Cystoid macular edema – eyewiki electricity outage sacramento


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 [1]. 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 [2].

A variety of risk factors may disrupt the normal interactions affecting the gas in california retinal environment. There is an intrinsic balance amongst the osmotic force, hydrostatic force, capillary permeability, and tissue compliance that occur within the vasculature [3] [4]. 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 gas finder map between the retinal and choroidal circulation, especially within the central retina due to its anatomical avascular zone [5]. 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 [6] [7] [8] [9]. However, typically CME associated with VMT does not demonstrate leak on FFA.

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 gas finder is better seen through retinal imaging [10]. Vitritis and optic nerve head swelling can also be seen in clinical examination.

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 [22] [23] [24] [25].

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. Intravitreal triamcinolone reduces fluid accumulation by stimulating endogenous adenosine signaling in Muller cells and decreasing VEGF production [36] [37]. 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 [38]. Triamcinolone acetonide can be given through various routes in CME- intravitreal, subtenon, peribulbar/trans-septal/orbital floor.

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 [43] [44] [45] [46] [47].

Pharmacologic vitreolysis agents – Chondroitinase, dispase, hyaluronidase, plasmin, and microplasmin induce a posterior vitreous detachment to relieve CME from VMT [48] [49] [50] [51]. Microplasmin is currently the agent that shows greatest promise with its stability, patient tolerance, and ease of storage and administration gas pain. Phase II trial has shown that a 125 μg dose repeated three times released VMT in 58% of patients one month after injection [52] [53] [54]. Phase IIb trial has shown that intravitreal injection of 125 μg seven days prior to vitrectomy resolved VMT in 28% of patients [55]. 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 [56].

PPV can help to relieve macula edema due to 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 [57].

Tractional components can be addressed by releasing the posterior hyaloid in VMT or conducting an internal limiting membrane peel gas tax 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 [58] [59]. 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 [60]. 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 [61] [62] [63] [64] [65] [66] [67] [68] [69] [70] [71] [72]. 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 [73] [74]. 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 [75]. 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 [76]. Furthermore, studies have shown that oxygen in the posterior segment and the rate of oxygen exchange in the vitreal cavity is increased after PPV [77] [78] [79] [80] [81] [82]. Specifically, PPV for nontractional components causing CME secondary to diabetes and uveitic macular edema has resulted in inconclusive data on improvement in visual acuity [83] [84] [85] [86] [87] [88]. Pendergast et al. demonstrated that vitrectomy in pseudophakic CME without any tractional component showed an improvement in visual acuity [89].

• ↑ Tripathy, Koushik, Rohan Chawla, Pradeep Venkatesh, Rajpal Vohra, Yog Raj Sharma, Varun Gogia, Shreyans Jain, and Alkananda gas efficient cars 2012 Behera. “Ultra-Wide Field Fluorescein Angiography in Retinitis Pigmentosa with Intermediate Uveitis.” Journal of Ophthalmic Vision Research 11, no. 2 (June 2016): 237–39.