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

Vitrectomy for diffuse macular edema associated to an attached premacular posterior hyaloidwithoutathickenedhyaloidmembrane has been shown to improve visual acuity outcomes. Tachi et al reported promising results with vitrectomy in these cases.4 They postulated that the edema in these cases can be the result of significant extravasation from retinal vessels secondary to vitreous traction as well as from breakdown of the inner and outer blood-retina barrier. These eyes showed vitreous attachment but no visible hyaloid membrane. In this series, macular edema re-

solved in 67% of eyes at 6 months and 98% at 1 year with visual acuity improvement in 53% of eyes at 1 year.

Diffuse Macular Edema

Diffuse macular edema occurs from generalized incompetence of the capillary vascular wall. Its treatment has been controversial and difficult. In the past, grid photocoagulation has been utilized with modest results.5 Intravitreal triamcinolone has been compared to

photocoagulation in the DRCR.net. Intravitreal triamcinolone, followed by photocoagulation has been utilized, as well as ranizumab and bevacizumab injections. Pars plana vitrectomy with or without ERM and /or ILM peeling has been utilized with varying results.

Aydin et al evaluated pharmacological management of diffuse macular edema. They concluded that intravitreal triamcinolone produced better visual results than grid-laser alone. IVTA followed by laser was better than IVTA alone or at the same time as the laser treatment.6

Frase-Bell et al demonstrated that the VEGF inhibitors bevacizumab and ranizumab both resulted in a significant reduction in foveal thickness in eyes with diffuse edema.7 Similar results were demonstrated with bevacizumab by Kook et al and Arevalo et al. Kook et al showed no change in visual acuity at 6 months but an improvement of 5 lines on average at 12 months.8 Arevalo et al showed an improvement in visual acuity at 24 months in 52% of eyes treated with bevacizumab.9

Beck et al reported the DRCR. net 3 year results of a comparison between grid laser photocoagulation and ICTA using 1 and 4 mg of IVTA.10 Between 2 and 3 years all eyes improved, but by 3 years the laser group had gained 5 letters of visual acuity whereas the IVTA group showed no gain in visual acuity. The incidence of cataract progression was 31% in the laser group, 46% in the 1mg IVTA, and 83% in the 4mg group. Intraocular pressure

increased 10mg in 4% of lasered eyes, 18% of 1mg IVTA and 33% 4mg IVTA.

Results of Vitrectomy for Diffuse Macular Edema

Park et al reported 66% of eyes showing resolution of edema at 12 weeks post vitrectotmy.11 He postulated that in diffuse edema macular flow is augmented and vitrectomy causes reduction and flow and thus of edema.

Kumagai et al reported results of 486 eyes treated with vitrectomy and posterior hyaloids removal.12 36% of these eyes had ILM removal also. At 5 years post-op 52.7% improved, 31.3% remained unchanged and 16% worsened visual acuity. Complications in this series included NVG in 3.9%, vitreous hemorrhage in 2.1%, increased hard exudates in the fovea in 4.3%.

In a series by Yamamoto et al of 65 eyes with diffuse diabetic macular edema, 45% improved, 49% remained unchanged and 6% decreasedvisualacuity.They foundthatcentral macular thickness fluctuated and decreased up to 4 months post vitrectomy.13

Whether or not to remove the internal limiting membrane (ILM) in cases of diffuse macular edema remains controversial. Hartley et al reported on 24 eyes treated with vitrectomy and ILM peeling for these eyes.14

In this series 25% improved, 54% remained unchanged and 21% decreased visual acuity. Despite the modest improvement in visual acuity, retinal thickness in the foveal region by OCT was reduced.

Others have attempted concomitant treatment. Figueroa et al treated 42 eyes with pars plana vitrectomy, ILM peeling and or intravitreal triamcinolone.15 They noted a reduction in macular thickness by OCT from 1-6 months only. Visual acuity only improved in 12%, remained unchanged in 76% and decreased in 12%. They concluded that the procedure produced a temporary reduction in foveal thickness but no anatomical or functional benefit at one year post vitrectomy.

