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QUESTION
HOW LONG SHOULD I WAIT TO PERFORM CATARACT SURGERY AFTER TREATMENT OF DIABETIC MACULAR EDEMA OR RETINOPATHY?
Linda A. Lam, MD, MBA
A frequent dilemma for cataract surgeons is when to perform surgery in a patient with diabetic retinopathy. Controversy exists regarding cataract surgery and its effects on the development and progression of diabetic macular edema (DME) and diabetic retinopathy. Previous studies reported that cataract surgery in diabetic eyes was complicated by worsening of macular edema and retinopathy with the development of vitreous hemorrhage, anterior segment neovascularization, and worsening visual acuity.1 Many of these studies were retrospective and included older surgical techniques associated with intra- and extracapsular cataract extraction.1,2 Recent prospective studies in eyes with relatively low-risk diabetic retinopathy undergoing small-incision phacoemulsification cataract surgery have shown no significant progression of diabetic retinopathy postoperatively compared with that in fellow eyes.3–6
In a patient with diabetes who needs cataract surgery, the following should be optimized or treated prior to cataract surgery in order to limit the development and progression of postoperative DME and diabetic retinopathy:
- Degree of glycemic control
- Preoperative severe nonproliferative and proliferative diabetic retinopathy (PDR)
- DME
- Presence of vitreomacular traction (VMT)
Degree of Glycemic Control
Normalizing and stabilizing systemic glucose levels is necessary to reduce the development and progression of diabetic retinopathy after cataract surgery. Poor preoperative glycemic control and poor renal function have been correlated with higher rates of diabetic retinopathy and DME following cataract surgery. Because transient worsening of diabetic retinopathy may occur during the first 6 months of intensive blood glucose management,7 deferring cataract surgery for at least 6 months is recommended in this scenario.
Preoperative Severe Nonproliferative and Proliferative Diabetic Retinopathy
Patients with severe nonproliferative diabetic retinopathy and PDR may benefit from having panretinal laser photocoagulation (PRP) performed prior to cataract surgery. Cataract surgery can then be delayed for 4 to 6 months afterward to allow the diabetic retinopathy to improve and stabilize. Following PRP, macular edema may subsequently develop or progress. As a result, waiting up to 6 months to perform cataract surgery is reasonable to allow for improvement and sometimes treatment of any secondary DME and regression of any PDR. This may not always be possible as the cataract may be interfere with the delivery of adequate PRP.
Preoperative Diabetic Macular Edema
Preexisting DME is a major contributor to postoperative visual loss in diabetic patients. In eyes with preoperative DME, treatment prior to cataract surgery is recommended as postoperative inflammation can exacerbate edema.3–6 Postoperative macular edema is common in patients with a history of DME; hence, it is prudent to treat the macular edema prior to cataract extraction.
The most effective treatment options for preoperative DME include anti-vascular endothelial growth factor (anti-VEGF) agents (ie, bevacizumab, ranibizumab, aflibercept). Other options include focal/grid laser, subtenon or intravitreal triamcinolone acetonide, or longer-acting intraocular steroid implants, such as dexamethasone or fluocinolone.
Anti-VEGF agents are the preferred first-line options to reduce DME in an eye with a visually significant cataract. The Diabetic Retinopathy Clinical Research Network explored the effectiveness of the 3 anti-VEGF agents in the treatment of DME.8 At 2 years, mean visual acuity improved by 12.8, 10, and 12.3 letters in the aflibercept, bevacizumab, and ranibizumab groups, respectively. The differences in visual outcomes among the 3 groups were not statistically significant. While all 3 anti-VEGF agents showed similar rates of improvement in letters gained at year 2 in eyes with initial good baseline vision (20/32 to 20/40), aflibercept showed a statistically significant improvement of visual outcomes in eyes with worse pretreatment vision (worse than 20/50) compared to bevacizumab. No advantage of aflibercept over ranibizumab was found at year 2, while aflibercept remained superior to bevacizumab.
In phakic eyes with DME with a view of the macula, my regimen is to initially start with anti-VEGF therapy for several injections prior to possible focal/grid laser or steroid, if the DME is recalcitrant. The choice of anti-VEGF agent is often dictated by the initial presenting visual acuity and the severity of DME, with aflibercept used more frequently in eyes with severe DME and worse vision. However, given that the visual acuity may be worse due to a cataract that is present, the central retinal thickness plays a more influential role in anti-VEGF drug selection in these eyes with visually significant cataracts. Eyes with worse central retinal thickness (eg, over 400 μm) are more likely to be treated with intravitreal aflibercept.
If the view is sufficient, then fluorescein angiography (FA) can delineate areas of leakage to guide focal/grid laser treatment. If significant DME remains following multiple anti-VEGF treatments or focal/grid laser, intravitreal (or subtenon) triamcinolone can be used to reduce the macular edema. However, steroid treatment may hasten cataract progression and may induce steroid-related intraocular pressure elevation. My preference is to administer intravitreal anti-VEGF injection(s) as first-line treatment followed by FA-guided focal/grid laser to treat DME prior to cataract surgery for an eye with an adequate view of the macula. Cataract surgery should then be delayed 4 to 6 months to allow for improvement of the macular edema.
Recent studies have shown that adjuvant intravitreal anti-VEGF treatment or triamcinolone at the time of cataract surgery may improve macular edema in the short term, up to 6 months.9 However, long-term data is lacking to support the role of intraoperative adjuvant therapy at this time in the management of preoperative DME.
