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Ординатура / Офтальмология / Английские материалы / Diabetes and Ocular Disease Past, Present, and Future Therapies 2nd edition_Scott, Flynn, Smiddy_2009

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204 Diabetes and Ocular Disease

15.American Academy of Ophthalmology Retina Panel. Preferred Practice Pattern Guidelines. Diabetic Retinopathy. San Francisco, CA: American Academy of Ophthalmology;2008. Available at http//www.aao.org/ppp.

16.Wilson DJ, Finkelstein D, Quigley HA, Green WR. Macular grid photocoagulation: an experimental study of the primate retina. Arch Ophthalmol. 1988;106:100–105.

17.Marshall J, Clover G, Rothery S. Some new findings on retinal irradiation by krypton and argon lasers. Doc Ophthalmol Proc Ser. 1984;36:21–37.

18.Weiter J, Zuckerman R. The influence of the photoreceptor-RPE complex on the inner retina: an explanation for the beneficial effects of photocoagulation. Ophthalmology. 1980;87:1133–1139.

19.Bresnick G. Diabetic maculopathy: a critical review highlighting diffuse macular edema. Ophthalmology. 1983;90:1301–1317.

20.Marshall J, Hamilton AM, Bird AC. Intra-retinal absorption of argon laser irradiation in human and monkey retinae. Experientia. 1974;30:1355–1357.

21.Arden G, Berninger T, Hogg CR, Perry S. A survey of color discrimination in German ophthalmologists. Ophthalmology. 1991;98:567–575.

22.Diabetic Retinopathy Clinical Research Network. Comparison of the modified Early Treatment Diabetic Retinopathy Study and mild macular grid laser photocoagulation strategies for diabetic macular edema. Arch Ophthalmol. 2007;125:469–480.

23.Diabetic Retinopathy Clinical Research Network. A randomized trial comparing intravitreal triamcinolone acetonide and focal/grid photocoagulation for diabetic macular edema. Ophthalmology. 2008;115:1447–1459.

24.Kaiser P, Riemann CD, Sears JE, Lewis H. Macular traction detachment and diabetic macular edema associated with posterior hyaloidal traction. Am J Ophthalmol. 2001;131:44–49.

25.Martidis A, Duker JS, Greenberg PG, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology. 2002;109:920–927.

26.Strom C, Sander B, Larsen N, et al. Diabetic macular edema assessed with optical coherence tomography and stereo fundus photography. Invest Ophthalmol Vis Sci. 2002;43:241–245.

27.Browning DJ, Zhang Z, Benfield JM, Scott AQ. The effect of patient characteristics on response to focal laser treatment for diabetic macular edema. Ophthalmology. 1997;104:446–472.

28.McDonald HR, Schatz H. Grid photocoagulation for diffuse macular edema. Retina. 1985;5:65–72.

29.Blankenship G. Diabetic macular edema and laser photocoagulation. Ophthalmology. 1979;86:69–75.

30.British MSG. Photocoagulation for diabetic maculopathy: a randomized controlled clinical trial using xenon arc. Diabetes. 1983;32:1010–1016.

31.Patz A, Schatz H, Berkow JW, et al. Macular edema: an overlooked complication of diabetic retinopathy. Ophthalmology. 1979;77:34–42.

32.Whitelocke R, Kearns M, Black RK, et al. The diabetic maculopathies. Trans Ophthalmol Soc UK. 1979;99:314–320.

33.Klein R, Klein BEK, Moss SE, Davis MD, DeMets DL. The Wisconsin Epidemiological Study of Diabetic Retinopathy. III. Prevalence and risk of diabetic retinopathy when age at diagnosis is 30 or more years. Arch Ophthalmol. 1984;102:527–532.

34.American Academy of Ophthalmology Retina Panel. Preferred Practice Pattern Guidelines. Diabetic Retinopathy. San Francisco, CA: American Academy of Ophthalmology;2008. Available at http//www.aao.org/ppp.

Photocoagulation for Diabetic Macular Edema and Diabetic Retinopathy

205

35.Diabetic Retinopathy Study Group. Clinical application of Diabetic Retinopathy Study (DRS) findings: DRS report number 8. Ophthalmology. 1981;88:583–600.

36.Early Treatment Diabetic Retinopathy Study (Research) Group. Early photocoagulation for diabetic retinopathy: ETDRS report number 9. Ophthalmology. 1991;98: 766–785.

37.Ferris F. Early photocoagulation in patients with either type I or type II diabetes. Trans Am Ophthalmol Soc. 1996;94:505–537.

