Rebound Iritis following Cataract Surgery
Rebound Iritis is described as inflammation of the anterior uveal tract. It is marked by the presence of leukocytes in the anterior chamber (AC) of the eye occurring after initiation of steroid taper regimens in the post-operative period following cataract surgery. Following cataract surgery, inflammation of the surrounding structures can result from the breakdown of the blood-aqueous barrier. Inflammation can be poorly controlled or can “rebound” during the steroid taper, leading to infiltration of cells into the AC accompanied by an acute flare of anterior uveitis.
“Rebound” Iritis following cataract surgery with steroid tapering regimens can be classified as a rare form of acute traumatic anterior uveitis.
Rebound Iritis is described as inflammation of the anterior uveal tract and is marked by the presence of leukocytes in the anterior chamber (AC) of the eye occurring after initiation of steroid taper regimens in the post-operative period following cataract surgery. Iritis is synonymous to anterior uveitis. Following cataract surgery, inflammation of the surrounding structures can result from the breakdown of the blood-aqueous barrier. Following breakage, white blood cells, inflammatory mediators, and/or other blood contents enter the eye and can lead to the development of an inflammatory state (1). This process typically peaks within the first week following cataract extraction and will slowly decrease back to normal levels after 2-3 weeks (2). Typically, the post-operative inflammation is well-controlled with steroid tapering regimens while the eye is still recovering. However, inflammation can be poorly controlled or can “rebound” during the steroid taper, leading to infiltration of cells into the AC accompanied by an acute flare of anterior uveitis.
The cause of rebound iritis following cataract surgery involves improper control of a newly imposed inflammatory state in the eye following trauma from the surgery itself. Specific causes include:
• Lack of proper post-operative anti-inflammatory medication adherence
• Improper response of the eye itself to standard tapering mechanism
• Lens material lodging in the anterior angle chamber, promoting both inflammation and potentially precipitating secondary glaucoma
Rebound Iritis following cataract surgery, while uncommon, is an important consideration in a country where more than 1 million cataracts are repaired annually. In one study, the overall incidence of post-operative iritis specifically was 1.20% with the exclusion of patients with prior ocular inflammation or pre-existing systemic inflammatory or autoimmune diagnosis (3). The incidence was higher in patients of African American descent (3). Other risk factors included diabetes and the use of pupil expansion device during surgery (3). Overall, the incidence of iritis is approximately 12 per 100,000 in the U.S (4). Iritis is by far the most common form of uveitis, comprising approximately 90% of all uveitis cases (5). In broad terms of uveitis, post-procedural uveitis encompasses 10% of total cases, with 48.7% of those specifically following cataract extraction and IOL (intraocular lens) implantation (6).
The promotion of inflammation following cataract surgery is a well-documented phenomenon that can lead to rebound iritis, among other more common complications including pseudophakic cystoid macular edema (PCME). Control of inflammation is largely well-controlled with topical steroid tapers and NSAIDs (nonsteroidal anti-inflammatory drugs), with most of the inflammatory process largely resolved after 1 month (3). Several studies have been performed to assess best specific treatment modality to prevent rebound, but current literature promotes steroid regimens (prednisolone acetate, difluprednate) alone or in combination with NSAIDs (Ketorolac or nepafenac commonly) as adequate measures of prophylactic inflammatory control (7-10). Other methods of inflammatory control in patients that are non-compliant or have potential loss to follow-up can include newer intracameral AC steroid and NSAID suspension delivery systems, which have been found to have similar safety and efficacy profiles when compared to standard steroid tapers while removing the burden of topical treatment options (11, 12).
Acute anterior uveitis from trauma following surgery will most likely be unilateral but can also occur bilaterally (13). Patients can present with a variety of symptoms including:
• Persistent redness of eye(s), characteristically noted at the limbus (circumlimbal)
• Complaints of visual change (blurry vision)
• Eye pain, more specific to acute anterior uveitis
Anterior uveitis can be confirmed via slit lamp examination (SLE). SLE will reveal leukocytes in the anterior chamber (diagnostic) with or without associated flare in patients with anterior uveitis. Patients may also have miosis secondary to iris sphincter spasm and altered IOP (decreased more commonly). Assessment of proper lens placement is also an important consideration. Dilated fundus examination is essential to assess for findings suggestive of panuveitis or posterior uveitis, including vitreous cell and/or chorioretinal inflammation, typically not seen in isolated anterior uveitis (14).
Patients with iritis closely following cataract surgery, especially within the first few months post-operatively, are very likely suspects of rebound inflammation as the causative factor. It is imperative to get a full history and to assess patients’ understanding of current or past eye drop regimen(s) in the post-operative period. Although not always the case, it is possible that the patient has not been following regimens as initially prescribed or intended. This may be due to multiple causes including negligence, misunderstanding and/or improper use, not shaking prednisolone acetate suspension drop before use, and lack of availability. In one study assessing the proper administration of eye drops in the post-operative period following cataract extraction, up to 92.6% of 54 patients included demonstrated improper administration technique (15). If the patient has been completely compliant with medications, further probing for other potential etiologies (infectious, autoimmune, additional trauma, idiopathic, etc.) of acute anterior uveitis should be explored.
Medical therapy for rebound iritis follows the same standard therapy for other cases of acute anterior uveitis, including:
• Topical corticosteroids, commonly prednisolone acetate 1% followed by dexamethasone 0.1% and prednisolone sodium phosphate 1% are prescribed via a tapering regimen to decrease inflammation (14).
• Cycloplegics (Homatropine 5%) are prescribed until there are maximum of 0.5% AC cells. Dilation of the pupil prevents synechiae development and decreases ciliary body spasm to help with pain management (14).
Medical follow up
Patient follow-up should be scheduled 7 days after the initial diagnosis is made. If anterior chamber cell has decreased appropriately and the patient has no pain or discomfort, cycloplegics can be discontinued at this time. The patient should be followed weekly until less than 5 cells per HPF (high power field) are detected in the AC. With proper improvement via strict monitoring and adherence to medications, drop frequency can be decreased and follow-up times can be extended slowly (14). Rebound iritis typically lasts 5-6 months, consequentially patients will need long-term monitoring, strict adherence to medications, and accessibility to an Ophthalmology clinic during an extended period (3).
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