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

Diabetics often present with “decortication” or separation of layers of the posterior hyaloid during posterior vitreal detachment. A surgeon may incorrectly believe that the posterior hyaloid has been completely removed, and not identify a persistent layer of vitreous cortex on the surface of the retina. Intraoperative triamcinolone greatly facilitates the identification of the anatomy of the posterior hyaloid. The surgeon may choose to engage the posterior hyaloid overlying the optic nerve with the vitreous cutter in suction mode or use intraocular forceps in the macular area to peel the hyaloid.

Identification of areas of retinal neovascularization (NV) that have persistent vitreous attachment is important, since these areas are often responsible for postoperative vitreous hemorrhages or retinal traction. These NVvitreous attachment sites should be removed with the vitreous cutter or intraocular scissors to decrease these postoperative problems.

c) Epiretinal Membrane Dissection

Epiretinal proliferation in diabetic traction retinal detachment usually has the conformation of plaques of fibrovascular tissue attached to the underlying retina by multiple discrete point vascular stalks. Each individual attachment site requires to be cut to safely remove the epiretinal tissue. If the attachment sites are not severed, but pulled on (by forceps instead of scissors, for example), there is a high risk of creating a retinal tear. Scissors delamination is the technique where the scissor blades are used parallel to the retinal

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surface and closed between the epiretinal tissue and the underlying retina, cutting the attachment sites. Scissors segmentation is the technique where the scissor blades are used perpendicular to the retinal surface to transect epiretinal tissue. Segmentation can be used to gain access to a specific epiretinal dissection plane for subsequent delamination, or can be used to relieve traction without further delamination.

Delamination and segmentation with the vitreous cutter has been made possible with the newer high speed cutters and with small gauge vitrectomy, since 25 and 23 G cutters have the port closer to the tip of the instrument than older 20 G cutters. Currently, after truncating the peripheral cone of posterior hyaloid, we use the cutter to perform access segmentation of the posterior epiretinal tissue. The cutter can also be used to delaminate plaques of dense epiretinal tissue without damaging the underlying retina. Fast cutting rates and low suction should be used to perform these difficult technique.

The most appropriate site for initiation of epiretinal tissue dissection is at or near the optic nerve, whenever possible. Whereas all other retinal areas may be detached and potentially mobile, the optic nerve is the only structure of the fundus that is not, facilitating dissection at its surface. In addition, once access to the epiretinal dissection space is achieved at the optic nerve, further centrifugal dissection towards the arcades is made significantly easier and safer. Dr. Steve Charles coined the term “inside-out delamination” to illustrate the notion of

initiation of the epiretinal tissue dissection at the epicenter (the safest location), and proceeding outwards rather than attempting to find the most peripheral edge of epiretinal tissue (usually overlying an area of retinal thinning) and proceeding inward.

Great care must be used when delaminating to avoid creating iatrogenic retinal tears. Many surgeons recommend bimanual dissection for traction retinal detachment dissection. To do this, a broad chandelier illumination system must be utilized, either through the infusion cannula (in 20 G surgery) or through a fourth entry port (in 25 G systems). This allows the surgeon to use a forceps in one hand and scissors in the other, facilitating delamination techniques. We do not regularly use chandelier illumination or bimanual techniques, since we are able to perform scissors delamination with the standard three port techniques, using the endoilluminator in one hand and the scissors or vitreous cutter in the active hand.

Although removal of all surface traction is optimal, the surgeon should remember that the goal of surgery is reattachment of the posterior retina and macula (Figures 11a-e). This becomes an issue when peripheral and nasal epiretinal tissue is encountered. Dissection over peripheral atrophic retina is very prone to creation of iatrogenic retinal tears. It is always best to leave peripheral traction present without retinal tears than attempt total peripheral dissection, creating peripheral retinal tears and further complicating the management of the retinal detachment.

