Cystoid Macular Edema
International Classification of Disease (ICD)
2014 ICD-9-CM 362.53 Cystoid Macular Degeneration
The American Academy of Ophthalmology Preferred Practice Patterns defines Cystoid Macular Edema (CME) as retinal thickening of the macula due to a disruption of the normal blood-retinal barrier; this causes leakage from the perifoveal retinal capillaries and accumulation of fluid within the intracellular spaces of the retina, primarily in the outer plexiform layer . Visual loss occurs from retinal thickening and fluid collection that distorts the architecture of the photoreceptors. CME is a leading cause of central vision loss in the developed world .
A delicate exchange of homeostatic mechanisms is in place with the vitreous, retina, retinal pigment epithelium (RPE), and choroid receiving their circulation through the retinal and choroidal vasculature.
A variety of risk factors may disrupt the normal interactions affecting the retinal environment. There is an intrinsic balance amongst the osmotic force, hydrostatic force, capillary permeability, and tissue compliance that occur within the vasculature . Specifically, the capillary filtration rate should equal the rate of fluid removal from extracellular retinal tissue, such as glial and RPE cells. Once these forces are disrupted an imbalance occurs and accumulation of fluid is seen in cystoid spaces within the inner layers of the retina, most commonly the outer plexiform layer (OPL). The OPL is more prone to fluid collection due to the watershed area that exists between the retinal and choroidal circulation, especially within the central retina due to its anatomical avascular zone . Accumulation of the fluid commonly occurs in the Henle’s fiber layer causing the classic petaloid pattern.
Specifically, a common factor that can cause CME is vitreomacular traction (VMT). VMT can cause stress at the Muller cell end-feet, exerting tractional forces and contributing to the release of inflammatory factors such as basic fibroblastic grown factor (bFGF), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF). This results in blood-retinal barrier breakdown from separation of the retina and RPE, lysis of muller cells, leakage and edema .
Using slit lamp or direct/indirect ophthalmoscopy, clinically significant foveal edema and retinal thickening more than 300 μm can be seen as a loss of foveal reflex; this is better visualized using green light to outline the cystic spaces. Subclinical foveal edema is described as edema less than 300 μm and is better seen through retinal imaging . Vitritis and optic nerve head swelling can also be seen in clinical examination.
Symptoms include decrease in visual acuity that is associated with retinal edema, loss of contrast sensitivity and color vision, metamorphopsia that can be demonstrated on Amsler grid, micropsia, and central scotoma. Leakage on fluorescein angiography does not seem to correlate with a decrease in visual acuity .
Diabetic macular edema (DME) is associated with leakage from microaneurysms and retinal capillaries causing circinate rings of hard exudates or lipoprotein deposits. Early Treatment Diabetic Retinopathy Study (ETDRS) defines clinically significant macular edema as:
One study indicated that 28% of aphakic eyes treated with epinephrine drops vs 13% of untreated aphakic eyes developed CME . Resolution of CME occurred with cessation of epinephrine drops.
In pars planitis, there is accumulation of T-cell inflammatory mediators such as interferon-Y, interleukin-2, interleukin-10, and tumor necrosis factor-α that has been associated with CME .
|Retinitis Pigmentosa (RP)|
Irvine-Gass is an inflammatory process occurring in up to 20% of cataract extraction with intraocular lens. 1% of these have a clinically significant decrease in visual acuity; in more complicated surgeries, such as those in which there is violation of the posterior capsule, this figure can reach 20%. CME usually occurs up to 6-10 weeks postoperatively. 95% of CME due to Irvine-Gass has been shown to resolve spontaneously within 6 months .
|E2-prostaglandin||E2-prostaglandins cause disruption of the tight junctions of the retinal capillaries.|
|Nicotinic acid and Niacin||Blurry vision associated with CME has been reported in doses greater than 1.5g/day .|
Various types of surgery can induce inflammation and alter the retinal blood flow. Treatment of CME prior to undergoing any procedures listed below can prevent the acceleration or persistence of pre-existing edema .
Risk factors that do not demonstrate leakage on FA include:
- Juvenile retinoschisis
- Goldmann-Favre disease
- certain types of RP
- Nicotinic Acid maculopathy
- antimicrotubule agents
Color Fundus Photography (CFP) depicts intraretinal cysts within the foveal region of the macula in Henle's layer (Figure 1).
