PATIENTS AND METHODS: In total, 100 eyes from 50 patients on long-term intranasal steroids (>2 y) for allergic rhinitis and 90 eyes from 45 controls were included in this study. Patients on other forms of steroids and risk factors for glaucoma were excluded. IOP was measured and nonmydriatic stereoscopic optic disc photos were taken for each eye. The vertical cup-to-disc ratio and the status of the optic disc were evaluated.
RESULTS: The mean IOP for intranasal steroids group was significantly higher (15.24±2.31 mm Hg) compared to the control group (13.91±1.86 mm Hg; P=0.000). However, there were no significant differences in the vertical cup-to-disc ratio and the status of glaucomatous optic disc changes between the groups.
CONCLUSIONS: Prolonged use of intranasal steroids cause statistical significant increase in IOP in patients with allergic rhinitis although no significant glaucomatous disc changes were seen. We suggest patients on long-term use of intranasal steroid have a yearly eye examination to be monitored for IOP elevation and those with additional risk factors for glaucoma is closely monitored for glaucoma.
DESIGN: A double-blind randomized controlled trial.
METHODS: This study comprised 295 patients who were randomized into the intracameral (ICM) mydriatic group or topical mydriatic group. Central corneal endothelial cell density (ECD), coefficient of variation (CV), and percentage of hexagonal cells were measured preoperatively and postoperatively at 1 week, 6 weeks, and 3 months with specular microscope.
RESULTS: There was no significant difference in endothelial cell density and endothelial cell loss between the topical and ICM mydriatic groups. At 3 months, the mean endothelial cell density in the ICM group was 2129.76 ± 423.53 cells/mm2 and 2100.54 ± 393.00 cells/mm2 in the topical group (P = 0.539). The endothelial cell loss was 18.60 ± 12.79% in the IC M group and 19.44 ± 11.24% in the topical group (P = 0.550). No significant difference was seen in the percentage of hexagonal cells and coefficient of variation of patients between the 2 groups.
CONCLUSIONS: Intracameral phenylephrine was not associated with increased risk of postoperative endothelial cell loss or morphological changes. It can be safely injected into the anterior chamber for pupil dilatation before phacoemulsification cataract surgery.
DESIGN: Multicenter retrospective case series.
METHODS: Retrospective review.
RESULTS: Seven patients presented with corneal findings ranging from superficial punctate epitheliopathy to bilateral corneal melt with subsequent perforation. Among those with mild corneal findings, resolution was achieved with topical steroids and lubrication, whereas some patients who developed progressive corneal melt required therapeutic penetrating keratoplasty. The history in all patients revealed exposure to aquarium zoanthid corals shortly before disease onset. A review of the literature revealed that there are few prior reports of coral-associated corneal toxicity and that some species of coral secrete a substance known as palytoxin, a potent vasoconstrictor that inhibits the membranous sodium-potassium ATPase pump across cell types and can cause rapid death if inhaled or ingested.
CONCLUSIONS: This is the largest case series to date demonstrating patients with aquarium coral palytoxin-associated corneal toxicity, and is the first to provide details of related histopathologic findings. Similar to other forms of toxic keratoconjunctivitis, a detailed history and careful clinical assessment are required, as well as timely removal of the offending agent from the patients' ocular milieu and environment. Mild ocular surface and corneal disease may be treated effectively with aggressive topical steroid therapy and lubrication. Given the potential severity of ocular as well as systemic adverse effects, there should be increased awareness of this entity among eye care professionals, aquarium enthusiasts, and the general public.