OCT choroidal thickness in diabetic macular edema
Omnia Salah El-Dien Hegazy;
Abstract
Diabetic macular edema (DME) is a leading cause of blindness in working class of developed countries. DME accounts for about 12% of new cases of blindness annually,being more prevalent in type 1 diabetes, and associated with longer duration of diabetes, high systolic blood pressure and elevated glycosylated hemoglobin.
The pathogenesis of DME is not well defined presently. Hyperglycemia is stated to cause capillary endothelial damage and changes in leukocyte function. Moreover, hyperglycemia has been described to stimulate oxidative stress agents, such as advanced glycation endproducts and the protein kinase C (PKC) pathway. Different inflammatory mediators seem to play a role in aggravating DME, including vascular endothelial growth factor (VEGF), placental growth factor (PlGF), and hepatocyte growth factor (HGF).
It has long been approved that diabetic macular edema can occur at all stages of diabetic retinopathy. Classically, patients suffer from a gradual onset of blurry vision, metamorphobsia and in severe cases, the macula becomes thickened and even cystic with significant visual loss.
Fluorescein angiography (FA)provides critical biological data in the diagnosis and characterization of DME disease, such as site, severity, and leakage source; additionally, various subtypes of DME have been suggested depending on differences in the pattern of fluorescein leakage as seen by FA
Optical coherence tomography (OCT) is a noninvasive method that evaluates diabetic macular edema. It can quantify the development and resolution of macular edema after treatment, and also evaluate choroid layer which play an important role in outer retinal nutrition.
Different studies reported progressive reduction of the choroidal thickness with age even in normal healthy person.
DME causes increase in the central foveal thickness with deterioration of vision. Different studies reported negative correlation between vision and macular thickness.
SFCT progressively reduced in DR according to its severity and presence of DME. This reduction may be due to decrease choroidal blood flow, which in turn disturbs RPE pump function, and possibly contributes to pathogenesis of DME and retina hypoxia. The choroid is the main source of nutrition to outer retina so its thinning may affect integrity of photoreceptors and its length which has high correlation with vision, but we did not find correlation between the choroid and outer retinal layer.
Different authors reported positive correlation between vision and outer retinal layer and choroidal thickness in DME cases. We found reduction of choroid below 215UM and /or reduction of outer retinal layer below 88Um is associated with reduced vision.
So tight control of blood sugar will reduce diabetic complications and routine fundus examination is mandatory for early detection and treatment of retinopathy
The pathogenesis of DME is not well defined presently. Hyperglycemia is stated to cause capillary endothelial damage and changes in leukocyte function. Moreover, hyperglycemia has been described to stimulate oxidative stress agents, such as advanced glycation endproducts and the protein kinase C (PKC) pathway. Different inflammatory mediators seem to play a role in aggravating DME, including vascular endothelial growth factor (VEGF), placental growth factor (PlGF), and hepatocyte growth factor (HGF).
It has long been approved that diabetic macular edema can occur at all stages of diabetic retinopathy. Classically, patients suffer from a gradual onset of blurry vision, metamorphobsia and in severe cases, the macula becomes thickened and even cystic with significant visual loss.
Fluorescein angiography (FA)provides critical biological data in the diagnosis and characterization of DME disease, such as site, severity, and leakage source; additionally, various subtypes of DME have been suggested depending on differences in the pattern of fluorescein leakage as seen by FA
Optical coherence tomography (OCT) is a noninvasive method that evaluates diabetic macular edema. It can quantify the development and resolution of macular edema after treatment, and also evaluate choroid layer which play an important role in outer retinal nutrition.
Different studies reported progressive reduction of the choroidal thickness with age even in normal healthy person.
DME causes increase in the central foveal thickness with deterioration of vision. Different studies reported negative correlation between vision and macular thickness.
SFCT progressively reduced in DR according to its severity and presence of DME. This reduction may be due to decrease choroidal blood flow, which in turn disturbs RPE pump function, and possibly contributes to pathogenesis of DME and retina hypoxia. The choroid is the main source of nutrition to outer retina so its thinning may affect integrity of photoreceptors and its length which has high correlation with vision, but we did not find correlation between the choroid and outer retinal layer.
Different authors reported positive correlation between vision and outer retinal layer and choroidal thickness in DME cases. We found reduction of choroid below 215UM and /or reduction of outer retinal layer below 88Um is associated with reduced vision.
So tight control of blood sugar will reduce diabetic complications and routine fundus examination is mandatory for early detection and treatment of retinopathy
Other data
| Title | OCT choroidal thickness in diabetic macular edema | Other Titles | استخدام التصوير المقطعى الضوئى فى قياس سمك المشيميه لحالات ارتشاح مقولة العين السكرى | Authors | Omnia Salah El-Dien Hegazy | Issue Date | 2016 |
Attached Files
| File | Size | Format | |
|---|---|---|---|
| G13031.pdf | 745.07 kB | Adobe PDF | View/Open |
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