Fluorescein Angiography (FA) studies the circulation of the retina and choroid. In the early phase of FA, capillary dilation in the perifoveal region is appreciated (Figure 2).
Less common but pathognomonic for CME is a smokestack pattern. FA can also show late staining of the optic disc. If leakage is elsewhere, such as in the peripheral retina or near the optic nerve, the appearance looks more honeycomb-like .
Optical Coherence Tomography (OCT) objectively obtains cross-sectional, high-resolution images of the retina. In CME, OCT can be diagnostic through measurement of the retinal thickening with depiction of the intraretinal cystic areas of low reflectivity in OPL  (Figure 4).
OCT can depict the mechanical forces induced by vitreomacular interface abnormalities, such as VMT or epiretinal membrane (ERM), via a hyperreflective band on the inner surface of the retina .
Autofluorescence (AF) depicts the health of the RPE and intraretinal cysts appear as hyperautofluorescent.
Retinal Thickness Analyzer (RTA) generates a wide 3D map of the retina.
Scanning laser ophthalmoscope (SLO) scans a small focused spot of the retina.
Therapeutic approaches, whether medical or surgical, in treating CME are dependent on the underlying etiology. Most cases are self-limiting within 3-4 months. If CME persists then medical or surgical therapy is warranted.
Medical therapy 
NSAIDS – Topical or systemic indomethacin inhibits cyclooxygenase enzyme that decreases the production of prostaglandins. Ketorolac tromethamine 0.5%, indomethacin 1%, and diclofenac 1% are used postoperatively for aphakic or pseudophakic CME .
Corticosteroids – Topical, periocular, systemic, intravitreal injection or implant corticosteroids inhibit phospholipase A2 that consequently inhibits prostaglandin and leukotriene production. Steroids specifically help in uveitic macular edema. In particular, intravitreal triamcinolone is used to visualize the posterior hyaloid to assist in surgical removal of traction. Also, intravitreal triamcinolone reduces fluid accumulation by stimulating endogenous adenosine signaling in Muller cells and decreasing VEGF production . Konstantinidis et al. demonstrated that intravitreal triamcinolone with PPV improved anatomic and visual outcome . There are currently four corticosteroid-based intravitreal implants: dexamethasone biodegradable implant, helical triamcinolone acetonide implant, fluocinolone acetonide implant, and an injectible version of the fluocinolone acetonide implant. Well-known side effects of steroid injection include glaucoma and cataract formation .
Carbonic anhydrase inhibitors (CAIs) – CAIs alter the polarity of the ionic transport systems in the RPE moving fluid away from the intracellular spaces . CAIs are helpful in paclitaxel and docetaxel induced CME  and RP induced CME .
Laser photocoagulation – Laser photocoagulation uses a light source to coagulate retinal and RPE tissue. One hypothesis to explain the effect of laser is that adjacent healthy RPE cells replace necrotic cells and reform a tight junctional retinal barrier . An alternative hypothesis depicts a reduction of oxygen consumption in the outer retina allowing diffusion of oxygen to the inner retina relieving hypoxia causing constriction of retinal vasculature and a decrease in fluid accumulation . A side effect of laser photocoagulation is scotoma that usually resolves in several weeks.
Anti-VEGF agents – Pegaptanib (anti-VEGF 165 RNA aptamer), ranibizumab (antibody fragment), and bevacizumab (full antibody) act by decreasing vascular permeability from disrupted endothelial cells. Marked reduction in retinal thickness and fluid accumulation has been noted in various studies with a significant improvement in visual acuity with minimal side effects .
Pharmacologic vitreolysis agents – Chondroitinase, dispase, hyaluronidase, plasmin, and microplasmin induce a posterior vitreous detachment to relieve VMT . Microplasmin is currently the agent that shows greatest promise with its stability, patient tolerance, and ease of storage and administration. Phase II trial has shown that a 125 μg dose repeated three times released VMT in 58% of patients one month after injection . Phase IIb trial has shown that intravitreal injection of 125 μg seven days prior to vitrectomy resolved VMT in 28% of patients . Phase III trial has shown that intravitreal injection of 125 μg for treatment of VMT associated with subjective visual dysfunction showed improvement of the adhesion .