Diagnosis

Patients with diabetic macular edema typically present with decreased visual acuity and metamorphopsia, although a central scotoma can occur in cases of foveal detachment or a large foveal exudate. The decreased vision is usually gradual but can be acute in cases in which a localized macular detachment is present. Slit lamp biomicroscopy reveals retinal thickening which can be accompanied by hard exudates or a glistening sheen. Fluorescein angiography reveals localized or diffuse leakage and areas of capillary non-perfusion. OCT is very useful as it demonstrates the degree of edema, cystoid components, epiretinal membranes, thickened hyaloids, and tractional components. It also shows areas of localized

retinal detachment. And any interfase pathology.

Management

Focal areas of edema caused by microaneurisms are best treated by focal laser photocoagulation. In cases of diffuse macular edema it is important to determine if it is caused solely by vascular leakage or if there is a tractional component associated. Cases without a tractional component can have a response when treated with triamcinolone, VEGF inhibitors or vitrectomy, but results are variable. Eyes with a tractional component, are best managed by vitrectomy

Vitrectomy can be performed with a three port system in either 20, 23 or 25g, although the recent trend is towards microincision surgery with sutureless techniques. Preoperative OCT is imperative to determine if the hyaloids is attached, if a thickened hyaloids is present and if there is a localized retinal detachment or a lamellar hole. Fluorescein angiography is important to determine if significant capillary loss or ischemia is present. These eyes can have a poor visual outcome.

It can be useful to use intraoperative triamcinolone to stain the vitreous and the hyaloid and facilitate their removal. The partially detached hyaloids can be incised with a pick or blade and peeled. A thickened hyaloids can be lifted with a pick or peeled directly with forceps. Tripan blue can also be

used to stain ERM’s or a thickened hyaloids to aid in visualization. In cases of significant traction or if a localized foveal retinal detachment is present an air/fluid exchange can be done to help resolve the detachment. Often, in cases of foveal detachment, after the traction is removed, the detachment can take months to resolve gradually. Eyes with significant traction can benefit from a longer acting gas and prone positioning. Post vitrectomy, the edema tends to resolve gradually.

Complications

Complications include iatrogenic retinal breaks and retinal detachment, iatrogenic macular hole, vitreous hemorrhage, RPE damage in the foveal region, cataract progression, phototoxicity, and endophthalmitis.

Conclusions

The benefit of pars plana vitrectomy for the management of diabetic macular edema in which there is a tractional or mechanical component has been established. Nevertheless the management of diffuse diabetic macular edema without a tractional component remains controversial. Published reports have shown conflicting results with a large variability. This can be explained by the multifactorial aspects of diabetic macular edema. Duration of edema, degree of associated capillary dropout and ischemia, degree of inflammation, quantity of hard exudates in the foveal region and the metabolic state and control of the patient are all variables that can affect visual outcomes in these eyes.

References

1.EarlyTreatmentDiabeticRetinopathyStudyResearch Group.Photocoagulationfordiabeticmacularedema: Early Treatment Diabetic Retinopathy Study report number 1. Arch Ophthalmol 1985;103:1796-1806.

2.EarlyTreatmentDiabeticRetinopathyStudyResearch Group.Photocoagulationfordiabeticmacularedema: Early Treatment Diabetic Retinopathy Study report number 9. Ophthalmology 1991;98:766-785.

3.Lewis HL, Abrams GW, Blumenkranz MS et al. Vitrectomy for diabetic macular traction and edema associated with posterior hyaloids traction. Ophthalmology 1992;99:753-759.

4.Tachi N, Ogino N. Vitrectomy for diffuse macular edema in cases of diabetic retinopathy. Am J Ophthalmol 1996;122:258-260.

5.Blankenship GW. Diabetic macular edema and argon laser photocoagulation: a prospective randomized study. Ophthalmology 1979;86:69-78.