38.Pavan PR, Folk JC, Weingeist TA, et al. Diabetic rubeosis and panretinal photocoagulation: a prospective, controlled, masked trial using fluorescein angiography. Arch Ophthalmol. 1983;101:882–884.

39.Jacobson D, Murphy RP, Rosenthal AR. The treatment of angle neovascularization with panretinal photocoagulation. Ophthalmology. 1979;86:1270–1275.

40.Glaser B. Extracellular modulatory factors and the control of intraocular neovascularization: an overview. Ophthalmology. 1988;106:603–607.

41.Glaser B. Retinal pigment epithelial cells release an inhibitor of neovascularization. Arch Ophthalmol. 1985;103:1870–1875.

42.Patz A. Retinal neovascularization: early contributions of Professor Michaelson and recent observations. Br J Ophthalmol. 1984;68:42–46.

43.Landers M, Stefanson E, Wolbarsht ML. Panretinal photocoagulation and retinal oxygenation. Retina. 1982;2:167–175.

44.Singerman LJ, Ferris FL III, Mowery RP, et al. Krypton laser for proliferative diabetic retinopathy: the Krypton Argon Regression of Neovascularization Study. J Diabet Complications. 1988;2:189–196.

45.The Krypton Argon Regression Neovascularization Study Research Group. Randomized comparison of krypton versus argon scatter photocoagulation for diabetic disc neovascularization. The Krypton Argon Regression Neovascularization Study Report Number 1. Ophthalmology. 1993;100:1655–1664.

46.Khairallah M, Chachia N. Post laser choroidal hematoma in a diabetic treated with an oral anticoagulant. J Fr Ophthalmol. 1994;17:138–140.

47.Ulbig M, Hamilton AM. Comparative use of diode and argon laser for panretinal photocoagulation in diabetic retinopathy. Ophthalmologe. 1993;90:457–462.

48.Bandello F, Brancato R, Trabucchi G, Lattazio R, Malegori A. Diode versus argongreen laser panretinal photocoagulation in proliferative diabetic retinopathy: a randomized study in 44 eyes with a long follow-up time. Graefes Arch Clin Exp Ophthalmol. 1993;231:491–494.

49.Early Treatment Diabetic Retinopathy Study (Research) Group. Techniques for scatter and local photocoagulation: Early Treatment Diabetic Retinopathy Study report no. 3. Int Ophthalmol Clin. 1987;27:254–264.

50.Ferris F III, Davis MD, Aiello LM. Treatment of diabetic retinopathy. NEJM. 1999;341:667–678.

51.Blankenship G. A clinical comparison of central and peripheral argon laser panretinal photocoagulation for proliferative diabetic retinopathy. Ophthalmology. 1988;95:170–177.

52.Ferris F III, Podgor MJ, Davis MD, The Diabetic Retinopathy Study Research Group. Macular edema in Diabetic Retinopathy Study patients: diabetic Retinopathy Study report number 12. Ophthalmology. 1987;95:754–760.

53.Doft B, Blankenship GW. Single versus multiple treatment sessions of argon laser panretinal photocoagulation for proliferative diabetic retinopathy. Ophthalmology. 1982;89:772–779.

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54.Aylward GW, Pearson RV, Jagger JD, Hamilton AM. Extensive argon laser photocoagulation in the treatment of proliferative diabetic retinopathy. Br J Ophthalmol. 1989;73:197–201.

55.Weinberger D, Ron Y, Lichter H, Rosenblat I, Axer-Siegel R, Yassur Y. Analgesic effect of topical sodium diclofenac 0.1% drops during retinal laser photocoagulation. Br J Ophthalmol. 2000;84:135–137.

56.Stevens JD, Foss AJ, Hamilton AM. No-needle one-quadrant sub-tenon anaesthesia for panretinal photocoagulation. Eye. 1993;7:768–771.

57.Han D, Mieler WF, Burton TC. Subretinal fibrosis after laser photocoagulation for diabetic macular edema. Am J Ophthalmol. 1992;113:513–521.

58.Guyer D, D’Amico DJ, Smith CW. Subretinal fibrosis after laser photocoagulation for diabetic macular edema. Am J Ophthalmol. 1992;113:652–656.

59.Lewis H, Schachat AP, Haimann, MH, et al. Choroidal neovascularization after laser photocoagulation for diabetic macular edema. Ophthalmology. 1990;97:503–510.

60.Schatz H, Madeira D, McDonald HR, Johnson RN. Progressive enlargement of laser scars following grid laser photocoagulation for diffuse diabetic macular edema. Arch Ophthalmol. 1991;109:1549–1551.