PPV can help to relieve macula edema through tractional or nontractional components, especially when refractory to medical therapy. The Vitrectomy-Aphakic-Cystoid Macular Edema Study, a prospective, multicenter study of patients with chronic aphakic CME, showed statistically significant improvement in visual outcomes following vitrectomy .
Tractional components can be addressed by releasing the posterior hyaloid in VMT or conducting an internal limiting membrane peel of an ERM. Specifically, PPV for the tractional component of VMT causing CME secondary to diabetes has been shown to improve macular edema in 80-92% of patients . Harbour et al. demonstrated that vitrectomy done on vitreous incarceration in the anterior segment and pseudophakic macular edema resulted in improvement in visual acuity in all patients . Though internal limiting membrane peeling in CME secondary to diabetes, central retinal vein occlusion (CRVO), uveitic macular edema, and RP has shown anatomical improvement, visual acuity results are inconclusive . Neodymium yttrium aluminum garnet (Nd:YAG) laser can also help to relieve tractional components, such as vitreous adhesions to iris.
Nontractional components are addressed by theoretically clearing the inflammatory factors when undergoing PPV . However, one study has shown that high vitreous levels of VEGF in CRVO patients correlated with less improvement in visual acuity after vitrectomy, suggesting that high VEGF levels may be associated with ischemia and permanent photoreceptor damage . However, one study showed an increase in VEGF levels in branch retinal vein occlusion (BRVO) patients correlated with an improvement in visual acuity after vitrectomy . Furthermore, studies have shown that oxygen in the posterior segment and the rate of oxygen exchange in the vitreal cavity is increased after PPV . Specifically, PPV for nontractional components causing CME secondary to diabetes and uveitic macular edema has resulted in inconclusive data on improvement in visual acuity . Pendergast et al. demonstrated that vitrectomy in pseudophakic CME without any tractional component showed an improvement in visual acuity .
Side effects of vitrectomy include cataract, retinal detachment, vitreous hemorrhage, and a rise in intraocular pressure.
CME is usually self-limiting and spontaneously resolves within 3-4 months. Depending on the etiology, resolution of the edema may be helped via medical or surgical options. If the edema is chronic (more than 6-9 months) permanent damage to the photoreceptors with retinal thinning and fibrosis can occur .
- ↑ Gass JD, Norton EW. Follow-up study of cystoid macular edema following cataract extraction.Trans Am Acad Ophthalmol Otolaryngol. 1969;73:665-682.
- ↑ Hogan P, Dall T, Nikolov P. American Diabetes Association: Economic costs of diabetes in the US in 2002. Diabetes Care. 2003;26:917-932.
- ↑ Scholl S, Kirchhof J, Augustin AJ. Pathophysiology of macular edema. Ophthalmologica. 2010;224:8-15.
- ↑ Bringmann A, Reichenbach A, Wiedemann P. Pathomechanisms of cystoid macular edema. Ophthalmic Res. 2004;36:241-249.
- ↑ Scholl S, Augustin A, Loewenstein A, et al. General pathophysiology of macular edema. Eur J Ophthalmol. 2010;21:10-19.
- ↑ Jampol LM. Niacin maculopathy. Ophthalmology. 1988;95:1704-1705.
- ↑ Lindqvist N, Liu Q, Zajadacz J, et al. Retinal glial (Muller) cells: sensing and responding to tissue stretch. Invest Ophthalmol Vis Sci. 2010;51:1683-1690.
- ↑ Augustin A, Loewenstein A, Kuppermann BD. Macular edema. General pathophysiology. Dev Ophthalmol. 2010;47:10-26.
- ↑ Praidou A, Klangas I, Papakonstantinou E, et al. Vitreous and serum levels of platelet-derived growth factor and their correlation in patients with proliferative diabetic retinopathy. Curr Eye Res. 2009;34:152-161.
- ↑ 10.0 10.1 Staurenghi G, Invernizzi A, de Polo L, et al. Macular edema. Diagnosis and detection. Dev Ophthalmol. 2010;47:27-48.
- ↑ Nussenblatt RB, Kaufman SC, Palestine AG, et al. Macular thickening and visual acuity. Measurement in patients with cystoid macular edema. Ophthalmology. 1987;94:1134-1139.
- ↑ Kearns TP, Hollenhurst RW. Venous-stasis retinopathy of occlusive disease of the carotid artery. Mayo Clin Proc. 1963;38:304-312.
