الفهرس 
Anatomy of the maculaOnly 14 pages are availabe for public view
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Abstract
CME can occur due to various ocular conditions among which diabetes, vein occlusions, Irvine Gas syndrome and wet AMD are the commonest causes. Regardless of the initial insult, the fluid accumulation in CME is the direct consequence of damage to the retinal vascular endothelium. The main method of diagnosing CME is both FFA and OCT.
There are many modalities for treating CME but the cause must be identified and accordingly the management will be decided. Generally treatment of CME is divided into four approaches; medical, surgical, laser photocoagulation and intravitreal injections.
Medical management may be either topical or systemic. One of the drugs is COI such as ketorlac which may be beneficial in prevention and treatment of post-operative CME. Another drug used topically is corticosteroid. It acts by inhibiting phospholipase A2 thereby blocking PG synthesis. Locally they decrease intracellular and intercellular edema, suppress macrophage activity, and de crease lymphokine production.
Carbonic anhydrase inhibitors (CAI) such as acetazolamide (Diamox) facilitate the transport of water across the RPE from sub retinal space to choroid. It is considered the second-line drug for CME as it is active in drying macular edema in Irvine Gass syndrome and RP.
Surgical treatment is not available for CME. However, removal of an epiretinal membrane or vitrectomy may lead to resolution of CME.
Focal or grid macular photocoagulation is currently the benchmark against which other treatment modalities are compared in treatment of DME.
Intra-vitreal injection is one of the most commonly used modalities nowadays in treatment of many ocular conditions. Among the drugs injected intravitreal is TA. It has both an anti-oedematous effect as well as an anti-neovascular effect therefore is useful in treatment of most conditions associated with CME such as diabetes, pseudophakic CME and vein occlusions. Unfortunately TA has been associated with serious side-effects such as secondary elevation of IOP and cataract.
Anti-VEGF therapy is the second type of drug which may be injected intravitreal. It targets VEGF molecule which has often been implicated in cases of neovascularisation. The role of anti-VEGF drugs in DME is affecting the endothelial tight junction proteins, and decreases vascular permeability thereby decreasing ME and yields a better visual outcome.
Pegaptanib is an aptamer targeting the heparin binding domain present in VEGF-A. It is currently used in treatment of CNV secondary to AMD. Ranibizumab is a potent, nonselective inhibitor of all VEGF-A isoforms and bioactive proteolytic products. Ranibizumab was created from a full-sized antibody developed previously as an anti-cancer agent. Bevacizumab is a recombinant full-length humanized murine monoclonal immunoglobulin antibody directed against human VEGF-A, and thus a closely-related drug to ranibizumab. Bevacizumab is highly effective, safe and is an attractive treatment option due to its cost advantage over ranibizumab.
Intravitreal injection anti-VEGF has the advantage of IOP stability compared with the intravitreal TA. Also the risk of cataract progression is significantly lower with anti-VEGF therapy.
Infectious endophthalmitis is the most feared complication of IV injections and has been reported after application of all currently used preparations. The prevention of postoperative endophthalmitis is one of the key issues influencing the organization and implementation of intravitreal injections on a larger scale.
Combination therapy of two of more of the above modalities may have a more beneficial role than either intravitreal injections or macular laser photocoagulation alone especially in DME and AMD.
Many emerging therapies are currently under trial as well for treatment of CME such as VEGF trap, small interfering RNAs, VEGF receptor tyrosine kinase inhibitors and nucleic acid therapies. The strategy of targeting VEGF has proven valuable in the treatment of blinding eye conditions. VEGF is only the first of many potential targets, and the continued development of other agents promises future combination therapies that may provide greater and sustained visual improvement. Additional advances in drug delivery will facilitate long-term intraocular delivery of such molecules, further enabling better and safer treatments.