected over a retinal break that is still under traction since the perfluorocarbon is likely to migrate into the subretinal space. However, if the traction has been released, it is possible to carefully and slowly inject the perfluorocarbon liquid over the retinal break, thereby stabilizing the

posterior retina and allowing for dissection of the anterior membranes.

Reoperations

Finally, reoperations after proliferative vitreoretinopathy repair are common. The most common indications for additional surgery include corneal opacification, cataract formation, recurrent retinal detachment with or without PVR, macular pucker, and silicone oil removal. One indication that is becoming more frequent is the development of hypotony despite retinal reattachment. Some patients after PVR surgery have total retinal reattachment or reattachment posterior to the scleral buckle but have very low intraocular pressures. If they are not treated, these eyes frequently progress to atrophia bulbi with shrinkage despite retinal reattachment. One of the causes of this hypotony is epiciliary proliferation. One of the causes of epiciliary proliferation is a massive output of fibrin, which is then deposited over the ciliary body. Cells are deposited on a scaffold made of fibrin matrix, and they contract and cause dysfunction of the ciliary body epithelium. In those cases the epiciliary proliferative membrane is dissected. If it is done earlier or soon after surgery, the intraocular pressure may increase and prevent atrophia bulbi. Surgery is not really designed to improve visual function because these patients already have an attached retina, but to decrease the likelihood of developing a blind and painful eye.

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During the last several years the ophthalmic industry has produced some tremendous technological advances in vitreoretinal surgery. Surgical instruments have become smaller, enhancing patient postoperative comfort and enabling transconjunctival sutureless surgery. PVR continues, however, to hamper successful retinal detachment surgery. To improve our success rates after retinal detachment, we must find ways to limit the production and proliferation of PVR, either through pharmacologic means or enhanced surgical techniques.

References

1.Spirn M, Regillo C.Proliferative vitreoretinopathy. Retinal Physician. 1-2008.

2.Lewis H. Proliferative vitreoretinopathy. In: retinal and Vitreoretinal Surgery. Highlights of Ophthalmology. 2002;459-484.

3.Bonnet M. Clinical findings associated with the development of postoperative PVR in primary rhegmatogenous retinal detachment. In: Heimann K, Wiedemann P, eds, Proliferative Vitreoretinopathy. Heidelberg, Germany: Kaden-Verlag; 1989:8-20.

4.Aguirrebeña A, Saornil MA, Giraldo A, Pastor JC. Incidencia de la vitreoretinopatía proliferante (VRP) en el desprendimiento de retina regmatógeno, Arch Soc Esp Oftalmol. 1986;51:229-234.

5.Bonnet M. Clinical factors predisposing to massive proliferative vitreoretinopathy in rhegmatogenous retinal detachment. Ophthalmologica. 1984;188:148152.

6.Cowley M, Conway BP, Campochiaro PA, et al. Clinicalriskfactorsforproliferativevitreoretinopathy. Arch Ophthalmol. 1989;107:1147-1151.

7.Schwartz D, de la Cruz ZC, Green WR, Michels RG. Proliferative vitreoretinopathy. Ultrastructural study of 20 retroretinal membranes removed by vitreous surgery. Retina. 1988;8:275-281.

8.Pastor JC. Proliferative vitreoretinopathy: an overview. Surv Ophthalmol. 1998;43:3-18.

9.Yao Y, Jiang L, Wang ZJ, Zhang MN. Scleral buckling procedures for longstanding or chronic rhegmatogenous retinal detachment with subretinal proliferation. Ophthalmology. 2006;113:821-825.

10.Coll GE, Chang S, Sun J, Wieland MR, Berrocal MH. Perfluorocarbon liquid in the management of retinal detachment with proliferative vitreoretinopathy. Ophthalmology. 1995;102:630-6 38; discussion 638-639.

11.Coll GE, Chang S, Sun J, Wieland MR, Berrocal MH. Perfluorocarbon liquid in the management of retinal detachment with proliferative vitreoretinopathy. Ophthalmology. 1995;102:630-6 38; discussion 638-639.

12.Quiram PA, Gonzales CR, Hu W, et al. Outcomes of vitrectomy with inferior retinectomy in patients with recurrent rhegmatogenous retinal detachments and proliferative vitreoretinopathy. Ophthalmology. 2006;113:2041-2047.

13.Tseng JJ, Barile GR, Schiff WM, Akar Y, Vidne-Hay O, Chang S. Influence of relaxing retinotomy on surgical outcomes in proliferative vitreoretinopathy. Am J Ophthalmol. 2005;140:628-636.

14.Silicone Study Group. Silicone Study report no. 1. Vitrectomy with silicone oil or sulphur hexafluoride gas in eyes with severe proliferative vitreoretinopathy: results of a randomized clinical trial. Arch Ophthalmol. 1992;110:779-779.