- ↑ Sturrock GD, Mueller HR. Chronic ocular ischaemia. Br J Ophthalmol. 1990;13:187-191.
- ↑ Sharma S, Brown GC. Ocular ischemic syndrome. In: Ryan SJ, ed. Retina. 4th ed. St Louis, MO: Mosby;2005:1483-1502.
- ↑ Sivalingam A, Brown GC, Magargal LE, et al. The ocular ischemic syndrome. II. Mortality and systemic morbidity. Int Ophthalmol. 1989;13:187-191.
- ↑ Shelsta HN, Jampol LM. Pharmacologic therapy of pseudophakic cystoid macular edema: 2010 update. Retina. 2011;31(1):4-12. Review.
- ↑ Early Treatment Diabetic Retinopathy Study Research Group. Photocoagulation for diabetic macular edema. Early Treatment Diabetic Retinopathy Study report no 1. Arch Ophthalmol. 1985;103:1796–1806.
- ↑ Thomas JV, Gragoudas ES, Blair NP, et al. Correlation of epinephrine use and macular edema in aphakic glaucomatous eyes. Arch Ophthalmol. 1978;96:625-628.
- ↑ Wakefield D, Lloyd A. The role of cytokines in the pathogenesis of inflammatory eye disease. Cytokine. 1992;4:1–5.
- ↑ Wright PL, Wilkinson CP, Balyeat HD, et al. Angiographic cystoid macular edema after posterior chamber lens implantation. Arch Ophthalmol. 1988;106:740-744.
- ↑ Ursell PG, Spalton DJ, Whitcup SM, et al. Cystoid macular edema after phacoemulsification: relationship to blood-aqueous barrier damage and visual acuity. J Cataract Refract Surg. 1999;25:1492-1497.
- ↑ 22.0 22.1 Ray S, D’Amico DJ. Pseudophakic cystoid macular edema. Semin Ophthalmol. 2002;17:167-180.
- ↑ Bradford JD, Wilkinson CP, Bradford RH, et al. Cystoid macular edema following extracapsular cataract extraction and posterior chamber intraocular lens implantation. Retina. 1988;8:161–164.
- ↑ Fraunfelder FW, Fraunfelder FT, Illingworth DR. Adverse ocular effects associated with niacin therapy. Br J Ophthalmol. 1995;79:54-56.
- ↑ Dowler JG, Sehmi KS, Hykin PG, et al. The natural history of macular edema after cataract surgery in diabetes. Ophthalmology. 1999;106:663–668.
- ↑ Shetty N. Cystoid macular edema. Atlas of fundus fluorescein angiography. New York, Informa Healthcare. 2004;130–4.
- ↑ Kim BY, Smith SD, Kaiser PK. Optical coherence tomographic patterns of diabetic macular edema. Am J Ophthalmol. 2006;142:405-412.
- ↑ Mavrofrides EC, Cruz-Villegas V, Puliafito CA. Miscellaneous retinal diseases. In: Schuman JS, Puliafito CA, Fujimoto JG, eds. Optical coherence tomography of ocular diseases. Thorofare, NJ: SLACK, Inc. 2004:457-482.
- ↑ Kim SJ, Bressler NM. Optical coherence tomography and cataract surgery. Curr Opin Ophthalmol. 2009;20(1):46-51. Review.
- ↑ Baskin DE. Optical coherence tomography in diabetic macular edema. Curr Opin Ophthalmol. 2010;21:172-177.
- ↑ Williamson TH, Grewal J, Gupta B, et al. Measurement of PO2 during vitrectomy for central retinal vein occlusion, a pilot study. Graefes Arch Clin Exp Ophthalmol. 2009;247:1019-1023.
- ↑ Flach AJ, Jampol LM, Weinberg D, et al. Improvement in visual acuity in chronic aphakic and pseudophakic cystoid macular edema after treatment with topical 0.5% ketorolac tromethamine.Am J Ophthalmol. 1991;112:514-519.
- ↑ Burnett J, Tessler H, Isenberg S, et al. Double-masked trial of fenoprofen sodium: treatment of chronic aphakic cystoid macular edema. Ophthalmic Surg. 1983;14:150–152.
- ↑ Reichenbach A, Wurm A, Pannicke T, et al. Muller cells as players in retinal degeneration and edema. Graefes Arch Clin Exp Ophthalmol. 2007;245:627-636.
