الفهرس 
Anatomy of the maculaOnly 14 pages are availabe for public view
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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.