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• W4360620056 abstract "Uveitis-glaucoma-hyphema (UGH) syndrome occurs because of contact between the iris or ciliary body and the intraocular lens (IOL). This contact results in mechanical irritation and erosion of uveal tissues, leading to the release of pigment from the iris pigment epithelium.1Durr GM Ahmed IIK. Intraocular lens complications: decentration, uveitis-glaucoma-hyphema syndrome, opacification, and refractive surprises.Ophthalmology. 2021; 128: e186-e194Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar Additionally, the breakdown of the blood–aqueous barrier results in the release of blood cells and proteins into the anterior chamber causing secondary glaucoma.2Zemba M Camburu G. Uveitis-glaucoma-hyphaema syndrome: general review.Rom J Ophthalmol. 2017; 61: 11-17Crossref PubMed Google Scholar We present a case of transient monocular heterochromia and transient monocular vision loss (TMVL) associated with UGH syndrome. A 66-year-old white female presented to the ophthalmology clinic with 7 episodes of TMVL of the left eye over a duration of 6 months. During each episode, the patient had a gradual onset of partial to complete vision loss that lasted from 2 to 6 hours and then recovered gradually. She also noted a change of her left iris color during these episodes from green to brown (Fig. 1). Two years prior to presentation, the patient underwent bilateral cataract surgery with multifocal IOL implantation, and there was a history of ocular hypertension in the left eye controlled with 2 topical antiglaucoma medications. Our patient presented to the local emergency department after her initial episode. The patient had computed tomography of the head and chest, carotid ultrasound, magnetic resonance imaging of the brain, magnetic resonance angiography of the head and neck, an echocardiogram, and Holter monitoring. Blood work-up was ordered and included hemoglobin A1C, a lipid panel, erythrocyte sedimentation rate, C-reactive protein, complete blood count, a complete metabolic panel, and a coagulopathy panel. Her extensive laboratory and imaging work-up revealed only mildly elevated levels of cholesterol, for which treatment was initiated. Patient also was started on clopidogrel by her cardiologist given the nature of her symptoms, but the intermittent episodes continued. On examination, the patient's best-corrected visual acuity was 20/15 in each eye, and intraocular pressures were 13 mm Hg OD and 10 mm Hg OS. Pupillary examinations were normal with full extraocular muscles movements. Slit-lamp examination showed symmetrically appearing light-coloured irises with a multifocal intraocular lens bilaterally. Detailed examination of the anterior segment of the left eye revealed superior iris transillumination defects without iris neovascularization (Fig. 2) and a 1-piece IOL with the inferior haptic within the capsular bag and the superior haptic in the ciliary sulcus (Supplementary Fig. 1, available online). Gonioscopy demonstrated open angles with extensive pigmentation of the trabecula meshwork (TM) in the left eye and no evidence of trabecular cleft or angle neovascularization (Supplementary Fig. 2, available online). Fundus examination of both eyes was normal. A review of the patient's cell phone photographs was performed and showed a small layered hyphema inferiorly in the left eye during an episode of transient vision loss (Supplementary Fig. 3, available online). Humphrey visual field testing and optical coherence tomography of the optic nerve of both eyes were normal. A diagnosis of UGH syndrome was established as the cause of the TMVL episodes. Intraocular lens repositioning was performed, resulting in complete resolution of TMVL and transient iris heterochromia in the left eye after 36 months of postoperative follow-up. Our patient developed transient monocular heterochromia, which is a rare ophthalmic entity that to our knowledge that has not been reported previously in association with UGH syndrome. We believe that the recurrent iris heterochromia and TMVL likely were due to the associated hyphema and IOL malposition. In UGH syndrome, the persistent uveal–IOL contact can lead to mechanical irritation and erosion of uveal tissues and anterior-chamber angle. This leads to release of pigment, red blood cells and hyphema formation, white blood cells, and protein into the anterior chamber, producing iritis. Glaucomatous optic neuropathy can develop due to multifactorial mechanisms, including blockage of the TM by released pigment, red or white blood cells, ghost cell glaucoma from vitreous hemorrhage, or synechial angle closure.1Durr GM Ahmed IIK. Intraocular lens complications: decentration, uveitis-glaucoma-hyphema syndrome, opacification, and refractive surprises.Ophthalmology. 