Diagnosing and Managing Toxic Anterior Segment Syndrome
By William L. Miller, OD, PhD, FAAO
One uncommon yet serious complication after any anterior segment surgery is toxic anterior segment syndrome (TASS), formerly referred to as sterile endophthalmitis. TASS is an inflammatory event that typically occurs after cataract surgery, but it has also been observed after penetrating keratoplasties. When the inflammation is isolated to the corneal endothelium, it is classified as toxic endothelial cell destruction (TECD) (Choi and Shyn, 2008).
TASS Etiology and Diagnosis
The etiology of TASS is multi-factorial. Patient-based factors such as retained lens material, pupil stretching, or other immunological events as well as intraocular irrigating fluids and medications are possible triggers. Other implicated causes include bacterial endotoxins, retained instrument cleaning detergents, and instrument debris. A recent case of a retained bolus of ophthalmic antibiotic ointment in the anterior chamber has also been reported (Ugurbas and Akova, 2010).
Because TASS can mimic endophthalmitis, that must be considered in your differential diagnosis. Both patients typically present with reduced or blurry vision and a severe anterior segment inflammation with fibrin deposition in the anterior chamber. Unlike infectious endophthalmitis patients who experience severe pain, TASS patients have minimal to no periocular pain.
TASS develops within the first 24 to 72 hours after surgery, distinguishing it from most cases of endophthalmitis, which occur between days three and seven. You will also observe pan-corneal edema along with possible folds in the posterior limiting lamina, but the corneal edema and anterior chamber reaction won't be as severe as in endophthalmitis cases.
Another hallmark clinical sign used to differentiate TASS from endophthalmitis is the absence of a vitritis. Other clinical clues to differentiate TASS from endophthalmitis include a lack of eyelid edema, conjunctival injection and chemosis, and eye discharge. An increase in intraocular pressure may manifest as well as an unreactive pupil, and in rare cases cystoid macular edema may occur.
When the clinical data is equivocal, it is best to treat the condition as infectious endophthalmitis until proven otherwise.
Because TASS is an inflammatory event isolated to the anterior segment, the mainstay of therapy is topical ophthalmic steroids, such as 1% prednisolone acetate, dosed at one drop every 30 to 60 minutes for the first three days with a gradual tapering thereafter. Examine patients every day after initiation of therapy. Continue to monitor the inflammation after tapering. Anti-glaucoma medications can be prescribed to control any increase in intraocular pressure.
Topical nonsteroidal anti-inflammatory agents such as Nevanac (nepafenac, Alcon), Voltaren (diclofenac, Novartis), Xibrom (bromfenac, Ista Pharmaceuticals), and Ocufen (flurbiprofen, Allergan) may be useful adjunctive medications to complement the topical steroid. When the cornea starts to clear, perform a gonioscopic exam to rule out any trabecular meshwork damage and peripheral anterior synechaie formation.
Long-term prognosis of mild-to-moderate TASS is good, the latter exhibiting a longer recovery (weeks) with typical persistent corneal edema and intraocular pressure increases. Severe cases of TASS may take many weeks to control, and patients may experience poorer visual outcomes. CLS
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Dr. Miller is an associate professor and chair of the Clinical Sciences Department at the University of Houston College of Optometry. He is a member of the American Optometric Association and serves on its Journal Review Board. You can reach him at email@example.com.
Contact Lens Spectrum, Issue: December 2010