DIABETIC RETINOPATHY
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.
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 3: Early retinal neovascularization with fibrovasular growth breaking the ILM and extending into the vitreous.
Figure 4: 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.
Suggested Readings:
RISE/RIDE
VISTA-DME and VIVID-DME Trials
READ 2
RETINAL VEIN OCCLUSION
Retinal vein occlusions (RVO) is categorized into branch (BRVO), hemiretinal (HRVO) or central retinal vein occlusion (CRVO) depending on the location of the occlusion. The condition can further be categorized by the presence or absence of macular edema and if the condition is ischemic or nonischemic.
Vision loss from retinal vein occlusions is secondary to macular edema and if ischemic, progress to neovascularization and neovascular glaucoma. OCT can assist in detecting macular edema secondary to retinal vein occlusions and track response to treatment with grid laser in BRVO or anti-VEGF therapies in BRVO, HRVO and CRVO. Macular edema in retinal vein occlusions are diffuse leakage, especially in CRVO. The macular edema is driven by ischemia and increases release of vascular endothelial growth factors (VEGF) that increases the inner retinal blood-brain barrier causing leakage of intraretinal fluid.
Figure 1: Hemiretinal vein occlusion (HRVO) with macular edema. Patient will benefit from anti-VEGF therapy.
Suggest readings:
BRAVO
CRUISE
COPERNICUS
GALILEO
VIBRANT
RETINAL ARTERY OCCLUSION
Retinal artery occlusions can be categorized into branch retinal artery occlusion (BRAO), hemiretinal artery occlusion (HRAO), central retinal artery occlusion (CRAO) or cilioretinal artery occlusion (CLRAO). The underlying pathophysiology is usually secondary to blockage of the retinal artery from a retinal emboli. The most common retinal emboli types are calcific, platelet-fibrin or cholesterol, also commonly referred to as Hollenhorst plaques. The occlusion can be transient or permanent leading to symptoms of amaurosis fugax, visual field defects or complete monocular blindness.
In an acute retinal artery occlusion, the retinal whitening seen on examination is secondary to significant swelling of the inner retinal layers from the ischemic event. The classic text book description of a “cherry red spot” in a CRAO describes the retinal whitening and thickening of the inner retinal layers and a normal fovea appearance. The fovea appears normal because there are no ganglion cell swelling to obscure the fovea. OCT is able capture the thickening/swelling of the inner retinal layers.
Figure 1: Acute branch retinal artery occlusion (BRAO) with retinal whitening. SD-OCT scan from left to right over the area of normal retina and the area involved. The inner retinal layers are significantly thicker and hyperreflective from the acute infaract.
After the initial acute phase of the retina artery occlusion, the swollen inner retinal layers will start to atrophy. OCT scans will display thin inner retinal layers with fairly normal outer retinal layers. On clinical examination, the area of retinal artery occlusion will sometimes be difficult to appreciate without the aid of OCT or fluorescein angiography. The macular cube 512x128 ILM-RPE layer map is useful at detecting areas of thinning outside the fovea.
Figure 2: Large branch retinal artery occlusion vs hemiretinal artery occlusion. The inferior of the retina was involved resulting in thinning of the inner retinal layers. Cirrus macular cube 512x128 scans reveal inner retinal thinning temporal to the fovea on the horizontal scan and severe thinning inferiorly on the vertical scan. The ILM-RPE layer map on the right of the scan reveals inferior thinning of the entire posterior pole.
Figure 3: Small branch retinal artery occlusion involving inferior to the fovea. Cirrus macular cube 512x128 reveals thinning on the ILM-RPE layer map. On clinical examination, the area of the BRAO was difficult to appreciate without the aid of the OCT.
Comments