2021; 128: e186-e194Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar UGH syndrome may present with various manifestations, including ocular hypertension, microhyphema or hyphema, anterior uveitis, iris transillumination defects, iris neovascularization, and cystoid macular edema.2Zemba M Camburu G. Uveitis-glaucoma-hyphaema syndrome: general review.Rom J Ophthalmol. 2017; 61: 11-17Crossref PubMed Google Scholar Gonioscopy evaluation can demonstrate blood within the anterior-chamber angle, increased pigmentation of the TM, and visualization the IOL haptic. Ultrasound biomicroscopy is often helpful to visualize malposition of the IOL and contact with uveal tissue.2Zemba M Camburu G. Uveitis-glaucoma-hyphaema syndrome: general review.Rom J Ophthalmol. 2017; 61: 11-17Crossref PubMed Google Scholar There are many causes of MTVL, including amaurosis fugax, retinal migraine, intermittent angle-closure glaucoma, papilledema, anemia and hypercoagulopathies, UGH syndrome, and hypotension.3Ahmed R Foroozan R. Transient monocular visual loss.Neurol Clin. 2010; 28: 619-629Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar Vision loss due to amaurosis fugax typically occurs suddenly, starts as a curtain covering the visual field, and recovers rapidly over seconds or minutes. Patients sometimes experience complete loss of light perception. However, UGH syndrome can cause diminution of vision that starts over a few minutes, recovers over hours to days, and occasionally is associated with red vision. Patients with TMVL due to UGH syndrome are unlikely to lose light perception during attacks.4Cates CA Newman DK. Transient monocular visual loss due to uveitis-glaucoma-hyphaema (UGH) syndrome.J Neurol Neurosurg Psychiatry. 1998; 65: 131-132Crossref PubMed Scopus (19) Google Scholar Ophthalmic evaluation during attacks may reveal microscopic hyphema that sometimes clears rapidly, making the diagnosis of UGH syndrome more difficult, as was noted in our patient. IOP spikes in UGH syndrome might lead to decreased ocular perfusion and subsequently transient retinal ischemia and TMVL.4Cates CA Newman DK. Transient monocular visual loss due to uveitis-glaucoma-hyphaema (UGH) syndrome.J Neurol Neurosurg Psychiatry. 1998; 65: 131-132Crossref PubMed Scopus (19) Google Scholar Treatment of UGH syndrome includes topical corticosteroid eye drops to control uveitis and IOP-lowering medications for ocular hypertension. In patients with hyphema, head elevation and topical cycloplegic and steroid drops are recommended. In eyes with recurrent hyphema or chronic inflammation with cystoid macular edema, surgical interventions may be required. A recent study showed that IOL surgeries (including IOL exchange, IOL suturing to the iris or sclera, haptic amputation, and IOL rotation) resulted in resolution of UGH syndrome in 77% of treated patients. There was a statistically significant IOP reduction and best-corrected visual acuity improvement in the operated cases compared with the conservative treatment group.5Iftikhar M Mir T Seidel N et al.Epidemiology and outcomes of hyphema: a single tertiary centre experience of 180 cases.Acta Ophthalmol. 2021; 99: e394-e401Crossref PubMed Scopus (6) Google Scholar Our patient did not develop any TMVL or heterochromia episodes during a 3-year follow-up after IOL repositioning. In summary, our case underscores the importance of maintaining a high index of suspicion for UGH syndrome as the cause of MTVL and transient iris heterochromia in patients with prior cataract surgery and signs of IOL malposition. IOL repositioning was successful in eradicating recurrence episodes with 36 months of postoperative follow-up. Exclusion of other mechanisms of transient vision loss is critical. The authors have no proprietary or commercial interest in any materials discussed in this correspondence. This work was supported by a National Institutes of Health Center Core Grant (P30EY01480) and a Research to Prevent Blindness Unrestricted Grant (GR004596). Download .jpg (.49 MB) Help with files Download .jpg (.39 MB) Help with files Download .jpg (.55 MB) Help with files" @default.
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• W4360620056 title "When my green eye turns brown: transient monocular heterochromia and vision loss due to uveitis-glaucoma-hyphema syndrome" @default.
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