6.AydinE,DemirHD,YardimH,ErkorkmazU.Efficacy of intravitreal triamcinolone after or concomitant with laser photocoagulation in non-proliferative diabetic retinopathy with macular edema. Eur J Ophthalmol. 2009 Jul-Aug;19(4):630-7.

7.Fraser-Bell S, Kaines A, Hykin PG. Update on treatments for diabetic macular edema. Curr Opin Ophthalmol. 2008 May;19(3):185-9.

8.Kook D, Wolf A, Kreutzer T et al. Long-term effect of intravitreal bevacizumab (Avastin) in patients with chronic diffuse diabetic macular edema.: Retina. 2008 Oct;28(8):1053-60.

9.Primary intravitreal bevacizumab for diffuse diabetic macularedema:thePan-AmericanCollaborativeRetina Study Group at 24 months. Arevalo JF, Sanchez JG, Wu L, Maia M, Alezzandrini AA, Brito M, Bonafonte S, Lujan S, Diaz-Llopis M, Restrepo N, Rodríguez FJ, Udaondo-Mirete P; Pan-American Collaborative Retina Study Group Ophthalmology. 2009 Aug; 116 (8): 1488-97, 1497.e1. Epub 2009 Jul 9.

The vitreous is the largest tissue in the human eye and is responsible for numerous ophthalmologic diseases. Its pre-programmed degeneration from early childhood through adult life leads to vitreous detachment and subsequent retinal problems, many of which are sight threatening. This chapter discusses the vitreous anatomy, its subsequent degeneration in diabetic patients leading to tractional retinal detachments and macular edema.

The vitreous gel in non-diabetic eyes generally goes through aging changes consisting of lacunae formation, syneresis and posterior separation. It has been observed that in diabetic eyes without retinopathy, there seems to be a lower incidence of lacunae formation compared to non-diabetic eyes of a similar age group. And among the diabetics, eyes with non-proliferative retinopathy are observed to have a higher incidence of posterior vitreous separation than eyes without clinical evidence

of diabetic retinopathy in the same age group. Therefore, it appears that the presence, and the activity of the diabetic retinopathy promote vitreous changes, and thus posterior vitreous separation.

In adults, the vitreous body volume is approximately 4 mL, which is 80% of the globe. The content of the vitreous is 99% water, and the remaining 1% is mostly composed of collagen and hyaluronic acid. Additionally, there are a few other soluble components such as ions, proteins, and trace cells. These components account for the gelatinous but clear nature of the vitreous.

The vitreous is avascular and inelastic. Pathological mechanisms of vitreous hemorrhage can include hemorrhage from diseased retina, traumatic insult, and/or spread of hemorrhage into the retina and vitreous from fibrous intraocular traction.

Vitreous Shrinkage

Vitreous fluorophotometric studies have demonstrated that in diabetic eyes, even without clinically detectable retinopathy, there occurs a breakdown in the blood-vitreous barrier. It is further suggested that leakage of blood constituents into the vitreous gel as a result of this barrier breakdown leads to shrinkage of the vitreous gel and therefore posterior vitreous separation with, and frequently without, lacunae formation and syneresis. In diabetic eyes with active retinopathy, retinal neovascularities also leak into the vitreous gel and further promote vitreous shrinkage and contraction.

Vitreoretinal Adhesions

In response to retinal ischemia in a diabetic eye, new retinal vessels proliferate. These proliferations are typically located in the surface of the retina and insinuate between the inner retinal surface and the vitreous posterior cortical surface. When fibrocytes are subsequently laid down and proliferate, the new proliferation gradually turns from a neovascular nature to fibrovascular and finally

into a fibrous proliferation in the form of membranes which bind the vitreous cortex with the retinal surface. These proliferations constitute points or areas of vitreoretinal adhesions of various tenacity which, depending on the nature of the adhesion (mainly vascularcortical, fibrovascular-cortical, or fibro-cortical) and also depending on the chronicity of the adhesion, result in complications.

