Glaucoma affects millions of people around the world. With the baby boom generation aging, the number of people affected by primary open-angle glaucoma in the US is expected to reach 3.3 million by 2020, and about half may not know they have the disease. The treatment of most forms of glaucoma includes the use of topical agents that enhance aqueous humour outflow, reduce aqueous production, or both. Topical intraocular pressure-lowering drugs must penetrate across the tissues of the eye to reach their therapeutic targets. Often, these tissues show the first signs and symptoms of drug toxicity and adverse effects. These include eyelid dermatitis, malpositions, lacrimal system scarring, ocular discomfort upon instillation, tear film instability, conjunctival inflammation, subconjunctival fibrosis, conjunctival epithelium changes, and corneal surface and endothelial impairment. For these reasons, ophthalmologists should evaluate the risks and benefits of ophthalmic medications before initiating therapy, identify the minimum dosages necessary to achieve a therapeutic benefit, and monitor patients for local and systemic adverse effects. Adverse events may be reduced by changing to a different class of topical medication, using corticosteroids, lubricating the eyes frequently, and reducing exposure to preservatives. This in turn can lead to higher levels of adherence to antiglaucoma therapy, improved outcomes and a reduction in the costs associated with long-term glaucoma complications. This article reviews the ocular adverse effects associated with the various classes of topical antiglaucoma drugs, with a particular focus on the ocular surface, eyelids and periorbital tissue.

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We report the history and clinical presentation of an 88-year-old female with Fuchs dystrophy who developed an acute anterior necrotizing scleritis in her left eye 23 months after an uncomplicated combined penetrating keratoplasty and phacoemulsification with intraocular lens implantation which progressed to slceral perforation with uveal prolapses. The patient underwent a complete systemic work-up for both autoimmune and infectious causes of scleritis. Surgical specimens of the area of scleral perforation were sent for histology and microbiologic studies. Analysis of surgical specimens revealed the presence of culture-proven Nocardia asteroides as a causative agent for the patient's scleral perforation. Results of her systemic autoimmune work-up were not conclusive. Successful treatment with tectonic scleral reinforcement with donor corneal tissue and preserved pericardium, oral and topical trimethoprim-sulfamethoxazole and topical amikacin salvaged the globe and increased vision. The patient's final best-corrected visual acuity sixteen months after her last operation remains 20/70. Prompt surgical intervention with submission of appropriate specimens for pathological diagnosis and microbiology, along with consultation with rheumatologic and infectious disease specialists, are mandatory to minimize visual loss in cases of suspected infectious necrotizing scleritis.

PurposeTo examine the relationships between sex and symmetry in the context of disease activity, severity, and thyroid status in thyroid eye disease.MethodsRetrospective chart review of 31 men and 31 women with untreated thyroid eye disease. Subjective complaints, smoking status, thyroid status, and objective findings pertinent to the clinical activity score (CAS) and “NO SPECS” classification were recorded. Overall disease asymmetry was defined as having simultaneous asymmetry of both more than one symptom and more than one external finding. Asymmetry was compared across sex and thyroid status. CAS and NO SPECS severity were compared across sex, symmetry, and thyroid status.ResultsAsymmetric appearance was reported by 58% of men and 19% of women. Asymmetric proptosis (>2 mm difference) was seen in 45% of men and 23% of women (P=0.036). Overall asymmetry was seen in 55% of men and 19% of women (P=0.017). Thyroid status and sex had a combined effect on symmetry, as 15 of 16 hyperthyroid females (94%) demonstrated symmetric disease. Average NO SPECS severity was 3.5 (standard deviation [SD] 1.4) in men and 3.3 (SD 1.1) in women (P=0.51), and was 3.8 (SD 1.4) in asymmetric patients versus 3.2 (SD 1.3) in symmetric patients (P=0.08). The CAS was higher in asymmetric than symmetric patients (1.84 versus 0.97; P=0.012).ConclusionMen demonstrated more asymmetric disease (proptosis and overall asymmetry) than women, while hyperthyroid females demonstrated more symmetry than euthyroid and hypothyroid males and females. NO SPECS severity score was unaffected by sex, thyroid status, or symmetry. Asymmetric patients demonstrated higher clinical activity scores.