Cataract- and Lens-Induced Uveitis
Somasheila I. Murthy
Phacoantigenic/phacoanaphylactic uveitis is the result of an immunologic response from disruption of the lens capsule with subsequent release of lens proteins.
The clinical diagnosis of phacoanaphylaxis, particularly in an eye with an intraocular lens implant, can be difficult, and on routine examination the condition may be indistinguishable from infectious endophthalmitis. Phacoantigenic uveitis is usually unilateral. The inflammation is predominantly anterior, with zonal granulomatous inflammation centered around the lens material. The process of granulomatous damage slowly involves the ciliary body and choroid, leaving the retina and sclera intact. Traditionally, phacolytic uveitis refers to nongranulomatous inflammation resulting from lens proteins leaking through an intact lens capsule in an eye with a hypermature cataract. All of these entities may represent varying manifestations of a similar disease process and can all be considered lens-induced uveitis.
Etiology and Epidemiology
• It can occur after cataract surgery or trauma, and occasionally occurs spontaneously if there is a hypermature cataract with a leaking capsule.
• The immune system generates inflammation against previously sequestered lens proteins. This leads to a delayed type hypersensitivity reaction in the surrounding ocular tissue.
• Pain, redness, photophobia, all of which are usually severe
• Yellow or whitish pupil reflex and decreased vision. The patient may report an antecedent history of trauma or preexisting decreased vision due to cataract.
• Circumciliary injection (ciliary flush)
• Corneal edema
• “Mutton fat” keratic precipitates
• Marked flare, abundant cells, lens matter in anterior chamber, and/or a hypopyon
• Posterior or peripheral anterior synechiae
• A pupillary membrane
• Irregular lens capsule, opaque lens, intense vitritis
• Glaucoma due to trabeculitis, lens debris in angles, or synechiae
• Endophthalmitis-like picture in extreme cases
• Hypotony caused by cyclitic membranes, ciliary shutdown, or choroidal effusion
• Phthisis bulbi
• Phacolytic glaucoma
• Sympathetic ophthalmia (in bilateral disease)
• Low-grade endophthalmitis (e.g., Propionibacterium acnes)
• Bacterial/fungal endophthalmitis
• A high degree of clinical suspicion is important.
• An anterior chamber tap with histopathology may help differentiate lens-induced inflammation from infectious endophthalmitis.
• Histopathology may reveal zonal granulomatous inflammation.
• Definitive treatment involves removal of the inciting agent (i.e., the lens or residual lens material).
• Control of inflammation and glaucoma with corticosteroids and ocular antihypertensive medications is important in order to prevent long-term morbidity.
Kalogeropoulos CD, Malamou-Mitsi VD, Asproudis I, Psilas K. The contribution of aqueous humor cytology in the differential diagnosis of anterior uvea inflammations. Ocul Immunol Inflamm. 2004;12(3):215-225.
Thach AB, Marak GE Jr, McLean IW, Green WR. Phacoanaphylactic endophthalmitis: a clinicopathologic review. Int Ophthalmol. 1991;15(4):271-279.
Takashi Y, Yasuaki F, Izumi N, et al. A murine model of experimental autoimmune lens-induced uveitis using Klebsiella 03 lipopolysaccharide as a potent immunological adjuvant. Int J Exp Path. 1993;74:573-582.
FIGURE 5-1. Phacolytic uveitis. Slit-lamp photograph of a case of trauma-related phacolytic uveitis. Note the granulomatous keratic precipitates and ruptured anterior lens capsule with cortical material in anterior chamber.
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