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Uveitis glaucoma

Intraorbital tumor Caroticocavernous fistula Retinal migraine Intracranial dural malformation Paraneoplastic retinopathy Reversible diabetic cataract Uveitis-glaucoma-hyphema syndrome... [Pg.104]

The primary vision-threatening manifestations of sarcoidosis are uveitis, glaucoma, and optic nerve involvement dry eye (keratoconjunctivitis sicca) is common but of lower risk. Anterior segment findings (including conjunctival granulomas, iris nodules, iridocyclitis, and keratoconjunctivitis sicca) occur in up to 70% of patients. In contrast, posterior uveitis occurs in up to 30% of patients. If only vasculitis, periphlebitis, or retinal neovascularization is considered, the frequency ranges from 4% to 17% of cases. Optic nerve involvement presents in up to 7% of patients. [Pg.631]

Hypersensitivity to any component of the formulation where constriction is undesirable (eg, acute iritis, acute or anterior uveitis, some forms of secondary glaucoma, pupillary block glaucoma, acute inflammatory disease of the anterior chamber). [Pg.2087]

Intravitreal triamcinolone injection is safe and effective for cystoid macular edema caused by uveitis, diabetic maculopathy, and central retinal vein occlusion, and for pseudophakic cystoid macular edema. Potential risks include glaucoma, cataract, retinal detachment, and endophthalmitis. Infectious endophthalmitis is extremely rare when appropriate sterile technique is practised. Seven patients developed a clinical picture simulating endophthalmitis after intravitreal injection of triamcinolone (71). The authors believed that this effect was a toxic reaction to the injected material and explained that the differential diagnosis of infectious endophthalmitis in eyes that have been injected with triamcinolone under sterile conditions includes a sterile toxic endophthalmitis that requires careful monitoring, perhaps every 8-12 hours, in order to determine whether the inflammation is worsening or improving. Resolution occurs spontaneously, and in the absence of eye pain unnecessary intervention can be avoided. [Pg.12]

The ocular adverse effects of latanoprost include conjunctival hyperemia, iris pigmentation, periocular skin color changes, anterior uveitis, and cystoid macular edema in pseudophakic patients (77,78). H. simplex dendritic keratitis has been reported after treatment with latanoprost (79). In patients with uveitic glaucoma, latanoprost can cause increased intraocular pressure and recurrence of inflammation (80). [Pg.106]

Several randomized double-blind trials provided evidence that oral acyclovir 800 mg, five times daily, is the most effective dosage for treating HZO. Studies also stressed the importance of initiating treatment within the first 72 hours to prevent severe complications of HZO (i.e., keratitis, uveitis, secondary glaucoma, scleritis, optic neuritis, and acute retinal necrosis [ARN]).When there is ophthalmic involvement, it is recommended to treat even if the rash has been present for more than 72 hours. In addition, there is evidence that 7 days of treatment may be adequate. Studies have been shown that oral acyclovir may lessen the incidence and duration of postherpetic neuralgia associated with HZO, as shown in Table 11-10. [Pg.201]

Topical ocular steroid administration also may cause the development of cataracts in both children and adults. Use of topical steroids for several years to eliminate redness associated with contact lens wear resulted in PSC formation as well as glaucoma and visual field loss. The opacities associated with steroid administration resemble those produced by ionizing radiation and ocular disease such as uveitis, retinitis pigmentosa, and retinal detachment. They differ from opacities associated with diabetes and trauma but are indistinguishable from lens changes associated with posterior subcapsular age-related cataract. [Pg.230]

All patients with blepharospasm should receive dry eye testing, because dry eye can exacerbate the spasms. Appropriate dry eye therapy with ocular lubricants or lacrimal occlusion should accompany any other treatment for blepharospasm. The clinician should search for and correct other treatable problems that may exacerbate the disease, such as corneal erosion, fiareign bodies, acute glaucoma, uveitis, entropion, eyelash abnormalities, and blepharitis. Emotional problems and neurosis usually are not a significant precipitating cause of blepharospasm in adults but may play a prominent role in affected younger individuals. [Pg.377]