We do not recommend intentional creation of a retinotomy for subretinal fluid drainage in traction retinal detachment surgery. Surgical removal of the retinal traction will lead to postoperative retinal reattachment through pumping of the subretinal fluid by the retinal pigment epithelial cells. Intentional retinotomies require air, gas or silicone oil tamponade, postoperative head positioning and increase the risk of postoperative reproliferation and cataract formation.

d) Management of Retinal Tears

Iatrogenic retinal tears occur frequently in traction retinal detachment surgery. Surgeon’s skill, experience and technique can minimize the creation of retinal tears, but the fact remains that retinal tears will be encountered. In addition to iatrogenic retinal tears, tractional cystic retinoschisis or full thickness retinal holes can be often found spontaneously after long standing retinal traction. The first step in management of intraoperative retinal tears is early detection of the tear, to stop further enlargement of the tear. Once the tear is detected, all retinal traction surrounding the tear must be resolved. If there is any traction acting on the tear, the edges of the tear will not settle properly over the retinal pigment epithelium postoperatively, and a rhegmatogenous retinal detachment will eventually occur. Subretinal fluid drainage with simultaneous fluid-air exchange can then be performed through the retinal tear. If all retinal traction has been removed, the retina should become reattached under air. If the retina doesn’t reattach completely, that is clear

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Figure 11 a-e: Active proliferative diabetic retinopathy in type 1 diabetes. Note the neovascularization of the disc that extends superonasally. b) Fluorescein angiography of the same patient, which demonstrates the neovascularization and peripheral capillary non-perfusion. c) Vitreous hemorrhage following panretinal photocoagulation, in the same patient. The patient received intravitreal bevazicumab. The hemorrhage resolved spontaneously after 3-4 weeks. d) Localized traction retinal detachment, following multiple intravitreal bevazicumab injections and panretinal photocoagulation sessions. Note almost complete resolution of intraretinal hemorrhages and retinal vascular dilatation. There is a nasal retinal detachment and macular striae. The patient complained of a localized scotoma that corresponded to the location of the retinal detachment. e) Postoperative result, following vitrectomy and scissors delamination of epiretinal membranes perfomed by the author. Note complete resolution of the retinal detachment and foveal striae. The diabetic retinopathy appears quiescent. The final visual acuity was 20/20, with resolution of the scotoma related to the retinal detachment.

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indication of persistent retinal traction and need for further dissection. The surgeon may choose to operate under air or to return to a fluid-filled eye for continuation of the retinal dissection. Once the retina is reattached, endolaser retinopexy should be performed around all retinal tears, in addition to the panretinal photocoagulation. We commonly use SF6 gas for postoperative surface tension management. In the event that the retinal traction cannot be safely removed completely, we utilize silicone oil tamponade.

e) Management of Intraoperative Hemorrhage

With the advent of preoperative intravitreal anti -VEGF, significant intraoperative hemorrhage has decreased significantly. In the event that such hemorrhages occur, the surgeon must be familiar with techniques to deal with this problem. It is inappropriate to simply stop surgery without addressing the retinal pathology because of intraoperative hemorrhage. The first step in the management of hemorrhage is the elevation of intraocular pressure above the retinal perfusion pressure. This is the equivalent of applying direct pressure on a general surgery wound. Once the bleeding has been stopped, intraocular cautery or direct laser photocoagulation can be utilized for hemostasis. Fluid-air exchange can also be done to let a blood clot to form over the area of hemorrhage, allowing visualization of all other retinal areas. Intraocular thrombin or other procoagulants have been used with some success,8 although we do not find much use for these medications. In the event that persistent hemorrhage precludes

finishing the removal of all retinal traction or adequate laser retinopexy around retinal tears, it is preferred to fill the vitreous cavity with silicone oil at the end of the procedure and plan for reoperation two to four weeks postoperatively than let untreated tears progress to rhegmatogenous retinal detachment in the postoperative period.

f) Endophotocoagulation

In the case of macular edema, the endolaser probe can be used to perform focal photocoagulation to microaneurysms in the macular area. We do not recommend performing grid endolaser photocoagulation, since this technique ablates potentially viable retina and doesn’t treat the underlying pathology of the macular edema.