- ↑ Zhang X, Bao S, Lai D, et al. Intravitreal triamcinolone acetonide inhibits breakdown of the blood-retinal barrier through differential regulation of VEGF-A and its receptors in early diabetic rat retinas. Diabetes. 2008;57:1026-1033.
- ↑ Konstantinidis L, Berguiga M, Beknazar E, et al. Anatomic and functional outcome after 23-gauge vitrectomy, peeling, and intravitreal triamcinolone for idiopathic macular epiretinal membrane. Retina. 2009;29:1119-1127.
- ↑ Loewenstein A, Goldstein M. Intravitreal triamcinolone acetonide for diabetic macula edema. Isr Med Assoc J. 2006;8:426–427.
- ↑ Cox SN, Hay E, Bird AC. Treatment of chronic macular edema with acetazolamide. Arch Ophthalmol. 1988;106:1190-1195.
- ↑ Joshi MM, Garretson B. Paclitaxel retinopathy. Arch Ophthalmol. 2007;125:709-710.
- ↑ Telender DG, Sarraf D. Cystoid macular edema with Docetaxel chemotherapy and the fluid retention syndrome. Semin Ophthalmol. 2007;22:151-153.
- ↑ Fishman GA, Gilbert LD, Fiscella RG, et al. Acetazolamide for treatment of chronic macular edema in retinitis pigmentosa. Arch Ophthalmol. 1989;107:1445–1452.
- ↑ Androudi S, Letko E, Meniconi M, et al. Safety and efficacy of intravitreal triamcinolone acetonide for uveitic macular edema. Ocul Immunol Inflamm. 2005;13:205–212.
- ↑ Molnar I, Poitry S, Tsacopoulos M, et al. Effect of laser photocoagulation on oxygenation of the retina in miniature pigs. Invest Ophthalmol Vis Sci. 1985;26:1410–1414.
- ↑ Iturralde D, Spaide RF, Meyerle CB, et al. Intravitreal bevacizumab (Avastin) treatment of macular edema in central retinal vein occlusion: a short-term study. Retina. 2006;26:279–284.
- ↑ Moschos MM, Moschos MN. Intraocular bevacizumab for macular edema due to CRVO. A multlifocal-ERG and OCT study. Doc Ophthalmol. 2008;116:147–152.
- ↑ Rotsos TG, Moschos MM. Cystoid macular edema. Clin Ophthalmol. 2008;2(4):919-930.
- ↑ Falavarjani KG, Parvaresh MM, Modarres M, et al. Intravitreal bevacizumab for pseudophakic cystoid macular edema: a systematic review. J Ophthalmic Vis Res. 2012;7(3):235-239.
- ↑ Waheed NK, Duker JS. OCT in the management of diabetic macular edema. Curr Ophthalmol Rep. 2013;1:128-133.
- ↑ Gandorfer A, Ulbig M, Kampik A. Plasmin-assisted vitrectomy eliminates cortical vitreous remnants. Eye (Lond). 2002;16:95-97.
- ↑ Sakuma T, Mizota A, Inoue J, et al. Intravitreal injection of autologous plasmin enzyme for macular edema associated with branch retinal vein occlusion. Am J Ophthalmol. 2010;150:876-882.
- ↑ Udaondo P, Diaz-Llopis M, Garcia-Delpech S, et al. Intravitreal plasmin without vitrectomy for macular edema secondary to branch retinal vein occlusion. Arch Ophthalmol. 2011;129:283-287.
- ↑ Sakuma T, Tanaka M, Inoue J, et al. Use of autologous plasmin during vitrectomy for diabetic maculopathy. Eur J Ophthalmol. 2006;16:138-140.
- ↑ Rheaume MA, Vavvas D. Pharmacologic vitreolysis. Semin Ophthalmol. 2010;25:295-302.
- ↑ de Smet MD, Gandorfer A, Stalmans P, et al. Microplasmin intravitreal administration in patients with vitreomacular traction scheduled for vitrectomy: the MIVI I trial. Ophthalmology. 2009;116:1349-1355.
- ↑ Stalmans P, Delaey C, de Smet MD, et al. Intravitreal injection of microplasmin for treatment of vitreomacular adhesion: results of a prospective, randomized, sham-controlled phase II trial (the MIVI-IIT trial). Retina. 2010;30:1122-1127.
