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العنوان
Recent trends in treatment of
Diabetic macular edema
المؤلف
Yousry Amin Elsherbeny,Doaa
هيئة الاعداد
باحث / Doaa Yousry Amin Elsherbeny
مشرف / Amin Gad Elrab
مشرف / Sherein Shafik Wahba
الموضوع
Role of sorbitol accumulation in pathogenesis of DME-
تاريخ النشر
2008 .
عدد الصفحات
86.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
طب العيون
تاريخ الإجازة
1/1/2008
مكان الإجازة
جامعة عين شمس - كلية الطب - opthalmology
الفهرس
Only 14 pages are availabe for public view

from 86

from 86

Abstract

The retinal microangiopathy caused by diabetes leads to ischemic retinopathy with sight-threatening neovascularization when a critical number of capillaries becomes nonperfused and obliterated.
The process begins in individual capillaries and then involves group of capillaries and advances centripetally to the arterioles and their branches.
VEGF is a potent vasopermeability factor which is a growth factor that is highly expressed under diabetic conditions and thought to induce neovascularization and blood-retinal barrier breakdown.
It acts on endothelial cell tight junctions and decreases their protein contents or increases phosphorylation which leads to increase paracellular permeability.
Diabetic macular edema is swelling of the retina in diabetes mellitus due to leaking of fluid from blood vessels within the macula which is believed to be the result of retinal microvascular changes that occur in patients with diabetes.
Thickening of the basement membrane and reduction in the number of pericytes lead to increased permeability and incompetence of retinal vasculature.
Clinically significant macular edema (CSME) occurs if:
- There is thickening of the retina involving the center of the retina (macula) or the area within 500 µm of it.
- if there are hard exudates at or within 500 µm of the center of the retina with thickening of the adjacent retina,
- or if there is a zone of retinal thickening one disk area or larger in size, any part of which is within one disk diameter of the center of the retina.
The current clinical classification into focal, diffuse, and ischaemic maculopathy is useful with respect to pathomechanism and therapy.
Risk factors of developing DME are type 1 and 2 DM with long duration of diabetes up to 10 years, poor control of hyperglycemia, renal diseases, systemic hypertension and serum hyperlipidemia.
Diagnosis of DME is done by visual acuity, Amsler grid, fundus biomicroscopy, fundus angiography, optical coherence tomography and scanning retinal thickness analyzer.
The benefits of early management, such as intensive diabetes control, persist for years, even with subsequent hyperglycemia
Regular screening and early treatment for DR/DME can potentially save years of vision and reduce social costs.
In patients with diabetes and diabetic retinopathy, single measurements of central foveal thickness using OCT correlate with visual acuity and are a successful means of monitoring macular thickening before and after therapy.
Both measurements of foveal and macular thickness with OCT may appear to be more sensitive than slit lamp examination for evaluating clinically significant macular edema.
Criteria for treatment depend on the presence of retinal thickening and its distance from the center of the fovea, which is clinically assessed by contact lens biomicroscopy or stereophotography.
The recommended values for HbA1c, blood pressure, and LDL cholesterol are <6.5–7%, <130/< 85 mmHg, and <100 mg/dl, respectively.
Older age of the patient, increasing size of CSME, poor pre laser visual acuity were associated with poor prognosis.
Involvement of the foveal centre was not an independent poor prognostic sign unless associated with poor baseline visual acuity.
The results of ETDRS suggest that diabetic maculopathy should be treated early when the visual acuity is normal or near normal and the size of CSME is still small provided it meets the diagnostic criteria of ETDRS
Treatment of DME is done by laser photocoagulation either focal, grid or modified grid laser, vitrectomy specially if there is taut posterior hyaloid membrane causing traction on the macula, medically through intravitreal injection of steroids .
New modalities of treatment of DME includes injection of anti VEGF is used and the use of ADI , AGE inhibitors , PKC-B inhibitors , antioxidants , anti- angiogenic agents and others are still in trials
Photocoagulation strategies (i.e., light laser photocoagulation and subthreshold micropulse diode laser) as well as pharmacological approaches (i.e., antioxidants, PKC inhibitors, aldose-reductase and AGE inhibitors, VEGF inhibitors, intravitreal triamcinolone) are emerging the new laser and pharmacological treatments currently investigated are promising and need to be confirmed by large, controlled clinical trials