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Edema cystoid macular

M/sce/Zaneoas. Atrial fibrillation and other cardiac arrhythmias, cystoid macular edema, decreased glucose tolerance, hypotension, orthostasis, toxic amblyopia, transient headache. [Pg.9]

Adverse reactions may include transient stinging and burning eye pain/ache browache headache allergic lid reaction conjunctival hyperemia conjunctival or corneal pigmentation ocular irritation (hypersensitivity) localized adrenochrome deposits in conjunctiva and cornea (prolonged use) reversible cystoid macular edema (may result from use in aphakic patients) palpitations tachycardia extrasystoles cardiac arrhythmia hypertension faintness. [Pg.2077]

Unlabeled Uses Treatment of vascular headaches (oral) to reduce the occurrence and severity of cystoid macular edema after cataract surgery (ophthalmic form)... [Pg.356]

Inflammation (iritis/uveitis) and macular edema, including cystoid macular edema, have been reported. [Pg.676]

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]

Hypopyon associated with non-infectious endophthalmitis after intravitreal injection of triamcinolone has been described previously (72). Pseudohypopyon and sterile endophthalmitis after intravitreal injection of triamcinolone for pseudophakic cystoid macular edema has been reported (73). [Pg.12]

Cystoid macular edema, iritis, Herpes simplex keratitis, periocular skin darkening, and headaches have been described in patients treated with prostaglandin analogues. These adverse effects occur rarely, and cystoid macular edema, iritis and H. simplex keratitis occur in eyes with risk factors. Repeated rechallenge with masked controls is required to establish a causal relation. However, even without firm establishment of a causal relation, caution is advised with the use of prostaglandin analogues in the eyes of patients with risk factors for macular edema, iritis, and H. simplex keratitis (76). [Pg.106]

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]

Cystoid macular edema developed in two patients treated with topical latanoprost for glaucoma (23). Latanoprost was withdrawn, and the cystoid macular edema was treated with topical corticosteroids and ketorolac, with improvement in visual acuity. The macular edema resolved in both cases. [Pg.124]

Cystoid macular edema has been reported in four other patients shortly after they started to use latanoprost (24) and other reports have appeared (25-29). A possible explanation is enhanced disruption of the blood-aqueous barrier induced by latanoprost (28). [Pg.124]

A review of the published literature (28 eyes in 25 patients) has shown that in all cases there were other associated risk factors, so that a definitive conclusion about a causal relation cannot be reached (30). Nevertheless, latanoprost should be used with caution in patients with risk factors for cystoid macular edema and special surveillance is necessary. [Pg.124]

Callanan D, Fellman RL, Savage JA. Latanoprost-asso-ciated cystoid macular edema. Am J Ophthalmol 1998 126(l) 134-5. [Pg.127]

Ayyala RS, Cruz DA, Margo CE, Harman LE, Pautler SE, Misch DM, Mines JA, Richards DW. Cystoid macular edema associated with latanoprost in aphakic and pseudo-phakic eyes. Am J Ophthalmol 1998 126(4) 602-4. [Pg.127]

Gaddie IB, Bennett DW. Cystoid macular edema associated with the use of latanoprost. J Am Optom Assoc 1998 69(2) 122-8. [Pg.127]

Heier JS, Steinert RF, Frederick AR Jr. Cystoid macular edema associated with latanoprost use. Arch Ophthalmol 1998 116(5) 680-2. [Pg.127]

Miyake K, Ota I, Maekubo K, Ichihashi S, Miyake S. Latanoprost accelerates disruption of the blood-aqueous barrier and the incidence of angiographic cystoid macular edema in early postoperative pseudophakias. Arch Ophthalmol 1999 117(l) 34-40. [Pg.127]

Moroi SE, Gottfredsdottir MS, Schteingart MT, Elner SG, Lee CM, Schertzer RM, Abrams GW, Johnson MW. Cystoid macular edema associated with latanoprost therapy in a case series of patients with glaucoma and ocular hypertension. Ophthalmology 1999 106(5) 1024-9. [Pg.127]

Schumer RA, Camras CB, Mandahl AK. Latanoprost and cystoid macular edema is there a causal relation Curr Opin Ophthalmol 2000 11(2) 94-100. [Pg.127]

There have been repeated reports of ophthalmic complications from tamoxifen, including irreversible retinopathy with seriously reduced visual acuity, retractile opacities, cystoid macular edema, retinal yellow-white dots, and keratopathy (SEDA-6, 356 SEDA-7, 391 SEDA-16, 466). [Pg.304]

A few cases of advanced cystoid macular edema have been reported in the older literature these took months to resolve once nicotinic acid was withdrawn (SEDA-14, 331 SEDA-20, 191 15,20). Four new cases have been added in patients who took nicotinic acid 2-4.5 g/day (21,22). The first symptoms of blurred vision appeared 1-18 months after the start of therapy. Withdrawal of nicotinic acid resulted in improvement of visual acuity and resolution of the cystoid macular edema within 1-2 months. A particular feature that distinguishes this form of maculopathy is the absence of leakage on fluorescein angiography. Retinal edema, when it occurs, will abate on withdrawal of nicotinic acid (15). [Pg.561]

