**4. OCTA in macular oedema of different pathologies**

Macular oedema is a pathological component of myriad ocular conditions and is a major cause of visual morbidity. Macular oedema can be due to inflammatory cause (as in uveitis), vascular, diabetes mellitus, retinal vein occlusion, CNV, metabolic, or in cases of retinal dystrophies. The high-resolution OCT B-scans allow for accurate description of macular oedema in terms of thickness, morphological pattern (cystoid, spongy or associated neurosensory detachment), and the anatomical involvement of selected retinal layers, the outer plexiform layer (OPL) (**Figure 5**). Such details can be useful not only for disease diagnosis but also for follow-up of treatment response. An advantage of OCTA over the traditional OCT B-scans is the ability to simultaneously correlate macular oedema with the underlying aetiological vascular process, for example ischemia and vascular drop-outs.

**In diabetic eyes**, OCTA can delineate successfully the enlarged FAZ with underlying non-perfusion that increases according to the severity of diabetic retinopathy, quantitative measurement of vascular density (mainly perfusion density and vessel density), reduced capillary density in the superficial and deep capillary plexuses,

#### **Figure 5.**

*Optical coherence tomography angiography (OCTA) of mild NPDR with diabetic maculopathy, the SCP (b, e) showed well-defined perifoveal and parafoveal vessels with areas void of flow representing area of capillary dropouts, more than those seen with the conventional FFA (a). SAME findings in the DCP (c, f) but more advanced regarding the areas of ischemia there is significant decrease in the perfusion as measured by the vessels density and flow index (d) more evident in the DCP.*

#### **Figure 6.**

*Mac Tel type 2 OCT-angiography shows temporal flow voids areas in the superficial and deep capillary plexuses, spacing between the vessels with increased vascular diameter, and minimal vascular invasion of the FAZ at the deep capillary plexus. The B scan shows multiple hyporeflective cavitations, focal loss of the inner/outer segment with no evidence of external limiting membrane disruption.*

microaneurysms (appear as focally dilated saccular or fusiform capillaries), choriocapillaris flow voids changes and increased vessel tortuosity. Moreover, OCTA may show DR before it is clinically detectable.

However, OCTA has certain limitations in the assessment of vascular retinal diseases associated with macular oedema. It is incapable of testing the structural and functional integrity of vessel walls and hence cannot demonstrate leakage (reflecting the breakdown of the blood-retinal barrier) as in FFA or ICGA. FFA has the advantage of showing abnormal blood vessels, such as retinal neovascularization or intraretinal microvascular abnormalities. In addition, OCTA has so far, a limited imaging field missing most of the peripheral retina which is the main site of pathology in a number of retinal diseases (the developing widefield OCTA technology). Therefore, for DR, fluorescein angiography will remain an essential vital diagnostic modality and OCTA will be the alternative or complementary method of angiography that can be safely (in risky patients especially with impaired kidney functions) and more frequently performed to assess the effectiveness of treatment in DR [11–14].

Macular telangiectasia Type 2 (MacTel2) is a neurodegenerative change affecting the Muller cells in the macular area. SD-OCT abnormalities in MacTel include; cyst formation in the inner retina, disruption of the external limiting membrane, loss of inner/outer segment, parafoveal venular dilation, hyporeflective cavitation of the outer retina, perifoveal capillary leakage, and subretinal neovascularization. In OCTA, Zeimer et al. noted vascular changes in the deep capillary network (enlargement of vessels, larger intervascular spaces, dilated, dendritic appearance

#### **Figure 7.**

*Advanced mac Tel type 2 OCT-angiography showed temporal flow voids areas in the superficial and deep capillary plexuses. Telangiectatic vessels are seen among the superficial and deep plexuses with increased vascular diameter as well as rarefied vessels; temporal and superior to the FAZ with right-angled configuration and, vascular invasion of the FAZ at the superficial and deep capillary plexuses. The B scan showed multiple hyporeflective cavitations with focal and diffuse loss of the inner outer segment as well as external limiting membrane disruption.*

of vessels, telangiectasis, reduction and/or loss of capillary density), and the extension of anastomoses toward the superficial capillary network with progression of the disease. RPE-proliferations were often associated with "contraction" of surrounding vessels [14, 15] (**Figures 6** and **7**).
