A 46-year-old healthy woman of Turkish ancestry was referred to our clinic for a second opinion. She had a history of seeking emergency assistance in another hospital 1 month before with redness, purulent discharge, and discomfort in her OS, with contralateral involvement after 4 days. At this time, she was diagnosed with bilateral bacterial conjunctivitis, being aggressively treated with topical 0.5% moxifloxacin/0.1% dexamethasone every 2 h, for a week.
Three weeks later, she developed ocular hypertension, ocular pain, severe photophobia, mild hyperemia, and decreased vision in her OS, being diagnosed with autoimmune hypertensive uveitis in both eyes. For this reason, treatment with topical prednisolone acetate 1% every 2 h, atropine 1% twice-daily, topical carbonic anhydrase inhibitor/beta-blocker combination, and oral steroids (1 mg/kg/day, tapered during 3 weeks) was prescribed, with no improvement of the symptoms. Past family and personal ocular history were negative, including for glaucoma.
During our initial examination, her best correct visual acuity was 20/25 in the right eye (OD) and 20/200 in OS, with normal color vision. Slit-lamp revealed severe pigment dispersion in the anterior chamber, iris transillumination defect, and mydriatic atonic pupils OU (Fig. 1). There were no inflammatory keratic precipitates and no inflammatory cells in the anterior chamber. Corneal sensibility was normal, with no hypoesthesia. Gonioscopy revealed wide-open angles (Shaffer IV), heavy pigment deposition in the trabecular meshwork, and no appearance of posterior iris bowing and/or peripheral anterior synechiae in OU (Fig. 2).
Even though she was not using steroids anymore, her IOP was 30 mm Hg in OD and 45 mm Hg in OS, despite the use of topical and oral antiglaucomatous medications described above. Fundus examination revealed tilted discs and increased cup-disc ratio in OU. In the OS, an edematous optic nerve, associated with peripapillary retinal hemorrhage, suggestive of nonarteritic optic neuropathy (NAION) was noticed (Fig. 3), and confirmed by optical coherence tomography, and high-frequency B-scan-ultrasonography. Fluorescein angiography did not show any signs of inflammation.
A routine laboratory workup was performed including complete blood cell count, erythrocyte sedimentation rate (11 mm/h), infectious - including VDRL, FTA-ABS, herpes simplex virus and cytomegalovirus serology - and inflammatory tests, quantiFERON-TB gold test, homocysteine, anticardiolipin antibody, lupus anticoagulant, antinuclear antibody, human leukocyte antigen-B27 (HLA-B27), all with negative results. Chest, orbit, and brain magnetic resonance imaging, as well as magnetic resonance angiography were unremarkable.
Since ocular hypertension persisted despite maximal medical therapy, and as the patient was not using any more steroids, a tube shunt was implanted in OU 3 weeks after her first appointment with us. After the procedure, the IOP gradually decreased, hence, topical hypotensive medications were reduced. Anterior chamber pigment was also significantly reduced in the second postoperative week.
After 6 months of follow-up, best correct visual acuity was still 20/25 in OD and 20/200 in OS. IOP was 12 mm Hg OU with topical use of carbonic anhydrase inhibitor/beta-blocker twice a day. Pigment dispersion in the anterior chamber resolved in OU, and optical coherence tomography of retinal nerve fiber layer showed a localized temporal inferior defect in the OD and a diffuse loss in the OS (Fig. 4). Visual field tests revealed a superior paracentral scotoma in the OD and a diffuse reduction in sensitivity in the OS. The presence of bilateral iris atrophy, heavy pigment dispersion in the anterior chamber and trabecular meshwork, in the absence of inflammatory cells and keratic precipitates, associated with high IOP, with no improvement with maximum medical therapy, in a patient with history of using topical moxifloxacin/dexamethasone drops led us to the diagnosis of BAIT syndrome.