15.Silicone Study Group. Silicone Study report no. 2. Vitrectomy with silicone oil or sulphur hexafluoride gas in eyes with severe proliferative vitreoretinopathy: results of a randomized clinical trial. Arch Ophthalmol. 1992;110:780-791.

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16.Silicone Study Group. Silicone Study report no. 3. Vitrectomy with silicone oil or perfluoropropane gas in eyes with severe proliferative vitreoretinopathy: results of a randomized clinical trial. Retina. 1993;13:278-284.

17.Berker N, Batman C, Ozdamar Y, Eranil S, Aslan O, Zilelioglu O. Long-term outcomes of heavy silicone oil tamponade for complicated retinal detachment. Eur J Ophthalmol. 2007;17:797-803.

35

Vitreoretinal Surgery

for Epiretinal Membranes

Javier A. Montero, MD, PhD.,

Jose M. Ruiz-Moreno, MD, PhD.,

Marta Fernández-Muñoz, MD, PhD., Pedro Amat-Peral, MD.

Introduction

Epiretinal membranes (ERM) are defined by the appearance of a more or less transparent avascular fibrous tissue which is adhered to the internal layers of the retina in the macular area. This entity has been referred to under different terms such as primary retinal folds, secondary retinal gliosis, cellophane maculopathy, vitreoretinal juncture-simple epiretinal membranes, macular pucker, astrocytic epiretinal membranes, and epimacular proliferation, among others. (1-8) Even though ERM may appear associated to certain vascular or inflammatory pathologies of the retina or following rhegmatogenous retinal detachment surgery, the most frequent scenario is that of primary ERM appearing in eyes that have not suffered diseases previously, in up to 80% of the cases. (9-11)

Idiopathic ERM may show a variable degree of adhesion to the macular retina and eventually cause retinal involvement with distortion of temporal vascular arcades and the appearance of foveal macular oedema.

ERM may eventually resolve and separate spontaneously from the retina. However, this event takes place rarely and most of the membranes will remain stable after an initial period of growth. ERM tend to remain unchanged and vision rarely improves or worsens dramatically. Presently, the only accepted procedure to remove ERM causing significant vision loss is vitreoretinal surgery, even though new advances are being made on other less aggressive, pharmacological therapies.

Vitrectomy is reserved for the cases of fast evolution with visual deterioration or threatening central vision.

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Epidemiology

The prevalence of ERM is high. Klein et al reported a prevalence of 11.8% according to the Beaver Dam Eye Study.(12) The association of ERM with age is clear and more than 90% of the patients are older than 50 years.(6,13) The Blue Mountains Eye Study (BMES) reported a prevalence of 7% on a population 49 years of age or older on the basis of detailed eye examination and stereo retinal photography, and was found to be bilateral in 31% of the cases. The prevalence was 1.9% in persons younger than 60 years of age, 7.2% in persons 60 to 69 years of age, 11.6% in persons 70 to 79 years of age, and 9.3% in persons 80 years of age and older, with slightly higher rates in women. This study identified an early form without retinal folds, termed “cellophane macular reflex” (which was present in 4.8%), and a later stage with retinal folds, termed “preretinal macular fibrosis” which was significantly associated with diabetes and had a small, significant effect on visual acuity (VA) in 2.2% of the population. ERM was more frequent among persons who had undergone cataract surgery (16.8%), or presented retinal vein occlusion (16.1%) or diabetic retinopathy (11%).(11)

Similar studies were later performed on AsianpopulationfromMalaysia,(10) andJapan.(9) Kawasaki et al reported an ERM prevalence of 7.9% in the Singapore Census population (higher in Malays than in Caucasians from the BMES, 15.8% vs 6.8%). Age, female gender, hyperopia and narrower retinal arteriolar

diameter were associated with higher prevalence of ERM.(10) The results of the Funagata study reported similar results for the Japanese population and for the BMES.(9)

Opticalcoherencetomography(OCT)seems to have increased the prevalence of ERM by increasing the sensitivity of the diagnostic procedure. A clinical-setting study on patients undergoing cataract surgery reported ERM in the baseline visit in 15.6% of the cases. ERM was detected adherent to the inner limiting membrane (ILM) and nervous fiber layer of the retina by OCT in the initial phases, although funduscopy did not reveal changes in most of the cases.(14) However, the Handan Eye Study (a population-based study of eye disease in rural China) reported ERM were present in 3.4% of participants and was bilateral in 20.3% of the cases on the basis of OCT and retinal photographs.(15)

Pathophysiology

Even though most of the cases of ERM are idiopathic(11,16) they have also been reported to occur in association with different ocular conditions such as retinal vascular diseases (obstructive vasculopathies, diabetic retinopathy and macro aneurysms),(11) ocular inflammation (sarcoidosis, pars planitis and almost any posterior uveitis),(17-19) intraocular tumours (hamartomas, angiomas),(20) blunt and perforating trauma,(21-23) surgery (especially laser, criotherapy and retinal detachment surgery)(24-26) and retinitis pigmentosa.(27,28)