on Vitreomacular Interface Abnormalities in Diabetic Retinopathy Clinical Trial
Official title:
Vitreomacular Interface Abnormalities Indiabetic Retinopathy Using Ocular Coherence Tomography
to evaluate vitreomacular interface abnormalities in diabetic retinopathy by using Ocular Coherence Tomography (OCT)
Diabetic retinopathy (DR) is a leading health concern and a major cause of blindness .DR can
be complicated by scar tissue formation, macular edema tractional retinal detachment. Optical
coherence tomography has found patient with DR has diffuse retinal thickening , cystoid
macular edema ,posterior hayaloid traction ,tractional retinal detachment.
The VMI in patient with DR can influence the emergence ,progression ,and treatment of DR.
The role of posterior hyaloid and vitreous on viteromacular interface abnormalities The
anomalous separation of vitreous cortex from ILM can lead to abnormal vitreomacular
interface. This separation can happen when liquefaction occur faster than detachment of the
vitreous cortex or when an abnormal adhesion of the vitreous cortex to the ILM occur.
The VMI abnormalities in DR include I. Vitreomacular adhesion The International Vitreomacular
Traction Study group has defined the vitremacular adhesion as specific stage of vitreous
separation when partial detachment of the vitreous in perifoveal area has occurred without
any abnormalities to the retinal contour.
II. Vitreomacular traction There is abnormal vitreous adhesion, there can be excessive
traction on the macula from the vitreous that change the contour of foveal surface. By OCT
any distortion of foveal contour together with partial posterior vitreous detachment is
considered vitreomacular traction . In accordance with the International Vitreomacular
Traction Study Group definition vitreomacular traction can be classified as focal or broad
based on horizontal area of adhesion.
III. Cystoid macular edema The vitreous has been implicated as a cause of macular edema via
mechanical and physiologic mechanisms.One of the most constructive hypothesis on how
vitreomacular traction may result in macular edema was given by Schubert in 1989,and was
summarized by Bringmann and Wiedmann Vitro retinal traction can also exert forces at the
level of retinal pigment epithelium ,which can eventually result in morphological retinal
pigment epithelial changes .
IV. Epiretinal membrane The epiretinal membrane is a cellular proliferation that creates a
semi translucent, fibrocellular proliferation on the surface of the inner retina. Because
epiretinal membrane contain contractile cellular elements they can be associated with retinal
folding and macular thickening thereby leading to decreased visual acuity, metamorphopsia,
monocular diplopia .
V. Full thickness hole Is a full thickness defect in the fovea, include the complete
interruption of all retinal layers from the ILM to the retinal pigment epithelium. antero
posterior traction, secondary to abnormal attachment at the fovea, and tangential contraction
of the perifoveal vitreous cortex may be responsible for the development of the macular hole.
VI. Lamellar holes These include an irregular foveal contour, a defect or break in the inner
fovea, a splitting of the inner and outer retina , lack of a full thickness foveal defect,
and intact photo receptors.
VII. Macular pseudo hole By OCT the pseudo hole has no loss of retinal tissue. They have
invaginated or heaped foveal edge, an epiretinal membrane with a central opening ,and a steep
macular contour to the central fovea .the steep foveal contour creates the appearance of
hole, even though there is no loss of retinal tissue.
Aim of work Primary outcome : To evaluate the changes in vitreomacular interface in diabetic
retinopathy by using Spectral Domain Ocular Coherence Tomography ( SD OCT) Secondary outcome
: To evaluate other macular changes in Spectral Domain Ocular Coherence Tomography ( SD OCT)
in diabetic patient with vitreomacular interface abnormalities
;