61.Mainster M, White TJ, Tips JH, Wilson PW. Retinal temperature increases produced by intense light sources. J Opt Soc Am. 1970;60:264–270.

62.Mainster M. Wavelength selection in macular photocoagulation: tissue optics, thermal effects and laser systems. Ophthalmology. 1986;93:952–958.

63.Blondeau P, Pavan PR, Phelps CD. Acute pressure elevation following panretinal photocoagulation. Arch Ophthalmol. 1981;99:1239–1241.

64.Mensher J. Anterior chamber depth alteration after retinal photocoagulation. Arch Ophthalmol. 1977;95:113–116.

65.Huamonte FU, Peyman GA, Goldberg MF, Locretz A. Immediate fundus complications after retinal scatter photocoagulation. 1. Clinical picture and pathogenesis.

Ophthalmic Surg. 1976;7:88–89.

66.Lobed L, Bourgon P. Pupillary abnormalities induced by argon laser photocoagulation. Ophthalmology. 1985;92:234–236.

67.McDonald HR, Schatz H. Visual loss following panretinal photocoagulation for proliferative diabetic retinopathy. Ophthalmology. 1985;92:388–393.

68.McDonald HR, Schatz H. Macular edema following panretinal photocoagulation. Retina. 1985;5:5–10.

11

Vitrectomy for Diabetic Retinopathy

WILLIAM E. SMIDDY, MD,

AND HARRY W. FLYNN, JR., MD

CORE MESSAGES

Indications for pars plana vitrectomy in the management of complications from diabetic retinopathy have changed substantially since the inception of vitrectomy.

Generally, vitrectomy is recommended early in the disease process, especially for type 1 diabetic patients, before irreversible changes occur.

Panretinal laser photocoagulation (PRP) is recommended before vitrectomy whenever the clinical presentation and course allow it.

New instrumentation and techniques, including high-speed vitrectomy instruments, wide-field viewing systems, and transconjunctival systems, have facilitated the objectives of diabetic vitrectomy.

There are many different surgical approaches, but all allow for acceptably good results.

Visual acuity outcomes of diabetic vitrectomy are best for clearance of media opacities and diminish as increasing traction causes retinal detachment.

The hallmark of proliferative diabetic retinopathy is ischemia-driven retinal vascular changes including neovascularization (NV). The most efficient strategies to preserve vision in diabetic patients are to prevent or mitigate complications through population screening and early detection, and timely and appropriate treatment of complications [1–3]. Prevention of retinopathy or reduction in rates of retinopathy progression via optimal glucose control [4,5] and laser treatment at earlier stages have been advocated and implemented [3]. Prospective clinical trial results have largely defined the management of complications of

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208 Diabetes and Ocular Disease

diabetic retinopathy. Timely application (and reapplication as needed) of panretinal laser photocoagulation (PRP) is the mainstay of treatment to reduce visual loss and to avoid the need for vitrectomy in patients with more advanced diabetic retinopathy complications [6–14]. Javitt has shown the cost-effectiveness of implementation of guidelines obtained from the results of collaborative, National Eye Institute sponsored laser studies to the diabetic population at risk [15].

However, despite timely treatment and preventative regimens, substantial numbers of eyes will develop complications of progressive retinopathy and may become candidates for vitrectomy [16]. Clinical trials together with case series form the foundation for defi ning treatment by vitrectomy [17,18].

SURGICAL INDICATIONS

The initial indications and surgical rationale for pars plana vitrectomy in diabetic patients were largely established by the mid-1980s [17–29]. As instrumentation and surgical techniques evolved, these indications have been refined. General categories of surgically approachable complications from diabetic retinopathy include eyes with media opacities and vitreoretinal traction (Table 11.1). The timing for vitrectomy has been generally accelerated as improvements in surgical instrumentation have resulted in better visual acuity outcomes. An addition to surgical indications is certain subsets of eyes with macular edema [29,30]. Optimal application for this indication is still undergoing definition and evaluation, but seems to be most effective if vitreomacular traction is present [31]. The DRCR network has recently reported that pars plana vitrectomy for eyes with vitreomacular traction and clinically significant macular edema was associated with significant improvement in

Table 11.1. Indications for Vitrectomy due to Complications of Severe Diabetic Retinopathy

A.Media Opacities:

1)Nonclearing hemorrhage

a)Vitreous hemorrhage

b)Subhyaloid, premacular hemorrhage

c)Anterior segment neovascularization with posterior segment opacity

2)Cataract preventing treatment of severe proliferative diabetic retinopathy

B.Tractional Defects:

