Systemic treatment of vitreous inflammation.

Non infectious vitreous inflammation is often vision threatening and can be associated with potentially life-threatening systemic conditions. Treatment is often challenging as it involves systemic medications that can be associated with adverse effects. The classes of drugs are ever expanding and include corticosteroids, antimetabolites, alkylating agents, T-cell and calcineurin agents, biologic agents, and interferons. Each class of systemic therapy for non-infectious vitreous inflammation is reviewed. We discuss the mechanisms of action, usual clinical dosages, the specific conditions that are treated, the adverse effects, and usual course of treatment for each class of therapy.

Intravitreal devices for the treatment of vitreous inflammation.

The eye is a well-suited organ for local delivery of therapeutics to treat vitreous inflammation as well as other pathologic conditions that induce visual loss. Several conditions are particularly challenging to treat and often require chronic courses of therapy. The use of implantable intravitreal devices for drug delivery is an emerging field in the treatment of vitreous inflammation as well as other ophthalmologic diseases. There are unique challenges in the design of these devices which include implants, polymers, and micro- and nanoparticles. This paper reviews current and investigational drug delivery systems for treating vitreous inflammation as well as other pathologic conditions that induce visual loss. The use of nonbiodegradable devices such as polyvinyl alcohol-ethylene vinyl acetate polymers and polysulfone capillary fibers, and biodegradable devices such as polylactic acid, polyglycolic acid, and polylactic-co-glycolic acid, polycaprolactones, and polyanhydrides are reviewed. Clinically used implantable devices for therapeutic agents including ganciclovir, fluocinolone acetonide, triamcinolone acetonide, and dexamethasone are described. Finally, recently developed investigational particulate drug delivery systems in the form of liposomes, microspheres, and nanoparticles are examined.

Optic nerve edema: complication of peripheral hemodialysis shunt.

Peripheral arteriovenous fistulas for hemodialysis can be complicated by infection, limb edema, venous thrombosis and stenosis, aneurysm, venous hypertension, and rarely, ophthalmic manifestations. We report an unusual case of unilateral optic nerve edema secondary to a contralateral peripheral hemodialysis shunt.

Brown syndrome associated with velocardiofacial syndrome.

Occurrences of Brown syndrome are rare, hence the difficulty in establishing the exact etiology. We report a patient with Brown syndrome associated with velocardiofacial syndrome (deletion of chromosome 22q11), which may implicate a candidate chromosomal region for some cases of this syndrome.

Optical coherence tomography findings of quinine poisoning.

PURPOSE: To report a case of acute quinine poisoning, document acute and chronic macular changes with optical coherence tomography imaging and fluorescein angiography (FA), and to review the literature on ocular toxicity of quinine. METHODS: A 32-year-old white female presented to our Emergency Department after ingesting over 7.5 g of quinine. She underwent a complete ophthalmologic examination, fluorescein angiography, Stratus time-domain optical coherence tomography (OCT), and electroretinography at 72 hours and 15 months postingestion. Stratus time-domain and Cirrus spectral-domain OCT, fundus autofluorescence, and FA were obtained at 28 months postingestion. RESULTS: Fluorescein angiography at 72 hours postingestion revealed normal filling times and vasculature. OCT showed marked thickening of the inner retina bilaterally. At 15 and 28 months follow-up, fundus photography and fluorescein angiography demonstrated optic nerve pallor, severely attenuated retinal vessels while OCT showed inner retinal atrophy. Fundus autofluorescence did not reveal any retinal pigmentary abnormalities. CONCLUSIONS: Quinine toxicity as seen by OCT reveals increased thickness with inner retinal hyperreflectivity acutely with development of significant retinal atrophy in the long-term. Fundus autofluorescence reveals an intact retinal pigment epithelial layer at 28 months. These findings suggest that quinine poisoning may produce a direct toxic effect on the inner retina in the acute phase resulting in long-term retinal atrophy.

Diagnostic challenges in retinitis pigmentosa: genotypic multiplicity and phenotypic variability.

Retinitis pigmentosa (RP) is a heterogeneous group of inherited retinal disorders. Diagnosis can be challenging as more than 40 genes are known to cause non-syndromic RP and phenotypic expression can differ significantly resulting in variations in disease severity, age of onset, rate of progression, and clinical findings. We describe the clinical manifestations of RP, the more commonly known causative gene mutations, and the genotypic-phenotypic correlation of RP.

Acute retinal necrosis after intraocular triamcinolone acetonide injection.

PURPOSE: The purpose of this study was to report a case of acute retinal necrosis after combined cataract surgery and intracameral triamcinolone acetonide injection in a healthy elderly patient. METHODS: Testing used was a clinical examination including fundus photographs, fluo-rescein angiography, and serologic testing. RESULTS: A 75-year-old healthy white woman undergoing cataract extraction received an injection of intracameral triamcinolone acetonide as a substitute for postoperative topical steroids. Two weeks later, the patient developed acute retinal necrosis, which responded well to systemic antiviral therapy. CONCLUSION: Acute retinal necrosis is a rare, but potentially devastating, complication that may be associated with intraocular triamcinolone acetonide injection.

In vivo three-dimensional imaging of neovascular age-related macular degeneration using optical frequency domain imaging at 1050 nm.

PURPOSE: To assess the application of optical frequency domain imaging (OFDI) at 1050 nm for the detection of choroidal neovascularization (CNV) in age-related macular degeneration (AMD) and its response to treatment. Three patients presenting with blurred vision and exudative AMD were imaged before and after anti-VEGF treatment with ranibizumab. METHODS: The patients were imaged with OFDI, a swept-source-based, high-speed optical coherence tomography (OCT) system developed at the Wellman Center for Photomedicine. A center wavelength of 1050 nm was used that has been demonstrated to provide better imaging of the deeper structures of the retina below the RPE, such as the choroidal vasculature. Three-dimensional data sets were acquired in 2 to 4 seconds. RESULTS: En face images were compiled from cross-sectional OFDI data and correlated with color fundus photography (CF) and fluorescein angiograms (FAs). Cross-sectional images were coregistered with CF and FA to obtain depth-resolved information about CNV, CNV volume, retinal thickness, subretinal fluid volume and height of neurosensory detachment before and after treatment with ranibizumab. A band of reduced reflectivity below the RPE was identified in all three subjects that corresponded to areas of confirmed and suspected occult CNV on FA. After treatment, this band was reduced in volume in all patients. CONCLUSIONS: High-speed 3-D OFDI at 1050 nm is a promising technology for imaging the retina and choroid in neovascular AMD. The developed system at 1050 nm provides good contrast for occult (type 1) CNV and may have advantages compared with time domain and current state of the art spectral domain OCT systems (SD-OCT) at 850 nm.

Rapamycin for treatment of refractory dysthyroid compressive optic neuropathy.

We report a patient with dysthyroid optic neuropathy refractory to steroids and orbital decompression treated with rapamycin, a fibroblast and T cell inhibitor. Symptoms, visual acuity, color plate testing, and visual fields improved. Aside from hypercholesterolemia, no complication related to this therapy was observed. By addressing the pathogenesis of thyroid eye disease, rapamycin may represent an alternative when standard treatments fail. Further investigation of rapamycin for treatment of dysthyroid orbitopathy is warranted.