Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2589_Библиотеки_им_академика_М_И_Перельмана

of MAs are recognized. These are focal bulging, saccular, fusiform, mixed saccular/fusiform, pedunculated, and irregularly shaped [20]. The morphological shape rather than the size of the MAs is responsible for leakage. The irregular, mixed type, and fusiform are more likely to leak than the saccular and pedunculated MAs [21]. Moreover, saccular MAs are more likely to be thrombosed than fusiform MAs [22]. Simulation studies have shown that reduced inlet velocity of the feeding vessel of the saccular MAs leads to increased adherence of the platelets to the aneu­rysmal wall where the blood is more stagnant and initiates thrombus formation. Reduced bold ow velocity may also lead to thrombus forma­tion in some fusiform MAs [17, 18]. It may be noted that before the development of retinopa­thy, the blood ow velocity in type 1 DM is reduced and is dependent on the blood glucose levels, but with the development of non-prolifer­ative diabetic retinopathy there is an increase in the ow velocity [23]. It is likely that this increase in ow velocity may be mediated through vascular endothelial growth factor (VEGF) [17, 18, 24].

On optical coherence tomography (OCT), MAs show either a complete, incomplete, or no ring. Compared to those with no or incomplete rings, MAs with complete rings are less likely to be associated with cystic spaces in the ret­ina. The complete ring likely indicates a thick­ened and hyalinized basement membrane. Hyperreectivity in the MAs indicates the

Optical coherence tomography angiography (OCTA) allows 3-D enface visualization of the various segmented layers of the retina with a caveat that all microaneurysms may not be visi­ble on OCTA [26]. On a 3-D rotational OCTA, most MAs are fusiform in shape and seem to arise from the DCP in the inner nuclear layer (Fig.1.9). Some of these are also present in the SCP and on the capillaries connecting the SCP and the DCP. MAs are also seen in the outer plexiform layer [27, 28]. Most MAs are associ­ated with two vessels originating in the DCP and, less commonly, from the SCP.Those arising from the DCP are in the inner nuclear layer, those from the SCP occupy the ganglion cell layer, and oth­ers may be seen in the outer plexiform layer and rarely in the outer nuclear layer [27].

Retinal microaneurysms are formed in response to hypoxia of the retina. In patients with hyper­tensive retinopathy, microaneurysms are seen surrounding cotton-wool spots formed by the occlusion of precapillary arterioles. These micro­aneurysms last only a few weeks and disappear with the disappearance of the cotton wool spots. Besides diabetes and hypertension, microaneu­rysms may be seen in carotid atherosclerosis (carotid insufciency). In contrast to diabetes, where MAs are predominantly seen in the poste­rior pole, in carotid insufciency, MAs are seen in the retinal periphery. Likewise, these may be seen in Takayasu’s arteritis (TA) if the arteries involve the common or the internal carotid artery (Figs.1.11 and 1.12). In the latter, MAs are seen

Microaneurysms may also be seen in long­standing branch retinal vein occlusion (BRVO) (Fig. 1.14) and central retinal vein occlusion (CRVO). These are also seen in congenital retinal vasculature abnormalities such as Coats’ disease which mostly affects young boys’ left eye. Large microaneurysm dilatations on telangiectatic reti­nal vessels characterize the latter. These pro­fusely leak uid and lipoproteins, forming massive deposits of hard exudates. Limited MAs are also seen in type 1 macular telangiectasia (Mac Tel type 1). The formation of MAs also characterizes radiation retinopathy.