Intravitreal bevacizumab for choroidal neovascularization secondary to presumed ocular histoplasmosis syndrome.

PURPOSE: The purpose of this study was to assess the efficacy of intravitreal bevacizumab for choroidal neovascularization resulting from presumed ocular histoplasmosis syndrome. METHODS: This is a chart review of retrospective consecutive case series in which intravitreal bevacizumab (1.25 mg) was injected into 24 eyes with choroidal neovascularization resulting from presumed ocular histoplasmosis syndrome. Visual acuity was measured in all patients. Optical coherence tomography and/or fluorescein angiography was performed before and after treatment. The minimum follow-up time was 3 months. Retreatment criteria included failure to improve visual acuity and/or persistent leakage as determined by optical coherence tomography or fluorescein angiography. RESULTS: Patients' mean age was 43.08 years (standard deviation, 13.58 years) and mean follow-up was 31.8 weeks (standard deviation, 20.79 weeks). The average number of bevacizumab injections was 6.8 injections/year. After 3 months, visual acuity improved from mean logMAR 0.76 +/- 0.48 (Snellen equivalent of 20/114) to mean logMAR 0.45 +/- 0.47 (Snellen equivalent of 20/55) (P < 0.001, paired t test; n = 24). After 12 months, visual acuity improved from mean logMAR 0.86 +/- 0.35 (Snellen equivalent of 20/150) to mean logMAR 0.34 +/- 0.33 (Snellen equivalent of 20/45) (P = 0.006, paired t test; n = 9). Fourteen (58.3%) eyes had final visual acuity of 20/40 or better compared with 5 (20.8%) eyes at baseline (P = 0.003, McNemar test). Ten patients (41.6%) had visual acuity of 20/200 or worse at baseline compared with 5 (20.8%) eyes at the final visit (P = 0.059, McNemar test). CONCLUSION: Intravitreal injection of bevacizumab seems to be an effective treatment for choroidal neovascularization resulting from presumed ocular histoplasmosis syndrome.

Effects of exercise on intraocular pressure and ocular blood flow: a review.

Glaucoma is a disease characterized by progressive optic neuropathy resulting in retinal ganglion cell death, which affects approximately 68 million people worldwide. Risk factors include intraocular pressure (IOP), genetics, race, age, and vascular factors. Exercise is known to affect IOP and systemic cardiovascular factors and, therefore, may affect glaucoma pathophysiology. This review discusses the results of articles relevant to glaucoma, IOP, ocular blood flow (OBF), and exercise. Isometric and dynamic exercises have been studied with respect to effects on IOP and OBF. Isometric exercise results in an acute decrease in IOP, which correlates with hypocapnia. Dynamic exercise results in a more pronounced but also short duration decrease in IOP. Physical fitness is associated with lower baseline IOP but diminished acute IOP-lowering response to exercise. Upon cessation of exercise, values return to pretrained levels within 1 month. In glaucoma patients, these IOP-lowering effects are greater than in healthy subjects. In healthy subjects, OBF is unchanged during exercise due to vascular autoregulation. This autoregulation fails at ocular perfusion pressures greater than 70% above baseline. In conclusion exercise in glaucoma patients results in acutely lowered IOP and lower baseline IOP. The effects of exercise on the prevention of glaucoma and glaucomatous progression remain unknown. The role of exercise in glaucoma management should be investigated.

Chlorhexidine gluconate 0.02% as adjunct to primary treatment for corneal bacterial ulcers.

BACKGROUND: It is common practice to use topical antiseptic formulations prior to specific therapy in superficial infections and injuries, but not in corneal bacterial ulcers. There is accumulating evidence proving chlorhexidine gluconate 0.02%, an antiseptic agent, as an effective treatment for infectious keratitis. OBJECTIVES: To investigate the safety and efficacy of chlorhexidine gluconate 0.02% as an adjunct therapy for corneal bacterial ulcers. METHODS: Twenty-six patients with corneal bacterial ulcers were treated with standard empirical antibiotic treatment. The study group was treated with chlorhexidine gluconate 0.02% while controls received placebo for one week. The patients were followed for at least 1 month. RESULTS: No allergic or toxic reactions were noted. Although a higher baseline severity of ulcers existed in the study group, no differences were found in final vision, scarring extent, or recovery duration. CONCLUSIONS: Chlorhexidine gluconate 0.02% may improve the clinical course of corneal ulcers.

Age-related ocular vascular changes.

BACKGROUND: The global society is aging at an increasing rate, with a continually larger proportion of the population consisting of those over the age of 65. Age-related vascular changes have been demonstrated in ocular tissue, and the incidence and prevalence of diseases such as macular degeneration, glaucoma and vascular occlusive diseases increase significantly with age. METHODS: This article reviews the current body of literature examining age-associated ocular vascular changes, and summarizes the aggregate findings. We discuss the potential role of the aging vasculature in the etiology of age-associated ocular disease, focusing on glaucoma. RESULTS: Our working hypothesis is that although advancing age is a physiological phenomenon, there are stepwise hemodynamic and vascular changes that occur, predisposing the eye and other tissue beds to pathological conditions. Advancing age does not independently give rise to disease, but does generate increasingly vulnerable vascular beds that are susceptible to further insults. CONCLUSIONS: These results compel a need for further investigation of age-related changes in ocular physiology and pathophysiology.

Age-related macular degeneration and the aging eye.

Age-related macular degeneration (AMD) is an ocular disease that causes damage to the retinal macula, mostly in the elderly. Normal aging processes can lead to structural and blood flow changes that can predispose patients to AMD, although advanced age does not inevitably cause AMD. In this review, we describe changes that occur in the macular structure, such as the retinal pigment epithelium and Bruch's membrane, with advancing age and in AMD. The role of genetics in AMD and age-related changes in ocular blood flow that may play a role in the pathogenesis of AMD are also discussed. Understanding the pathophysiology of AMD development can help guide future research to further comprehend this disease and to develop better treatments to prevent its irreversible central vision loss in the elderly.