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Pathogenesis of Pseudophakic Cystoid Macular Oedema

Published Online: May 22nd 2012 European Ophthalmic Review, 2012;6(3):178 –84 DOI: http://doi.org/10.17925/EOR.2012.06.03.178
Authors: Conceição Lobo
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Abstract:
Overview

Cystoid macular oedema (CMO) is a primary cause of reduced vision after cataract surgery even after uneventful surgery. The incidence of clinical CMO following modern cataract surgery is 1.0–2.0 % but the high number of surgeries performed worldwide makes this entity an important problem. Pre-existing conditions such as diabetes and intra-operative complications increase the risk of developing CMO post-operatively. CMO is caused by an accumulation of intra-retinal fluid in the outer plexiform and inner nuclear layers of the retina, as a result of the breakdown of the blood–retinal barrier. The mechanisms that lead to this condition are not completely understood. However, the principal hypothesis is that the surgical procedure is responsible for the release of inflammatory mediators, such as prostaglandins. Optical coherence tomography is at present an extremely useful non-invasive diagnostic tool. Guidelines for the management CMO should be focused essentially on prevention and are based on the principal pathogenetic mechanisms, including the use of anti-inflammatory drugs.

Keywords

Cataract surgery, cystoid macular oedema, pathogenesis, inflammatory mediators, anti-inflammatory drugs, management

Article:

Modern cataract extraction using phacoemulsification and posterior intraocular lens (IOL) implantation is one surgical procedure considered extremely safe and successful.1,2 The constant innovations in instrumentation, lens design and surgical technique lead to improved outcomes following this surgery.3,4 Although the procedure is efficient, and uneventful surgery is generally associated with good visual results,1,2,5 complications, as cystoid macular oedema (CMO) may develop, and this can result in sub-optimal post-operative vision.6–8 It can occur after uncomplicated surgery in patients with otherwise healthy eyes, after complicated surgery, or after surgery in patients with ocular diseases such as uveitis or diabetic retinopathy.9

CMO following cataract surgery was an entity reported first time by Irvine in 1953. Thirteen years later, Gass and Norton demonstrated its typical presentation using fluorescein angiography (FA); therefore, it is known as Irvine–Gass syndrome.10–12

The pathogenesis of CMO following cataract surgery remains uncertain, but clinical observations and experimental studies indicate that the pathophysiology of this post-operative problem may be multifactorial.13,14 Prostaglandin-mediated inflammation7,14–20 and the subsequent breakdown of the blood–aqueous barrier (BAB) and blood–retinal barrier (BRB) are probably the more important facts involved.21–26

Clinical CMO is diagnosed in those patients who have detectable visual impairment as well as angiographic and/or biomicroscopic findings. Some patients who are asymptomatic with respect to visual acuity, but have detectable leakage from the perifoveal capillaries on FA, are diagnosed as angiographic CMO. Optical coherence tomography (OCT) confirms the clinical diagnosis. So, the incidence of pseudophakic CMO depends not only on the surgical technique or pre-existing conditions, but also on the methodology used in its detection. The actual guidelines recommend the use of non-steroidal anti-inflammatory drugs (NSAIDs) pre-operatively, and the combination of steroids and NSAIDs in the post-operative period, to reduce the incidence of pseudophakic CMO.

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Disclosure

The author has no conflict of interest to declare.

Correspondence

Conceição Lobo, Association for Innovation and Biomedical Research on Light and Image, Azinhaga de Santa Comba, Celas, 3000-548 Coimbra, Portugal. E: clobofonseca@gmail.com

Received

2011-10-07T00:00:00

References

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