Eyes without preoperative DME that then develop DME postoperatively usually experience resolution of the edema within the first postoperative year after cataract surgery.10 Postoperative macular edema therapy should be tailored to whether the edema is related to the Irvine-Gass Syndrome or DME which may be differentiated on FA. If the macular edema shows petaloid leakage (cystoid macular edema) with a hot disc (disc leakage) on FA, then the edema is most likely due to Irvine-Gass Syndrome, and as such, topical anti-inflammatory agents such as topical steroids and topical non-steroidal anti-inflammatory agents are advised as first-line therapy. However, if the FA shows focal leakage from microaneurysms and/or diffuse leakage of diabetic origin, a combination of anti-VEGF treatment and focal/grid laser is recommended. In recalcitrant postoperative macular edema, I also consider intravitreal preservative-free triamcinolone in addition to anti-VEGF agents.11
Presence of Vitreomacular Traction
Optical coherence tomography (OCT) can be used to assess the degree of macular edema and evaluate the treatment effect. OCT may reveal the presence of coexisting pathology such as VMT or posterior hyaloidal traction, which may contribute to persistent DME, despite treatment. If significant VMT is present, then vitrectomy may be needed to eliminate the tractional forces contributing to the edema.
If any lens opacity precludes a clear view of the macula for vitreous surgery, then consider either performing cataract surgery prior to vitrectomy or performing both surgeries at the same time. Some retinal surgeons prefer to have the cataract removed first to allow for any associated corneal edema to subside in order to optimize the intraoperative view of the macula.
If the cataract is not severe and the view of the macula is clear enough to allow vitrectomy, I prefer to perform vitrectomy to relieve the VMT and reduce as much of the macular edema as possible prior to cataract surgery. The presence of the macular edema may influence intraocular lens calculations. Allowing the macular edema to resolve prior to cataract surgery would result in a more accurate axial length calculation and consequently, a more appropriate intraocular lens selection. It is possible that intravitreal pharmacotherapeutic agents may have a shorter half-life in some vitrectomized eyes.12–15
Summary
Recent data demonstrate that the progression of diabetic retinopathy is not significantly affected by small-incision cataract surgery. However, it is important to treat any preoperative diabetic retinopathy and DME and then allow up to 6 months for improvement and stabilization prior to elective cataract surgery. Key factors such as glycemic control, presence of untreated severe nonproliferative or PDR, DME, and any coexistent VMT need to be addressed prior to proceeding with cataract surgery.
References
1. Mittra RA, Borrillo JL, Dev S. et al. Retinopathy progression and visual outcomes after phacoemulsification in patients with diabetes mellitus. Arch Ophthalmol. 2000;118:912-917.
2. Dowler, JG, Sehmi KS, Hykin PG, et al. The natural history of macular edema after cataract surgery in diabetes. Ophthalmology. 1999;106:663-668.
3. Romero-Aroca P, Fernández-Ballarat J, Almena-Garcia M, Méndez-Marín I, Salvat-Serra M, Buil-Calvo JA. Nonproliferative diabetic retinopathy and macular edema progression after phacoemulsification: prospective study. J Cataract Refract Surg. 2006;32(9):1438-1444.
4. Squirrell D, Bhola R, Bush J, Winder S, Talbot JF. A prospective, case-controlled study of the natural history of diabetic retinopathy and maculopathy after uncomplicated phacoemulsification cataract surgery in patients with type 2 diabetics. Br J Ophthalmol. 2002;86(5):565-571.
5. Rashid S, Young LH. Progression of diabetic retinopathy and maculopathy after phacoemulsification surgery. Int Ophthalmol Clin. 2010;50(1):155-166.
6. Shah AS, Chen SH. Cataract surgery and diabetes. Curr Opin Ophthalmol. 2010;21(1):4-9.
7. Diabetes Control and Complications Trial Research Group. Early worsening of diabetic retinopathy in the diabetes control and complications trial. Arch Ophthalmol. 1998;116(7):874-886.
8. Wells JA, Glassman AR, Ayala AR, et al. Aflibercept, bevacizumab, or ranibizumab for diabetic macular edema: two year results from a comparative effectiveness randomized clinical trial. Ophthalmology. 2016;123(6):1351-1359.
9. Cetlin EN, Yildirim C. Adjuvant treatment modalities to control macular edema in diabetic patients undergoing cataract surgery. Int Ophthalmol. 2013;33(5):605-610.
10. Murtha T, Cavallerano J. The management of diabetic eye disease in the setting of cataract surgery. Curr Opin Ophthalmol. 2007;18(1):13-18.
11. Grover D, Li TJ, Chong CC. Intravitreal steroids for macular edema in diabetes. Cochrane Database Syst Rev. 2008;(1): CD005656.
12. Ahn J, Kim H, Woo SJ, et al. Pharmacokinetics of intravitreally injected Bevacizumab in vitrectomized eyes. J Ocul Pharmacol Ther. 2013;29(7):612-618.
13. Ahn, SJ, Ahn J, Park S, et al. Intraocular pharmacokinetics of Ranibizumab in vitrectomized versus nonvitrectomized eyes. Invest Ophthalmol Vis Sci. 2014;55(1):567-573.
14. Christoforidis JB, Carlton MM, Wang J, et al. Anatomic and pharmacokinetic properties of intravitreal bevacizumab and ranibizumab after vitrectomy and lensectomy. Retina. 2013;33(5):946-952.
15. Papastefanou, V. Pharmacokinetics of anti-VEGF and steroid agents in vitrectomized eyes with diabetic macular edema. Acta Ophthalmol. 2015;93. doi: 10.1111/j.1755-3768.2015.0127.
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