Ocular surface disease: a known yet overlooked side effect of topical glaucoma therapy.

Ocular surface disease (OSD), a disorder affecting the lacrimal and meibomian glands and the corneal and conjunctival epithelium, is a well-known complication of topical glaucoma therapy. OSD can present as a new or pre-existing condition that virtually any anti-glaucoma formulation can exacerbate. As such, both glaucoma and OSD frequently coexist. Typical OSD symptoms include ocular discomfort, redness, burning, and dryness, whereas signs include periorbital and eyelid skin pigmentation, conjunctival scarring, and superficial punctate keratitis. Pressure-lowering eyedrops can cause toxic, allergic, and inflammatory reactions on the ocular surface. The latter can result from either preservatives or direct toxicity from the active molecule. Although usually mild, OSD can cause significant symptoms that lead to poor quality of life, decreased compliance to therapy, glaucoma progression, and worse visual outcomes. Given the chronic nature of glaucoma, lack of curative therapy, and subsequent lifelong treatment, addressing OSD is necessary. This manuscript aims to provide an up-to-date overview of OSD's signs, symptoms, and pathogenic mechanisms from glaucoma therapy toxicity.

X-linked juvenile retinoschisis associated with an RS1 in-frame deletion and bilateral central serous chorioretinopathy.

PURPOSE: To report the case of a patient with X-linked juvenile retinoschisis (XLRS), caused by an in-frame deletion of the RS1 gene, who presented visual loss due to bilateral central serous chorioretinopathy (CSC).Methods: Observational case report. RESULTS: A 34-year-old man, with type-A personality, presented with a one-month history of decreased visual acuity and metamorphopsia in his right eye. Funduscopic examination showed a dome-like foveal elevation in both eyes (OU), as well as subtle pigmentary changes of the retinal pigment epithelium with a tapetal reflex in the fovea. Spectral-domain optical coherence tomography revealed intraretinal cystic foveal changes and serous retinal detachment in OU. Fundus fluorescein angiography of OU showed a focal area of intense hyperfluorescence with leakage in late phases. Electroretinogram revealed a markedly attenuated b-wave and a diminished a-wave in photopic and scotopic phases. Genetic testing revealed a hemizygous c.282_284delCTT deletion in the RS1 gene, predicting a p.Ser95del change at the protein level. The patient was diagnosed with XLRS and central serous chorioretinopathy as a coexisting condition. Patient was observed during a 3-month period but showed no improvement. Therefore, subthreshold micropulse laser was applied, achieving complete resolution of signs and symptoms of CSC. CONCLUSION: CSC can be a cause of acute or subacute visual loss in patients with XLRS when other complications such as vitreous hemorrhage and retinal detachment have been excluded.

Unilateral Orbital Emphysema Secondary to Vitreoretinal Surgery.

PURPOSE: To describe preoperative, intraoperative, and postoperative characteristics, imaging findings, and clinical evolution of patients who developed orbital emphysema after vitreoretinal surgery. DESIGN: Retrospective, descriptive, observational case series. PARTICIPANTS: Patients with orbital emphysema after vitreoretinal surgery who were diagnosed and treated between January 2006 and October 2018 at a single ophthalmology referral center. METHODS: Medical records and orbital computed tomography images were reviewed and analyzed. A minimum follow-up of 3 months was required. MAIN OUTCOME MEASURES: Final best-corrected visual acuity (BCVA). RESULTS: This study included 16 patients with a mean age of 47.9 ± 14.7 years, 50% were women, and 25% had a history of previous ocular trauma. A diagnosis of rhegmatogenous retinal detachment was established in 75% of patients. Twenty-five percent of patients underwent pars plana vitrectomy (PPV), 50% underwent encircling scleral buckling plus PPV, 18.8% underwent repeat PPV, and 6.2% underwent scleral buckling plus repeat PPV. Additionally, 62.5% received silicone oil endotamponade. The median time between vitreoretinal surgery and orbital emphysema was 8 days (interquartile range [IQR] 5-15 days). Mean proptosis was 6.7 ± 4.6 mm. Orbital cellulitis was considered as a differential diagnosis in 31.2% of patients, and tomographic evidence of fracture was observed in 25% of patients. Treatment with compressive patching was prescribed for 87.5% of patients, transpalpebral drainage was prescribed for 75% of patients, hyperbaric oxygen therapy was prescribed for 43.8% of patients, and surgical management was prescribed for 31.2% of patients. The comparison between BCVA before vitreoretinal surgery (median, 1.8 logarithm of the minimum angle of resolution [logMAR]; IQR, 1.33-2.3 logMAR) and at the last follow-up (median, 2.3 logMAR; IQR, 1.42-2.8 logMAR) was not statistically significant (P = 0.125, Wilcoxon matched-pairs signed-rank test). No association was found between surgeon experience and lower final BCVA (P = 0.604, Fisher exact test); however, development of ocular hypertension was associated with worse final BCVA (P = 0.0101; relative risk, 7; 95% confidence interval, 1.01-44.63). CONCLUSIONS: Although orbital emphysema constitutes a very unusual complication of vitreoretinal surgery, it is important to identify this condition promptly and treat patients efficiently to avoid potential vision loss.