Endopanretinalphotocoagulationshouldbe performed in cases with proliferative diabetic retinopathy. Several authorities recommend panretinal photocoagulation extending to the ora serrata in cases of severe proliferative diabetic retinopathy. We have not found this to be necessary, and, on the other hand, it increases the risk of peripheral retinal tears, damage to the lens in phakic patients, and increases surgical time, which is an important consideration in diabetics that often have coexisting systemic morbidities.

g) Management of the Lens

Removal of the lens during vitrectomy for diabetic retinopathy can increase postoperative complications, so cataract surgery should be decided cautiously. If the view to the retina

is sufficient for achievement of the goals of vitrectomy surgery, then it is best to leave the lens alone, even in the presence of a mild to moderate cataract. It is always safer to perform standard phacoemulsification with intraocular lens implantation as a separate procedure after recovery from the vitrectomy surgery than attempt to combine them in a single operation.

If a cataract is dense enough to preclude adequate vitrectomy then cataract surgery is in order. In these cases we perform standard phacoemulsification through a clear corneal incision and place a foldable acrylic lens in the capsular bag. Regarding intraocular lens selection, silicone IOLs should be avoided, given the possibility of silicone oil tamponade after the vitrectomy. There is not enough data at this time to recommend multifocal IOLs in the setting of diabetic vitrectomies, so we currently prefer simple monofocal IOLs to provide optimal visual input to these diseased maculas. Great care should be taken during the cataract surgery to maintain constant anterior chamber depth and avoid touching the iris with the surgical instruments, since this would increase the likelihood of intraoperative miosis and postoperative inflammation. If the pupil is small or if there are significant posterior synechiae that require synechiolysis, it is best to use iris hooks or a similar pupilary expansion device during surgery. Once placed, these devices can be left in place until the vitrectomy surgery has been finished. While most well constructed cataract surgery wounds are water tight without

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suturing, postoperative hypotony secondary to the sclerotomies can deform the corneal wound and cause it to leak. Due to this, we prefer to place a single 10-0 nylon suture on the corneal wound after the cataract surgery portion of the procedure. If there are any difficulties with placing a posterior chamber IOL in the bag or even in the ciliary sulcus, it is best to leave the eye aphakic than to hastily place an anterior chamber IOL. Secondary IOL placement can be performed in the future. The surgeon should always keep in mind that the primary goal of the surgery is to fix the retinal pathology, and that cataract surgery and IOL implantation should not interfere with this primary goal.

References

1.Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy. Four-year results of a randomized trial: Diabetic Retinopathy Vitrectomy Study Report 5. Arch Ophthalmol. 1990 Jul;108(7):958-64

2.Arevalo JF, Wu L, Sanchez JG, Maia M, Saravia MJ, Fernandez CF, Evans T. Intravitreal bevacizumab (Avastin) for proliferative diabetic retinopathy: 6-months follow-up. Eye. 2007 Sep 21.

3.Kaiser PK, Riemann CD, Sears JE, Lewis H. Macular traction detachment and diabetic macular edema associated with posterior hyaloidal traction. Am J Ophthalmol. 2001 Jan;131(1):44-9.

4.Sander B, Thornit DN, Colmorn L, Strøm C, Girach A, Hubbard LD, Lund-Andersen H, Larsen M. Progression of diabetic macular edema: correlation with blood retinal barrier permeability, retinal thickness, and retinal vessel diameter. Invest Ophthalmol Vis Sci. 2007 Sep;48(9):3983-7.

