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Aqueous Shunts
Published in Neil T. Choplin, Carlo E. Traverso, Atlas of Glaucoma, 2014
Brian J. Song, JoAnn A. Giaconi, Anne L. Coleman
Complications associated with aqueous shunts can be categorized as those associated with the reduction of intraocular pressure, with the functioning and placement of the tube, with the episcleral plate and the response of surrounding tissues to it, and with intraocular surgery per se. A complete list of complications is provided in Table 18.4. Information about the steps of the surgery and potential associated complications are illustrated by Figures 18.1 through 18.38. Suprachoroidal hemorrhage is a complication that can occur in any eye predisposed to develop it regardless of the presence of a device to restrict flow. Ocular hypotony with or without consequent serous choroidal effusion may occur with both valved and nonvalved devices with which flow is restricted. Ocular hypotony can have many etiologies, including inadequate restriction of aqueous flow, leakage of aqueous around the tube, or the decreased production of aqueous humor by the ciliary body. Phthisis bulbi has been reported in 2%–18% of eyes following shunt placement with neovascular glaucoma having a greater risk.5,28 Complications associated with intraocular surgery per se also occur with glaucoma drainage devices. The incidence of retinal detachment has been reported as 0%–14% and that of vitreous hemorrhage is 0%–11% (although vitreous hemorrhages may be secondary to underlying disease, such as proliferative diabetic retinopathy).29–32 The incidence of epiretinal membranes and/or cystoid macular edema have been reported in 0%–14% of eyes, and that of endophthalmitis after aqueous shunt implantation is 0%–3%.20,32–36
Use of Anti-Tumour Necrosis Factor-Alpha Agents in the Management of HLA-B-27-Associated Uveitis: The First Case Series from India
Published in Ocular Immunology and Inflammation, 2021
Ruchika Lakra, Amravi Shah, Viswanath Kaushik, Jyotirmay Biswas, Parthopratim Dutta Majumder
Twenty eyes of 14 patients with HLA-B-27-associated uveitis were included in the study. Twelve patients (85.7%) were male and median age was 31.5 years (IQR 15) (range 17–53 years). In eight patients, ocular involvement was unilateral and in six patients ocular involvement was bilateral when biological therapy was considered. Only one patient had simultaneous bilateral involvement and in rest of the patients, the ocular involvement was alternating bilateral. The most common underlying systemic disease was ankylosing spondylitis (92.8%). Anterior uveitis was the most common subtype of uveitis (10 patients;71%) followed by anterior uveitis and intermediate uveitis seen in in 4 patients (28.6%). Of the 20 eyes of 14 patients, all eyes had anterior uveitis; severe fibrinous reaction was seen in 7 eyes (35%) and 3 eyes had hypopyon (15%). Posterior segment involvement was seen in the form of vitritis in 9 eyes (45%), (Figure 1a) CME in 2 eyes (10%) (Figure 1d) and papillitis in 1 eye (5%) (Figure 1b). Pars plana exudates (Figure 1c) were observed in 5 eyes (25%) of 4 patients. None of the patients had clinical evidence of retinal vasculitis. Fundus fluorescein angiography was done only in two patients, both the angiograms did not reveal any retinal vessel inflammation. Seven patients had developed posterior subcapsular cataract during the course of the disease. Details of medications prior to administration of biologicals were as follows. Topical corticosteroid (1% prednisolone acetate) and cycloplegic (2% homatropine) were used in all patients to control anterior chamber reaction. Oral corticosteroid was used in all patients. Two patients were on sulphasalazine as advised by the rheumatologist for the treatment of joint involvement in ankylosing spondylitis elsewhere. Immunosuppressive treatment was administered in 11 patients (78.5%) and methotrexate was the only immunosuppressive used in these patients. Intravenous methylprednisolone was administered in two patients––both patients had severe, persistent intraocular inflammation with protracted hypotony. Eleven patients received one or more posterior subtenon corticosteroid. The median frequency of topical corticosteroid application was 12 (range: 6–24) times per day and the median oral prednisolone therapy was 60 (range: 0–64) mg/day at the time of shifting to biological therapy. Ocular hypotony was present in 6 patients which resolved in five patients (83.3%). Two patients (14.2%) had CME which resolved with increase in BCVA. Two patients (14.2%) with recurrent anterior uveitis who were steroid responders had achieved good control of IOP without anti-glaucoma medications when they were shifted to biologicals. Seven patients in our case series developed posterior subscapular cataract; only three of them required cataract surgery. Two of them underwent successful phacoemulsification with foldable intraocular lens implantation with very minimal anterior chamber in the postoperative period, while the other patient declined to undergo cataract surgery. Another patient who developed rhegmatogenous retinal detachment with horse shoe tear successfully underwent retinal detachment surgery under corticosteroid cover. Details of these patients are outlined in Table 1.