1)Progressive fibrovascular proliferation

2)Traction retinal detachment involving the macula

3)Combined tractional and rhegmatogenous retinal detachment

4)Macular edema associated with taut, persistently attached posterior hyaloid

C.Other Miscellaneous Indications (often following previous vitrectomy):

1)Vitreous hemorrhage/ghost cell glaucoma

2)Anterior hyaloidal fibrovascular proliferation

3)Fibrinoid syndrome

4)Epiretinal membrane (nonvascularized)

5)Macular heterotopia

6)Macular hole

7)Macular edema without traction

Vitrectomy for Diabetic Retinopathy

209

Figure 11.1. Diabetic vitreous hemorrhage most commonly presents as a fairly sudden decrease in vision. Depending upon the degree of hemorrhage, the posterior pole may not be visible. The hemorrhage is usually due to vitreous traction on elevated neovascularization. The neovascularization can be isolated or more broadly distributed. This schematic illustrates the subhyaloid hemorrhage in all areas except at the optic nerve head where a stump of neovascularization is present. (Source: Redrawn with permission of Johns Hopkins University from Michels RG: Proliferative diabetic retinopathy: pathophysiology of extraretinal complications and principles of vitreous surgery. Retina 1981;1:1–17.)

optical coherence tomography (OCT) outcomes but visual acuity outcomes were relatively unchanged at six months follow-up.

Media Opacities. Severe nonclearing diabetic vitreous hemorrhage was the first indication for diabetic vitrectomy [32,33] (Fig. 11.1). Vitreous hemorrhage probably results from vitreous traction on the vascular stalk of fibrovascular complexes [34–36]. Timely application of PRP has decreased the incidence of dense vitreous hemorrhage by truncating the extent of retinal NV. Newer vitrectomy techniques and instrumentation now allow successful surgery on more complex cases, expanding the indications for diabetic vitrectomy.

Probably the greatest change in clinical practice during the last decade is the timing for vitrectomy, which has generally come to be undertaken after a shorter waiting period. Several clinical features may influence the decision on timing of vitrectomy for diabetic vitreous hemorrhage. Surgical intervention is usually considered within several weeks to a few months after onset of symptoms. However, a substantial proportion of such cases will have spontaneous clearing, and careful clinical assessment is necessary during the initial observation period. Earlier surgical intervention is generally recommended for type 1 diabetic patients, especially when no previous PRP has been performed, when the proliferative complexes are more extensive, and when the retinopathy in the fellow eye has been more aggressive. Conversely, surgical intervention may be more appropriately deferred,

210 Diabetes and Ocular Disease

at least temporarily, when there is a posterior vitreous detachment (PVD), when extensive prior PRP has been delivered, and when other labile medical conditions coexist. Patients with sustained hypertension or elevated levels of glycosylated hemoglobin should have prompt and appropriate treatment for these systemic conditions. Echographic monitoring for retinal detachment is important when media opacities prohibit visualization of the fundus.

Other coexisting clinical features define subsets of vitrectomy indications for vitreous hemorrhage. Rubeosis iridis in an eye with a recent vitreous hemorrhage, especially when no PRP has been applied, constitutes an urgent indication for intervention (Fig. 11.2). An extensive subhyaloid macular hemorrhage (SHMH) constitutes another surgical indication (Fig. 11.3). The confinement of blood in the subhyaloid space indicates that the posterior hyaloid has not fully separated and remains as a scaffold for progressive fibrovascular proliferation (FVP) [35–37]. Although the hemorrhage may clear over several months, this SHMH is often associated with broad-based areas of vitreoretinal adhesions. Because of the relatively poor visual prognosis in eyes with substantial SHMH even with spontaneous clearing, surgical intervention should be considered relatively early in the course (probably within 2 months of onset). As with the conventional form of

A

B

Figure 11.2. Rubeosis iridis characteristically appears first at the pupillary border and then extends onto the iris surface, but in progressive cases, may be visible in the anterior chamber angle. Subsequent neovascular glaucoma and precipitous loss of vision may result, especially without prompt and extensive panretinal photocoagulation treatment.

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211

A

B

Figure 11.3. (A) This patient presented with extensive subhyaloid hemorrhage and vision of 2/200. (B) Postoperative appearance following vitrectomy with supplementation of panretinal photocoagulation. Vision is 20/40.

vitreous hemorrhage, intervention is generally recommended earlier for type 1 diabetic patients compared to type 2 diabetic patients. While waiting for clearing of SHMH, however, PRP should be applied in more peripheral areas, as breakthrough bleeding into the central vitreous may later prevent this.