- ↑ Benz MS, Packo KH, Gonzalez V, et al. A placebo-controlled trial of microplasmin intravitreous injection to facilitate posterior vitreous detachment before vitrectomy. Ophthalmology. 2010;117:791-797.
- ↑ Dugel PU, Group M-TS. A single injection of microplasmic for the treatment of symptomatic vitreomacular adhesion (sVMA): results of the Phase III MIVI-TRUST Program [abstract]. Invest Ophthalmol Vis Sci (suppl.). 2011;52:6628.
- ↑ Fung WE. Vitrectomy for chronic aphakic cystoid macular edema. Results of a national, collaborative, prospective, randomized investigation. Ophthalmology. 1985;92:1102–1111.
- ↑ Lewis H, Abrams GW, Blumenkranz MS, et al. Vitrectomy for diabetic macular traction and edema associated with posterior hyaloidal traction. Ophthalmology. 1992;99:753-759.
- ↑ Pendergast SD, Hassan TS, Williams GA, et al. Vitrectomy for diffuse diabetic macular edema associated with a taut premacular posterior hyaloid. Am J Ophthalmol. 2000;130:178-186.
- ↑ Harbour JW, Smiddy WE, Rubsamen PE, et al. Pars plana vitrectomy for chronic pseudophakic cystoid macular edema. Am J Ophthalmol. 1995;120:302-307.
- ↑ Stolba U, Binder S, Gruber D, et al. Vitrectomy for persistent diffuse diabetic macular edema. Am J Ophthalmol. 2005;140:295-301.
- ↑ Stefaniotou M, Aspiotis M, Kalogeropoulos C, et al. Vitrectomy results for diffuse diabetic macular edema with and without inner limiting membrane removal. Eur J Ophthalmol. 2004;14:137-143.
- ↑ Bahadir M, Ertan A, Mertoglu O. Visual acuity comparison of vitrectomy with and without internal limiting membrane removal in the treatment of diabetic macular edema. Int Ophthalmol. 2005;26:3-8.
- ↑ Patel JI, Hykin PG, Schadt M, et al. Pars plana vitrectomy with and without peeling of the inner limiting membrane for diabetic macular edema. Retina. 2006;26:5-13.
- ↑ Kumar A, Sinha S, Azad R, et al. Comparative evaluation of vitrectomy and dye-enhanced ILM peel with grid laser in diffuse diabetic macular edema. Graefes Arch Clin Exp Ophthalmol. 2007;245:360-368.
- ↑ Gentile RC, Milman T, Eliott D, et a.: Taut internal limiting membrane causing diffuse diabetic macular edema after vitrectomy: clinicopathological correlation. Ophthalmologica. 2011;226:64-70.
- ↑ Hoerauf H, Bruggemann A, Muecke M, et al. Pars plana vitrectomy for diabetic macular edema. Internal limiting membrane delamination vs posterior hyaloid removal. A prospective randomized trial. Graefes Arch Clin Exp Ophthalmol. 2011;249:997-1008.
- ↑ DeCroos FC, Shuler Jr RK, Stinnett S, et al. Pars plana vitrectomy, internal limiting membrane peeling, and panretinal endophotocoagulation for macular edema secondary to central retinal vein occlusion. Am J Ophthalmol. 2009;147:627-633.
- ↑ Schaal S, Tezel TH, Kaplan HJ. Surgical intervention in refractory CME – role of posterior hyaloid separation and internal limiting membrane peeling. Ocul Immunol Inflamm. 2008;16:209-210.
- ↑ Gutfleisch M, Spital G, Mingels A, et al. Pars plana vitrectomy with intravitreal triamcinolone: effect on uveitic cystoid macular oedema and treatment limitations. Br J Ophthalmol. 2007;91:345-348.
- ↑ Garcia-Arumi J, Martinez V, Sararols L, et al. Vitreoretinal surgery for cystoid macular edema associated with retinitis pigmentosa. Ophthalmology. 2003;110:1164-1169.
- ↑ Hagiwara A, Yamamoto S, Ogata K, et al. Macular abnormalities in patients with retinitis pigmentosa: prevalence on OCT examination and outcomes of vitreoretinal surgery. Acta Ophthalmol. 2011;89:122-125.
