Treating inflammation after lens surgery

Cataract surgery is, with more than 20 to 25 million procedures estimated annually, the most performed surgical intervention worldwide. Due to the invasive nature of modern cataract surgery 2 outcomes are common: infection and intraocular inflammation.1 Infection, while an area of great concern and somewhat controversial in the ways to prevent it, is a long discussion delving into topics such as intracameral and postoperative care2 and as such is not the topic of this editorial. Intraocular inflammation occurs due to the breakdown of cell membranes as a result of tissue injury. In effect, an inflammatory cascade occurs that involves the step-by-step enzymatic conversion of cell membrane phospholipids to bioactive prostaglandin molecules. First, surgical trauma activates phospholipase A2, which releases arachidonic acid from the membrane phospholipids (fats that form the lipid bilayer). Arachidonic acid is then metabolized by cyclooxygenases (COX-1 and COX-2) into unstable endoperoxide intermediates (prostaglandin G2 and prostaglanden H2). This ultimately leads to the formation of prostaglandins. Prostaglandin H2 is then isomerized into different prostanoids.3 All of this leads to local vasodilation and increased vascular permeability. This results in a number of symptoms including hyperemia, miosis, pain, photophobia, diminished visual acuity, and cystoid macular edema.1 Inflammation is classically treated with steroids as well as with nonsteroidal antiinflammatory drugs (NSAIDs).4 Nonsteroidal antiinflammatory drugs, in particular, reduce inflammation and pain by blocking prostaglandin synthesis by inhibiting COX activity.5 Treatment using topical NSAIDs after cataract surgery began in the 1970s,6 and studies have shown that they offer efficacy comparable to steroids in reducing postoperative inflammation but with a lower risk for adverse events in most patients.1 Nonsteroidal antiinflammatory drugs play a number of important roles in postoperative care including the management of postoperative inflammation as well as macular leakage7 and a reduction in pain, photophobia, and intraoperative miosis. However, the development of topical formulations has been problematic due to the acidic nature of NSAIDs which can lead to ocular irritation.4 As a result, continued research into the efficacy and optimum use of the current formulations available on the market is required. In this issue Sahu et al. do just that (pages 2043–2048); they report on the effect of topical ketorolac 0.4%, nepafenac 0.1%, and bromfenac 0.09%, all commonly used topical NSAIDs, on postoperative inflammation in patients after phacoemulsification surgery. The outcomes indicate that all the formulations are effective, but nepafenac was shown to be significantly more effective in terms of anterior chamber flare reduction. This supports previous research by Modi et al.8 showing that nepafenac 0.3% instilled once daily was as effective as nepafenac 0.1% instilled 3 times daily in postoperative treatment of ocular inflammation and pain. The research suggests that postoperative inflammation could be treated with 1 drop a day after surgery, which is very convenient for both patients and doctors.8 Further research is required to determine the effects of this treatment, particularly in relation to its use with steroids, as the standard treatment protocol. The question remains—do we still need steroids in small-incision fast–rehabilitation cataract and refractive lens surgery with their associated higher level of side effects, or can their use be abandoned in favor of NSAIDs?