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Current Use of Non-steroidal Anti-inflammatory Drugs in the Treatment of Ocular Inflammation Related to Cataract Surgery

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Published Online: May 22nd 2012 European Ophthalmic Review, 2012;6(3):173–7 DOI:
Authors: Eric D Donnenfeld
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Ocular inflammation and pain are a common consequence of cataract surgery, and if left untreated, may lead to extensive ocular damage, resulting in impaired vision as well as decreased satisfaction with the procedure. Effective management of ophthalmic inflammation after surgery is therefore vital. Topical ophthalmic non-steroidal anti-inflammatory drugs (NSAIDs) have become a mainstay of management of ocular pain and inflammation as a result of their anti-inflammatory activity, analgesic property and established safety record. Numerous studies have demonstrated the efficacy of topical NSAIDs in post-operative prevention of ocular inflammation, inhibition of intra-operative miosis, reduction of pain associated with cataract surgery and pre-operative use to prevent cystoid macular oedema. Studies have also indicated that NSAIDs and steroids act synergistically when administered together, and that a combination of steroid and NSAID therapy is recommended to achieve successful outcomes. With appropriate administration, NSAIDs are safe and effective therapeutic agents, which rarely result in serious local and systemic responses.


Cataract surgery, cystoid macula oedema, miosis, non-steroidal anti-inflammatory drugs


Cataract surgery is an invasive procedure involving an incision and manipulation of ocular tissue, leading to intraocular inflammation. The latter is characterised by redness, swelling, and/or pain. Inflammation arises from the release of prostaglandins (PGs). Activation of phospholipase A2, following tissue injury during surgery, breaks down cell membrane phospholipids to arachidonic acid. This is then converted to PGs by activation of cyclo-oxygenase (COX) enzymes via the COX-1 and COX-2 pathways. Production of PGs causes local vasodilation and increased vascular permeability resulting in a number of symptoms including hyperaemia, miosis, pain, photophobia and diminished visual acuity secondary to cystoid macular oedema (CMO) – the most common complication of cataract surgery and potentially the most adverse ocular outcome of PG production.1

Two agents are primarily employed for the reduction of intraocular inflammation: non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids. NSAIDs are potent inhibitors of cyclo-oxygenase enzymes and hence of PG synthesis. Together with corticosteroids, they act on the COX-1 and COX-2 pathways. While corticosteroids inhibit phospholipase A2, preventing arachidonic acid release from phospholipids, NSAIDs act downstream and more specifically in the cascade by direct inhibition of COX-1 and COX-2 enzymes (see Figure 1).2 Post-operative ocular inflammation is a complex condition owing to the diverse types of tissues that may be affected, including the conjunctiva, retina, sclera, aqueous and vitreous humour, cornea, iris, ciliary body, choroid and retina.3

Corticosteroids have a long history of use in the management of ocular inflammation but their efficacy is tempered by serious adverse effects including impairment of wound healing, elevation of intraocular pressure (IOP), progression of cataracts, increased susceptibility to microbial infections owing to a suppressed host immune response, delayed corneal epithelial and stromal wound healing, and safety issues associated with long-term use including glaucoma.1

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Article Information:

The author has no conflicts of interest to declare.


Eric Donnenfeld, Ophthalmic Consultants of Long Island, 2000 North Village Avenue, Suite 402, Rockville Centre, NY 11570, US. E:


The publication of this article was funded by Alcon. The views and opinions expressed are those of the author and not necessarily those of Alcon.




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