- ↑ Noma H, Funatsu H, Mimura T, et al. Pigment epithelium-derived factor and vascular endothelial growth factor in branch retinal vein occlusion with macular edema. Graefes Arch Clin Exp Ophthalmol. 2010;248:1559-1565.
- ↑ Matsunaga N, Chikaraishi Y, Izuta H, et al. Role of soluble vascular endothelial growth factor receptor-1 in the vitreous in proliferative diabetic retinopathy. Ophthalmology. 2008;115:1916-1922.
- ↑ Noma H, Funatsu H, Mimura T, et al. Visual acuity and foveal thickness after vitrectomy for macular edema. Ophthalmologica. 2010;224:367-373.
- ↑ Yamasaki M, Noma H, Funatsu H, et al. Changes in foveal thickness after vitrectomy for macular edema with branch retinal vein occlusion and intravitreal vascular endothelial growth factor. Int Ophthalmol. 2009;29:161-167.
- ↑ Williamson TH, Grewal J, Gupta B, et al. Measurement of PO2 during vitrectomy for central retinal vein occlusion, a pilot study. Graefes Arch Clin Exp Ophthalmol. 2009;247:1019-1023.
- ↑ Stefansson E, Novack RL, Hatchell DL. Vitrectomy prevents retinal hypoxia in branch retinal vein occlusion. Invest Ophthalmol Vis Sci. 1990;31:284-289.
- ↑ Holekamp NM, Shui YB, Beebe DC. Vitrectomy surgery increases oxygen exposure to the lens: a possible mechanism for nuclear cataract formation. Am J Ophthalmol. 2005;139:302-310.
- ↑ Siegfried CJ, Shui YB, Holekamp NM, et al. Oxygen distribution in the human eye: relevance to the etiology of open-angle glaucoma after vitrectomy. Invest Ophthalmol Vis Sci. 2010;51:5731-5738.
- ↑ Giblin FJ, Quiram PA, Leverenz VR, et al. Enzyme-induced posterior vitreous detachment in the rat produces increased lens nuclear pO2 levels. Exp Eye Res. 2009;88:286-292.
- ↑ Quiram PA, Leverenz VR, Baker RM, et al. Microplasmin-induced posterior vitreous detachment affects vitreous oxygen levels. Retina. 2007;27:1090-1096.
- ↑ Massin P, Duguid G, Erginay A, et al. Optical coherence tomography for evaluating diabetic macular edema before and after vitrectomy. Am J Ophthalmol. 2003;135:169-177.
- ↑ Bandello F, Battaglia Parodi M, Lanzetta P, et al. Diabetic macular edema. Dev Ophthalmol. 2010;47:73-110.
- ↑ Haller JA, Qin H, Apte RS, et al. Vitrectomy outcomes in eyes with diabetic macular edema and vitreomacular traction. Ophthalmology. 2010;117:1087-1093.
- ↑ Kiryu J, Kita M, Tanabe T, et al. Pars plana vitrectomy for cystoid macular edema secondary to sarcoid uveitis. Ophthalmology. 2001;108:1140-1144.
- ↑ Wiechens B, Reichelt JA, Urbat C, et al. Pars plana vitrectomy in cystoid macular edema of different forms of chronic uveitis. Ophthalmology. 2003;100:33-43.
- ↑ Stavrou P, Baltatzis S, Letko E, et al. Pars plana vitrectomy in patients with intermediate uveitis. Ocul Immunol Inflamm. 2001;9:141-151.
- ↑ Pendergast SD, Margherio RR, Williams GA, et al. Vitrectomy for chronic pseudophakic cystoid macular edema. Am J Ophthalmol. 1999;128:317-323.
- ↑ Guex-Crosier Y. The pathogenesis and clinical presentation of macular edema in inflammatory diseases. Doc Ophthalmol. 1999;97:297–309.
- ↑ Henderly DE, Genstler AJ, Rao NA, et al. Pars planitis. Trans Ophthalmol Soc UK. 1986;105:227–232.
- ↑ Henderly DE, Haymond RS, Rao NA, et al. The significance of the pars plana exudates in pars planitis. Am J Ophthalmol. 1987;103:669–671.
- ↑ Agarwal A. Gass’ Atlas of Macular Diseases. 5th ed. Waltham, MA: Elsevier Inc;2012:500-508.