Management of the ocular aspects of Reiter s syndrome is directed toward control of inflammation.The uveitis can be fairly severe and resistant to therapy. In most instances such topical steroids as 1% prednisolone acetate or 0.1% dexamethasone are recommended. Dosage is variable but in severe cases should be administered initially every 1 to 2 hours and accompanied by such cycloplegic agents as 5% homatropine or 0.25% scopolamine two to three times daily. Aggressive treatment reduces formation of synechiae and subsequent secondary glaucoma. In patients who have severe uveitis, either sub-Tenon s capsule or oral steroids may be used in conjimction with topical management. [Pg.473]

Although cataract surgery is a potential precursor to bullous keratopathy, there are many other causes. Fuchs endothelial dystrophy, infection, trauma, retained foreign body, posterior polymorphous dystrophy, chronic uveitis, chronically elevated intraocular pressure (lOP), and vitreous touch are all known causes of bullous keratopathy. Other less common causes of bullous keratopathy include corneal thermal injury secondary to carbon dioxide laser skin resurfacing, air bag trauma, the use of topical dorzolamide hydrochloride in glaucoma patients with endothelial compromise, and use of mitomycin C during trabeculectomy surgery. [Pg.493]

Band keratopathy was first described in 1848 and is a chronic degenerative condition characterized by the deposition of calcium carbonate salts in the superficial corneal layers, most frequently in the interpalpebral area. Although there are many reported cases of idiopathic band keratopathy, some of which seem to have a hereditary component, the most common causes are associated with chronic ocular inflammation and systemic conditions resulting in altered calcium metabolism. Band keratopathy is typically seen in eyes with chronic uveitis, severe superficial keratitis, corneal ulcers, chemical burns, interstitial keratitis (IK), trachoma, phthisis bulbi, and prolonged glaucoma. The chronic anterior uveitis of juvenile idiopathic arthritis is frequently associated with band keratopathy, with one study reporting its development in 66% of patients with juvenile idiopathic arthritis. [Pg.494]

Epithelial bullae can be found in some cases of disciform keratitis, as can a Wessley ring, which is composed of immune cells surrounding the discoid edema.A mild to moderate uveitis with keratic precipitates is usually present, although it may not be visible due to corneal edema. Secondary glaucoma can also develop, primarily the result of intraocular inflammation (trabeculitis). [Pg.528]

Because intermediate uveitis does not involve the ciliary body or trabecular meshwork, lOP is rarely impacted by this disease course. However, should late-stage changes occur in the anterior chamber (e.g., synechiae, iris neovascularization), the clinician is obligated to perform tonometry and monitor for secondary glaucoma. Also, use of topical, injectable, and/or systemic corticosteroids in the treatment of uveitis may induce a precipitous rise in lOP, resulting in steroid-induced glaucoma. [Pg.592]

Complications associated with anterior uveitis may include cataracts, glaucoma, band keratopathy, and CME. Posterior subcapsular cataracts are the most commonly encountered lenticular change associated with chronic uveitis. Additionally, it is well known that long-term topical steroid use can induce or accelerate posterior subcapsular cataract development. [Pg.596]

Anticholinesterase agents are potent drugs with many potential adverse effects iris cysts and anterior subcapsu-lar lens cataracts are the most serious and well known. Other significant but less common ocular manifestations include retinal detachment, angle-closure glaucoma, and uveitis. Common but less serious adverse effects include... [Pg.666]


See other pages where Uveitis glaucoma is mentioned: [Pg.624]    [Pg.39]    [Pg.582]    [Pg.610]    [Pg.296]    [Pg.624]    [Pg.624]    [Pg.39]    [Pg.582]    [Pg.610]    [Pg.296]    [Pg.624]    [Pg.628]    [Pg.2101]    [Pg.84]    [Pg.84]    [Pg.48]    [Pg.124]    [Pg.125]    [Pg.174]    [Pg.72]    [Pg.232]    [Pg.510]    [Pg.529]    [Pg.588]    [Pg.590]    [Pg.596]    [Pg.100]    [Pg.100]   
See also in sourсe #XX -- [ Pg.631 ]




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