We present a technique that uses intracameral lidocaine to induce pupil dilation without using preoperative mydriatic eyedrops. After 1 or 2 drops of topical lidocaine hydrochloride 1% (Xylocaine-MPF 1%) are applied to the ocular surface, a 1.0 mm side-port incision is created through which Xylocaine-MPF 1% is injected into the anterior chamber. The lidocaine paralyzes the pupil sphincter, and adequate mydriasis occurs within 90 seconds. Epinephrine (0.3 cc of 1:1000) is added to the irrigation fluid comprising balanced salt solution (BSS), and standard phacoemulsification with intraocular lens implantation is performed. Pupil dilation is maintained or increased during the procedure. Postoperatively, the pupil returns more quickly to normal size and reaction. Using lidocaine for mydriasis instead of standard dilating drops eliminates the cardiac risk of topical sympathetic agents, decreases the time patients wait in the holding area before surgery, reduces the risk of superficial punctate keratopathy, and provides faster recovery of normal pupil function.

Ophthalmic involvement in sarcoidosis may cause significant sight-threatening illness for patients. Studies of patients with histologically proven sarcoidosis have found 25 to 50% of patients to have ocular manifestations. The frequency in which eye disease is seen and the course that it takes vary with age, race, and geography. This article discusses relevant aspects of the ocular manifestations of sarcoidosis for the internist and pulmonologist. Overall disease presentation, specific types of ocular involvement, evaluation strategies, and treatment considerations are discussed.

Ligneous conjunctivitis is a rare form of chronic pseudomembranous conjunctivitis that is associated with systemic membranous pathological changes. A probable link between plasminogen and ligneous conjunctivitis has been indicated by the recent diagnoses of plasminogen deficiency in five patients suffering from ligneous conjunctivitis. The current study reports that plasminogen-deficient mice develop conjunctival lesions indistinguishable from human ligneous conjunctivitis in both appearance and histology. Both human and mouse lesions contain acellular material rich in fibrin, and aberrant or disrupted epithelium. The incidence of lesion development in mice increases with age and is strongly influenced by genetic background. Interestingly, ligneous conjunctivitis was not observed in plasminogen-deficient mice simultaneously lacking fibrinogen. This study provides direct evidence that plasminogen deficiency is one cause of ligneous conjunctivitis and suggests that plasminogen-deficient mice may be an excellent model for the development of therapeutic strategies for the treatment of this debilitating disease.

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Objective: To describe the efficacy and complications of intracameral tissue plasminogen activator (tPA) in a large series of glaucomatous eyes with valved glaucoma drainage implants (GDIs). Methods:A retrospective analysis of 620 Ahmed and Krupin aqueous shunts implanted between December 1992 and May 2001 identified 36 eyes treated with intracameral tPA for total or imminent tube obstruction by fibrin and/or blood. For a successful ocular outcome, tPA use must prevent the need for additional glaucoma surgery to replace or revise an occluded drainage implant.Results: Intracameral tPA successfully cleared or prevented tube occlusion by fibrin/blood clots in 32 (88.9%) of 36 eyes. Multiple tPA injections were administered in 38.9% of eyes, and the mean number of injections required to achieve successful outcomes was 1.6. The mean±SD tPA dose per injection was 9.8±3.1 µg, and the mean ± SD total tPA dose required to achieve successful outcomes was 15.5±9.9 µg. For injections to be successful in totally occluded tubes (n=31), the mean±SD intraocular pressure change 24 hours after tPA administration was -21.2±15.6 mm Hg. Significant complications, including severe hyphema, profound hypotony, and anterior chamber flattening, occurred after 10.9% of tPA administrations.Conclusion: Intracameral tPA clears and prevents obstruction of valved GDIs by fibrin and/or blood clots.

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