Diabetic retinopathy can lead to severe vision loss secondary to diabetic macular edema, tractional retinal detachment from fibrovascular proliferation, macular ischemia and complications from neovascular glaucoma. OCT has increased the sensitivity to detect diabetic macular edema and track progression of treatment from focal/grid laser and anti-VEGF therapies. The RISE/RIDE studies on treatment of diabetic macular edema with Lucentis was one of the initial studies to incorporate time-domain OCT.
The definition of clinically significant macular edema (CSME) is based on a clinical assessment of diabetic macular edema with a specific criterias defined by the ETDRS in report 1 prior to the development of OCT.
Figure 1: Diabetic macular edema with intraretinal edema secondary to leakage from the microaneurysm located in the center of the cyst.
Figure 2: Diabetic macular edema with intraretinal edema/cysts and subretinal retinal fluid. Leakage can occur from microaneurysms located in the intraretinal layers and leak into the subretinal space causing a serous detachment.
Figure 3: Diabetic macular edema with large intraretinal cysts located in multiple retinal layers, especially the outer nuclear layer (ONL). Temporal to the fovea, there is RPE disruption and loss of the COST and EPIS lines secondary to s/p panretinal photocoagulation (PRP) laser treatment. A window defect is seen from the disrupted RPE allowing the OCT scans to penetrate deeper into the choroid.
In diabetic retinopathy, hard exudates with associated retinal thickening located within 500 microns of the center of the fovea is referred to as clinically significant macular edema (CSME). The ETDRS report 22 found an association of hard exudates with elevated serum lipid levels.
Figure 4: Retinal hard exudates located mainly in the outer plexiform and some in the outer nuclear layer appear as hyperreflective on SD-OCT.
OCT can also be utilized in differentiating between intraretinal microvascular abnormalities (IRMA) versus early retinal neovascularization. Retinal neovascularization first develops in the intraretinal layers but will extend into the vitreous cavity and disrupt the inner limiting membrane (ILM) forming fibrovascular proliferations. SD-OCT when scanned over retinal neovascularization will reveal hyperreflective lesions that disrupt the ILM and protudes into the vitreous cavity connecting to the posterior hyaloid membrane if present.
Figure 5: Early retinal neovascularization with fibrovasular growth breaking the ILM and extending into the vitreous.
Figure 6: Neovascularization of the disc (NVD) with fibrovascular membane growing over the optic disc. The fibrovascular membrane is attaching to the posterior hyaloid membrane and blocking the view of the optic disc cup. This patient has high-risk proliferative diabetic retinopathy.
Figure 7: Tractional retinal detachment secondary to proliferative diabetic retinopathy. The retinal detachment is threatening fixation. The BCVA was 20/30. The patient had already previously received scatter pan-retinal photocoagulation (PRP) as seen on the photograph.
Figure 8: Tractional retinal detachment secondary to proliferative diabetic retinopathy. The retinal detachment is macula-on and detached superior to the macula. The tractional fibrovascular bands can be seen on the retinal photograph bridging the superior and inferior arcades with attachment to the optic nerve.
Figure 9: Tractional retinal detachment secondary to proliferative diabetic retinopathy.
Suggested Readings:
ETDRS report 1- http://www.ncbi.nlm.nih.gov/pubmed/2866759?dopt=Abstract
RISE/RIDE- http://www.ncbi.nlm.nih.gov/pubmed/23706949
Da Vinci Study- http://www.ncbi.nlm.nih.gov/pubmed/22537617
VISTA-DME and VIVID-DME Trials http://www.ncbi.nlm.nih.gov/pubmed/?term=VISTA-DME+and+VIVID-DME+Trials
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