The new vessels leak blood constituents into the cortical vitreous which subsequent undergoes shrinkage and contraction, separating from the posterior retinal surface at places where there are no firm vitreoretinal adhesion and a partial posterior vitreous separation results.

Some years ago, I have conducted a pilot study of looking at the status of the vitreous in eyes of diabetic patients at first presentation to my retinal clinic before any treatments were given. Those eyes which were found to have proliferative diabetic changes at initial presentation, 64% had a partial posterior vitreous separation and only 2% had a complete separation, whereas in eyes in non-proliferative changes initially, 7% had partial separation and 22% had complete posterior vitreous separation (Table 1).

Partial Posterior Vitreous

Separation

Clinically, the vitreous could best be observed using a +78 preset lens and a slit lamp biomicroscope which can produce a thin but strong slit beam. The preset lens facilitates observation of the vitreous cortical movement on eye excursions. It is also important for the observer to become dark adapted before vitreous examination. Turning off all the lights in the examination room and the observer closing his eyes for 30 seconds before the examination would help. Ensuring that the

TheVitreous in Diabetes

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patient’s pupil is widely dilated would also facilitate the examination although unfortunately, in many diabetic eyes, the pupils do not dilate well.

A partial posterior vitreous separation is frequently accompanied in a diabetic eye with a dense posterior hyaloid surface which can be traced posteriorly to the area of vitreo retinal adhesion (Figure 1). The hyaloid surface is thickened, tight and taut, and demonstrates very little movement on ocular excursion. The vitreous cortical gel is dense, hazy and may contain particles, bleaches blood, or even fresh hemorrhage.

Complications from proliferative diabetic retinopathy arise as a result of the interaction between the vitreoretinal adhesions, and the vitreous contraction and can be viewed as consequences of partial posterior vitreous separation in diabetic eyes. There are mainly three complications:

1)vitreous hemorrhage;

2)tractional and/or rhegmatogenous retinal detachment; and

3)rapid neovascular growth.

Vitreous Hemorrhage

In the presence of a partial posterior vitreous separation, and the vitreo retinal adhesion of the vitreous cortex to the new vessels on the retinal surface, vitreous traction from eye movements on these new vessels may cause a rupture of these flimsy vessels and bleeding into the vitreous cavity may promote more vitreous condensation, more vitreous shrinkage, and more vitreous traction until the vitreo-neovascular adhesions were broken by the traction.

However, when the traction is mild and not severe enough to break the vitreo-neo- vascular adhesions, but just enough to cause leakage or small bleeding into the vitreous cortex or the subcortical/preretinal space, a partial posterior vitreous separation may persist. When the neovasular tissue is quickly replaced by a fibrovascular proliferation and a fibrous proliferation, the vitreoretinal adhe-

sions become more firm, and when further vitreous contraction and traction may transmit the pulling force onto the retinal surface instead of breaking the vitreo retinal adhesion, a tractional retinal detachment or retinal break may then occur.

Tractional Retinal Detachment

When the cortical vitreous is tethered to the retinal surface through strong fibrorascular or fibrotic proliferations and membranes, and when the vitreoretinal adhesions involve a wide area, and when the neighboring retina has close to normal tensile strengths, insidious vitreous contraction may result in a centripetal traction on the retina leading to a tractional retinal detachment (Figure 2).

Retinal Break and Rhegmatogenous Retinal Detachment

However, if the dense vitreo retinal adhesion involves only a small focal area, such as a pinpoint, and if the surrounding retina has compromised tissue tensile strength such as atrophic retina after extensive laser treatment, or when the surrounding retina is chronically edematous, and when the vitreous shrinkage and contraction occurs precipitously and forcefully, the centripetal tractional force onto a focal area of weakened retina may result in a retinal break. A rhegmatogenous retinal detachment may then result.