الفهرس | Only 14 pages are availabe for public view |
Abstract Cystoid macular oedema represents a common pathologic sequel of the retina associated with a broad spectrum of potential insults. It consists of a localized expansion of the retinal intracelluar and/ or extracellular space in the macular area. This predilection to the macular region is probably associated with the loose binding of inner connecting fibers in Henle’s layer . The leakage may be generalized. resulting in a diffuse thickening of the posterior pole (diffuse macular oedema) . However cystic spaces consisting of ophthalmoscopically clear fluid are often detectable clinically in the macular area. so-called cystoid macular oedema. A wide variety of conditions can disrupt either the inner or the outer blood-retinal barrier. The list includes metabolic diseases, ischemic diseases, mechanical disruption, hydrostatic factors, inflammation with release of chemical mediators, hereditary diseases, and toxic conditions. Cystoid macular oedema is a common cause of visual impairment in patients with diabetic retinopathy, which occurs of visual impairment in diabetic patients with at least 20 years duration of the disease. The pathogenesis of diabetes macular oedema is more complex than other forms of macular edema and includes poorly demarcated leakage from abnormal retinal capillaries and microaneurysms. Other mechanisms that had been postulated include these changes. Although, it is not clearly defined, its origin may be the RPE, pericytes, retinal capillary endothelial cells, muller cells and astrocytes.It is known to be up regulated by ischaemia, reactive oxygen intermediates, advanced glycation end products and insulin like growth factors. Retinal vascular obstruction can cause disruption of the blood- retinal barrier ,good examples of this are central and branch retinal vein occlusion where the obstruction of a vein results in abnormal leakage from the distal capillary bed .this leakage can dissect into the macular area resulting in CME. Aphakic or pseudophakic CME is a relatively frequent complication of cataract surgery. It has been described with greater frequency after complicated surgery or in patients with eye diseases, but aslo in normal eyes after uncomplicated surgery. The vitreomacular traction syndrome is a well-recognized complication of partial posterior vitreous detachment (PVD). the vitreous is separated from the retina throughout the peripheral fundus but remains adherent posterioly, resulting in anteroposterior traction on the macular area and optic nerve. Associated findings typically include epiretinal membrane and varying degrees of macular oedema with fluorescein leakage, macular puckering and tractional macular detachment. CME is a common complication of inflammation in the eye and often seen in patients with intermediate uveitis. Prostaglandins, complement, platelet- activating factor (PAF), lysosmal enzymes, cytokines, nitric oxide, and endothelin had also been implicated in inflammatory conditions such as postoperative inflammation. clinical examination of patients with suspected cystoid macular edema begins with stereoscpic visualization using either indirect fundus ophthalmoscope or fundus biomircroscopic examination using fundus contact lens or the 60 or 90 D lens. Various methods of investigation are utilized to detect disruption of the BRB in order to determine the presence and the extent of cystoid macular edema. Fundus fluorescein angiogram is clinically the most widely available and useful test. Apart from being a significant diagnostic modality also it improves the accuracy of planning treatment.It is useful in estimating the retinal thickness, the level of the leakage and the location and extent of cystic spaces. Evaluation of macular oedema by OCT has become particularly useful in cases of diabetic maculopathy, retinal vein occlusions, uveitic and postoperative inflammations, as well as in vitreomacular traction syndromes. The OCT images demonstrate reproducible patterns of retinal morphology that corresponded to lacation of retinal layers seen on light microscopic overlays. The subclinical foveal oedema that has been proposed in some cases of deteriorated visual acuity with normal stereofundus photography, was detected by OCT. variety of approaches to the treatment of macular oedema had been attempted with a variable degree of success. these options have included topical and systemic steroids, topical and oral non-steroidal anti- inflammatory agents and laser photocoagulation treatment. Other therapeutic modalities, including immunomodulators, intravitreal injection of triamcinolone, and parsplana vitrectomy have also been employed. clinical trials are currently looking into the use of a steroid slow-release intravitreal device for the management of cystoid macular oedema secondary to uveitis and diabetes. In aphakic or pseudophakic CME, NSAIDs are useful as they inhibit the enzyme cyclooxygenase, which is required for the production of the prostaglandins as a degradation product of arachidonic acid. Corticosteroids may be administered topically, orally, parenterally, or by periocular injection . periocular injections may be delivered via posterior subtenon ’s or peribulbar routes. They have advantages over topical application as they allow administration of a large bolus of drug ,also allow a more sustained release of drug. They also exert a maximal, long-lasting response at the site of injection. Due to the Potentially severe systemic complication, oral steroids should be used with caution. Intravitreal corticosteroids are another therapeutic modality that can be used in patients with intractable CME attributable to chronic uveitis and more to diabetic or pseudophakic cystoid macular oedema. The exact mechanisms by which intravitreal corticosteroids act on the BRB remain unclear , corticosteroids reduce retinal capillary permeability by increasing the activity and/or density of the tight junction in the retinal capillary endothelium . Intravitreal corticosteroids inhibit the expression of the VEGF gene and also corticosteroids inhibit the metabolic pathway of VEGF via their modulation of signals or effectors’ proteins downstream of the VEGF receptor . If long-term, high-dose corticosteroids are required the use of Steroid-sparing agents should be considered . several studies had Evaluated the effect of intravitreal sustained-release cyclosporine (5mg) in the treatment of experimental uveitis. Hyperbaric oxygen has been reported to improve visual function in patients with chronic macular oedema associated predominantly with retinal vein occlusion. Laser photocoagulation is a therapeutic modality using a strong laser to coagulate tissues. The ETDRS used two types of treatment for diabetic macular oedema : focal and grid laser treatment . Surgery in cystoid macular oedema in its broadest sense aims to relieve vitreomacular traction and remove the cytokine-laden vitreous. Peeling of epiretinal membranes, removal of the posterior vitreous face. and peeling the ILM may all lead to breaking the possible points of vitreoretinal adhesion underlying the traction. In cases where the direct VMT leads to a shallow traction retinal detachment, this can also be relieved by surgery. Also, there is a proposal that the vitreous may limit rates of fluid flow in the posterior segment if it is removed,a higher amount of oxygenated aqueous would be able to circulate and enhance inner retinal circulation. Recently, Anti – VEGF including bevacizumab (Avastin) is being Used for treatment of DME, oedema due to vein occlusion and edema secondary to uveitis. The use of intravitreal avastin for BRVO offers significant advantages over triamcionlone and grid – laser treatment. Novel intavitreal drug deliver system (DDS) ( dexamethasone Posterior segment drug delivery system) has been developed, that gradually releases 350or 700 µm of dexamethasone after it has been inserted into the eye through a small pars plana incision or puncture. Dexamethasone DDS can be used to treat cystoid macular oedema. |