Posterior snb-Tenon s injection of corticosteroids is most often nsed in the treatment of chronic eqnatorial and mid-zone posterior uveitis, including inflammation of the macnlar region. Cystoid macular edema after cataract extraction and diabetic macular edema are treated occasionally with snb-Tenon s repository steroids. [Pg.49]

Cystoid macular edema Anterior uveitis Punctate corneal erosions Corneal pseudodendrites... [Pg.141]

Numerous cases have been reported in which latanoprost therapy has been associated with the development of cystoid macular edema (CME). Considering the role that prostaglandins play in the pathogenesis of CME, it may be reasonable to assume that topically applied latanoprost can increase the risk of CME. However, latanoprost itself is not known to be vasoactive or to affect vascular permeability. Furthermore, pharmacokinetic studies have feiled to demonstrate significant levels of latanoprost in the posterior segment of the eye after topical application. Indeed, controlled clinical studies... [Pg.142]

An additional clinical use of acetazolamide is unrelated to its ocular hypotensive properties.The 500-mg acetazolamide capsule administered daily for 2 weeks may produce either a partial or a complete resolution of macular edema in patients with cystoid macular edema (CME), retinitis pigmentosa, and chronic intermediate uveitis (pars planitis). Macular edema produced by primary retinal vascular diseases (branch and central retinal vein occlusion and macular telangiectasia) did not respond to acetazolamide therapy. It is believed that acetazolamide may improve visual function if the macular edema stems from retinal pigment epithelial dysfunction. Improved macular edema in these conditions may be associated with fluid movement from the retina to the choroid. However, acetazolamide does not appear to alter macular blood flow. [Pg.161]

Grover S, Apushkin MA, Fishman GA. Topical dorzolamide for the treatment of cystoid macular edema in patients with retinitis pigmentosa. Am J Ophthalmol 2006 141 850-858. [Pg.171]

Halpem DL, Pasquale LR. Cystoid macular edema in aphakia and pseudophakia after use of prostaglandia analogs. Semin Ophthalmol 2002 17 181-186. [Pg.171]

Although oral NSAIDs have application to ophthalmic pain management, topical NSAIDs have the more immediate utility. Some of the earliest indications for topical NSAIDs were prophylaxis and treatment for cystoid macular edema (CME) as well as pain and inflammation management after cataract surgery.This pioneering work ras done befiare the introduction of less traumatic procedures such as clear corneal incisions. The seminal investigations using... [Pg.234]

Cupples HP Lefler WH, Pulido JS, et al. Improvement in visual acuity in chronic aphakic and pseudophakic cystoid macular edema after treatment with topical 0.5% ketorolac tromethamine.Am J Ophthalmol 1991 112 514-519. [Pg.243]

Kraff M, et al. Prophylaxis of pseudophakic cystoid macular edema with topical indomethacin. Ophthalmology 1982 89 885-890. [Pg.243]

Various ocular conditions may benefit from medication delivered via a subconjimctival injection. Applications include recalcitrant uveitis, cystoid macular edema, felling trabeculectomy, and severe corneal ulcer in a noncompli-ant patient. One to two drops of topical anesthesia should be instilled. Additionally, an anesthetic-soaked pledget of 4% lidocaine applied to the area of injection may enhance comfort, particularly if the conjunctiva is to be lifted with forceps before introducing the needle into the subconjunctival space (Figure 19-4). [Pg.323]

A thorough examination should be performed to determine the cause of bullous keratopathy. The specific treatment plan depends on both the cause and severity. Examination of the endothelium, internal structures, and fundus can be enhanced by the use of topical hyperos-motics to decrease epithelial edema. Internal examination is essential to determine if there is corneal touch by the intraocular lens or vitreous face and to rule out cystoid macular edema or intraocular inflammation. [Pg.493]

Figure 30-15 Fluorescein angiogram demonstrating clinical cystoid macular edema. Figure 30-15 Fluorescein angiogram demonstrating clinical cystoid macular edema.
Figure 31-10 Cystoid macular edema, late phase of fluorescein angiogram. (Photo courtesy Sheila E Anderson, O.D.)... Figure 31-10 Cystoid macular edema, late phase of fluorescein angiogram. (Photo courtesy Sheila E Anderson, O.D.)...
HeierJS, Topping TM, Baumann W, et al. Ketorolac versus prednisolone versus combination therapy in the treatment of acute pseudophakic cystoid macular edema. Ophthalmology 2000 107 2034. [Pg.641]

Jonas JB, Kreissig I, Degeming RE Intravitreal triamcinolone acetomde for pseudophakic cystoid macular edema. AmJ Ophthalmol 2003 136 384. [Pg.641]


See other pages where Edema cystoid macular is mentioned: [Pg.919]    [Pg.920]    [Pg.12]    [Pg.13]    [Pg.212]    [Pg.6]    [Pg.8]    [Pg.25]    [Pg.308]    [Pg.338]    [Pg.588]    [Pg.602]    [Pg.613]    [Pg.618]    [Pg.632]    [Pg.641]   
See also in sourсe #XX -- [ Pg.632 , Pg.633 , Pg.633 , Pg.634 ]




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