Fig. 12.1
Image of a case with focal diabetic macular edema (DME) by SS-OCT. Arrows indicate the region that has focal thickening of both the retina and choroid
Fig. 12.2
(a) SS-OCT image of diffuse retinal thickening. Note the area of the thin choroid (arrows). (b) SS-OCT image of a case with cystoid macular edema. Both intraretinal cystoid cavities and choroidal vasculature are well documented. The chorio-scleral interface is indicated by arrowheads. (c) SS-OCT image of serous retinal detachment without posterior hyaloidal traction (PHT). A slight subretinal fluid is observed beneath the dome-like elevation of detached retina (arrow). Arrowheads indicate the region showing focal thinning of the choroid. (d) SS-OCT image of PHT without traction retinal detachment (TRD). The PHT is clearly identified as a highly reflective strand arising from the inner retinal surface (arrow). Note the relatively thin choroid. (e) SS-OCT image of PHT with TRD. The traction exerted by the PHT is identified as a highly reflective strand between the inner retinal surface and the posterior hyaloid (arrows). The TRD is detected as an area of low signal underlying the highly reflective border of detached retina (arrowhead)
12.2 Photocoagulation Treatment
Focal laser photocoagulation is the standard treatment for focal DME. The Early Treatment Diabetic Retinopathy Study (ETDRS) reported a 50% reduction in moderate vision loss (>3 lines) with laser treatment compared to observation (Figs. 12.3, 12.4, 12.5, and 12.6) [13]. In diffuse DME, however, the significant effectiveness of laser photocoagulation has not been demonstrated.
Fig. 12.3
(a) Fundus photograph (left) and fluorescent fundus angiography (right) of a case with CME. Note the microaneurysm (arrowhead) treated with focal laser photocoagulation. (b) Preoperative spectral-domain OCT image. Note the CME and the adhesion of posterior hyaloid membrane to the foveola (arrows). The choroidal vasculature is not well visualized. (c) Preoperative SS-OCT image. Note the detail structure of the choroid is well visualized, compared to (b) (arrowheads)
Fig. 12.4
Preoperative retinal (left) and choroidal thickness map (right) by SS-OCT. Arrowhead indicates the area where the photocoagulated microaneurysm is located
Fig. 12.5
SS-OCT at 1 month after focal photocoagulation. Note the adhesion of posterior hyaloid membrane is released
Fig. 12.6
Retinal thickness map (left) at 1 month after focal photocoagulation shows reduction of the retinal thickness in the photocoagulated area (arrowhead) and also the central fovea. The choroidal thickness map (right) shows that the choroidal thickness remains largely unchanged
Recent reports showed a significant decrease in choroidal thickness in patients treated with pan-retinal coagulation (Figs. 12.7, 12.8, 12.9, and 12.10) [14, 15]. On the other hand, it has been reported that focal laser photocoagulation did not alter choroidal thickness in eyes with DME [16].
Fig. 12.7
A case that required pan-retinal photocoagulation. Preoperative SS-OCT shows CME and hard exudates (arrows)
Fig. 12.8
Preoperative retinal (right) and choroidal thickness map (left)
Fig. 12.9
SS-OCT at 2 weeks after pan-retinal photocoagulation. The increase of macular edema was observed (arrowhead)
Fig. 12.10
Retinal thickness map (left) at 2 weeks after pan-retinal photocoagulation shows increase of the retinal thickness. The choroidal thickness map (right) shows that the choroidal thickness remains unchanged
12.3 Medical Treatment
The two major medical treatments for DME are corticosteroids and anti-VEGF agents. The anti-inflammatory effect of corticosteroids helps to reduce retinal edema and may also inhibit neovascularization [17, 18], while significant side effects, including cataracts and glaucoma, have been reported [19, 20].
The efficacy and safety of intravitreal anti-VEGF treatment for DME have recently been demonstrated by various clinical trials [21–23]. To date, both ranibizumab and aflibercept are approved for the treatment of DME by the U.S. Food and Drug Administration. The recent reports showed anti-VEGF treatment for DME reduces choroidal thickness (Figs. 12.11, 12.12, 12.13, and 12.14) [24–26].
Fig. 12.11
A case treated with intravitreal injection of aflibercept (IVA). Preoperative SS-OCT shows CME and a slight subretinal fluid (arrow)
Fig. 12.12
Preoperative retinal (left) and choroidal thickness map (right) show diffuse retinal thickening and localized choroidal thickening in the fovea, respectively
Fig. 12.13
SS-OCT image at 1 month after the initial IVA shows complete resolution of the macular edema
Fig. 12.14
Retinal thickness map (left) at 1 month after IVA shows a remarkable decrease of the retinal thickness and the choroidal thickness is also slightly reduced (right)
12.4 Vitrectomy
The vitreous is implicated as a cause of DME by some mechanical and physiologic mechanisms, all of which lead to increased vascular permeability [27–29]. When there is an evident traction over the macular, vitrectomy has been reported to be effective (Figs. 12.15, 12.16, 12.17, and 12.18) [30, 31]. Vitrectomy also can improve DME by removing the growth factors and cytokines such as VEGF, IL-6, and platelet-derived growth factor. These factors have been reported to be abundantly detected in the vitreous fluid of DME and associated with macular edema and retinal neovascularization [32]. Furthermore, the evidence that decreased oxygenation can exacerbate DME [33] supports an additional advantage of vitrectomy since it provides the inner retina with additional oxygen by improving the flow of oxygen rich aqueous into the vitreous cavity [34]. The increase of oxygen concentration at the inner retina can decrease the flow of oxygen from choroid to retina and constrict the choroidal vessels [35]. Nevertheless, the role of vitrectomy in treatment of DME remains elusive because the potential benefits and risks have not been clearly evaluated in long-term, adequately sized, randomized clinical trials.