Diabetic macular edema can be caused by a number of different pathologies. These include focal edema caused by microaneurysms, diffuse macular edema caused by incompetence of the capillary wall, thickened posterior hyaloid, vitreomacular traction and epiretinal membranes. Argon laser photocoagulation has been the mainstay of treatment as evidenced by the EDTRS for clinically significant macular edema secondary to capillary leakage.1,2 With the advent of optical coherence tomography (OCT) for diagnostic evaluation, a tractional component of macular edema has been disclosed in some cases. This tractional etiology has shown to be responsive to management by vitrectomy. Pars plana vitrectomy has shown to be beneficial in the management of macular edema associated to macular traction from epiretinal membranes or a thickened posterior hyaloid, vitreomacular traction syndrome and pre-retinal hemorrhage. Nevertheless, the treatment of diffuse macu-

lar edema without an associated tractional component has been controversial. Treatment modalities of photocoagulation, vitrectomy, and intravitreal pharmacotherapy have been attempted with varying results.

Etiologies of Diabetic Macular

Edema

Diabetic macular edema secondary to a tractional component can be divided into several subgroups depending on the underlying pathology. These include traction from a thickened premacular posterior hyaloid membrane, diffuse edema from a partially attached premacular posterior hyaloid without a thickened membrane or traction from an epiretinal membrane in an eye with a posterior vitreous detachment (PVD). The widespread use of the optical coherence tomography (OCT)

has increased the accuracy of the diagnosis of the underlying vitreoretinal pathologies in these cases. It has made it possible for the clinician not only to determine if there is a tractional component but also to assess the degree of retinal edema present. Small, shallow localized macular detachments can be easily visualized with this modality.

Vitreomacular Traction

This diagnosis was very difficult to make prior to the advent of OCT. Previously, gliosis

observed by contact lens slit lamp biomicroscopy as well as diffuse leakage by fluorescein angiography were used for diagnosis. Nevertheless, the gold standard for diagnosis is the OCT. In these eyes, vitreomacular traction on the fovea causes diffuse edema, and/or foveal detachment. These eyes have shown positive responses to management with pars plana vitrectomy to remove the hyaloid. The edemaandlocalizedfovealdetachmentresolves slowly over time with slow improvement of visual acuity (Figures 1 and 2).

Figure 1a-b: a) Posterior hyaloids exerting traction on foveal region Va 20/400. b) Resolved traction and edema 6 months post vitrectomy Va 20/50.

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Figure 2a-d: a) 65 years old IDDM patient with posterior hyaloids traction, stable for 8 months. Va 20/30. b) Patient experienced sudden reduction of visual acuity. A localized foveal detachment can be observed by OCT. Va 20/400. c) 2 months post vitrectomy, small localized foveal detachment remains but is reduced. Va 20/80. d) 3.5 years post vitrectomy edema has resolved. Va is 20/50.

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In eyes with a partially attached premacular posterior hyaloid or vitreomacular traction syndrome, the tractional forces are anteroposterior (Figure 1). These cases can develop cystoid macular edema changes and a localized foveal neurosensory detachment which can cause severe, acute visual acuity loss. They can also develop lamellar holes (Figure 3). In 1992 Lewis et al reported promising results in eyes with diabetic macular edema from traction from a taut premacular posterior hyaloids membrane.3 In these eyes fluorescein angiography (FA) demonstrated

deep retinal diffuse leakage. The pathogenesis of this leakage was speculated to be at the level of the retinal pigment epithelium (RPE) from traction on the fovea and tangential tractional forces causing a shallow macular detachment. In this series of 10 eyes visual acuity improved in 90% at 6 months. All eyes showed glistening on biomicroscopy which can be confused with an epiretinal membrane, but no tortuosity was seen (Figure 4). This study was done prior to the use of OCT and biomicroscopy and fluorescein angiography were utilized for diagnosis.

Figure 3 a-b: a) Vitreomacular traction causing a localized foveal detachment and a lamellar hole. Right eye Va 20/100. b) Vitreomacular traction causing a lamellar hole. Left eye Va 20/25.

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