Lens opacities may be sufficient to impair not only the patient’s vision but also the physician’s ability to diagnose, monitor, and apply laser treatment to the retina. In such cases, cataract removal may be considered either as a separate procedure or in combination with vitrectomy. In eyes with vitreous hemorrhage, the accurate assessment of the degree of cataract may be difficult. Reports before the availability of endolaser photocoagulation documented a substantial rate of rubeosis iridis and poor visual prognosis in aphakic eyes, or in those eyes undergoing lensectomy at the time of vitrectomy [38–41]. However, more recent experience with better techniques for lens removal and the ability to deliver intraoperative photocoagulation have improved outcomes with combined lens removal and intraocular lens (IOL) implantation during vitrectomy in selected cases [42–44].

212 Diabetes and Ocular Disease

Two general approaches for combined vitrectomy and cataract surgery have been reported. In the first approach, pars plana lensectomy is combined with vitrectomy maneuvers, and the anterior capsule (with central capsulotomy) is preserved for posterior chamber (PC) IOL support. Using this approach, the visual acuity has been reported to improve in over 75% of eyes, including about 25% with ≥20/40 vision [42,43]. In the second approach, a standard clear corneal phacoemulsification is performed, with IOL insertion into the capsular bag, followed by the vitrectomy. Using that approach, visualization was reported to be excellent, but visual acuity outcomes were not as good in one study [44]; the discrepancy in visual results between the two approaches is most probably accounted for by case selection. Modern techniques for cataract surgery allow successful outcomes even in the presence of rubeosis iridis [45].

Vitreoretinal Traction. Vitreoretinal traction constitutes the second general indication category for diabetic vitrectomy. The spectrum of tractional involvement includes macular heterotopia [46], progressive FVP without retinal detachment, tractional retinal detachment, and rhegmatogenous retinal detachment where the retinal break formed because of progressive traction. Frequently, tractional elements and media opacities coexist, and a dual set of indications for vitrectomy must be assessed (Fig. 11.4).

Progressive FVP may occur despite appropriate PRP and may be especially aggressive in type 1 diabetics (Fig. 11.5). Although FVP may be very extensive in some cases, visual loss may only be slight in its earlyto mid-stages. Ultimately, FVP usually progresses and induces marked visual loss, and a more guarded prognosis for vitrectomy. The lack of a complete PVD is commonly the determining factor influencing anatomic extent and visual prognosis. Broad-based posterior hyaloid attachment usually allows the FVP to be more extensive, requiring more prolonged scissors dissection. In general, the more chronic the FVP, the more adherent its retinal attachment. On the other hand, more acute onset is frequently associated with a more active vascular component that allows more complete removal, but leads to more intraoperative and postoperative vitreous hemorrhage. Incomplete removal may form a nidus for reproliferation. Surgical relief of traction is accomplished with fewer complications when the zone of vitreoretinal attachment is less extensive, extends less anteriorly, and is of recent onset.

The pathogenesis of retinal detachment involves progressive vitreoretinal traction (Fig. 11.6). Since peripheral or mid-peripheral tractional retinal detachments progress to involve the macula in only about 15% of cases per year [47], caution is advised in recommending vitrectomy for localized, non−macular-involving detachments; they may never lead to visual loss, whereas surgical removal might accelerate visual loss. Vitrectomy is generally reserved for cases in which the macula is involved or clearly threatened by progressive tractional retinal detachment. Currently, tractional retinal detachment is probably the most common specific indication for vitrectomy in patients with progressive FVP.

As with cases of nonclearing diabetic vitreous hemorrhage, additional factors may influence the timing of surgical intervention. Patients with type 1 diabetes, coexisting media opacities (which may have prevented delivery of adequate PRP),

A

B

C

Figure 11.4. (A) Frequently, media opacities and tractional components coexist. In this schematic representation, there is vitreous hemorrhage admixed with fibrovascular proliferation, which is causing a tractional retinal detachment. However, this may not be clinically evident due to the obscuration of the posterior pole by the media opacities. (B) This patient presented with vision of hand motions. Clearly, there is vitreous hemorrhage, but the view is clear enough to depict fibrovascular proliferation along the superotemporal arcade. (C) Appearance postoperatively following vitrectomy with extensive membrane peeling and silicone oil infusion. Vision is 20/400. (Source: Part A redrawn with permission of Johns Hopkins University from Michels RG: Proliferative diabetic retinopathy: pathophysiology of extraretinal complications and principles of vitreous surgery. Retina 1981;1:1–17.)

213