In the acute phase following retinal artery occlusion, there is an isolated increase in the inner retinal thickness and hyper-reflectivity. Importantly, there is an absence of hyporeflective cystic spaces from fluid accumulation that differentiates retinal oedema from retinal artery occlusion from other vascular causes (Rodrigues 2013). This is because oedema from retinal artery occlusion is due to cytoplasmic swelling from coagulation necrosis rather than extracellular fluid accumulation (Coady et al. 2015; Chu et al. 2013). The area of retinal swelling is typically well demarcated and corresponds to the area subserved by the occluded artery (Mathew et al. 2010). Shadowing of underlying structures can mask the outer retinal layers that lead to the layers appearing hyporeflective or widened (Rodrigues 2013; Mathew et al. 2010) (Fig. 12.3).

In BRAO, the OCT findings associated with ischaemia are striking when contrasted to the adjacent perfused retina. The temporal changes are similar to what is seen in CRAO (Ritter et al. 2012). While differentiating the types of retinal emboli is clinical in nature, OCT has been used to demonstrate complete occlusion of an obstructed artery (Shah et al. 2010) and can be used to show recanalisation (Fig. 12.4). Prominence of middle limiting membrane has been described as a reliable indicator of acute retinal ischaemia. Histologically, it is thought to correspond to cytoplasmic swelling of bipolar cell synapses in the inner OPL (Chu et al. 2013). Figure 12.5 contrasts the presence of p-MLM in the affected retina to the normal retina (Fig. 12.6).

In the chronic phase, there will be isolated inner retinal thinning with the absence of stratification of the inner retinal layers. The outer retinal layers are always spared (Cruz-Villegas et al. 2004; Ghazi et al. 2010; Rodrigues 2013). Normal foveal depression is lost as the thinned retina extends up to the level of foveal depression (Ghazi et al. 2010). The inner retinal atrophy is coupled with increase outer retinal reflectivity and better visualisation of the outer choroid and large choroidal vessels (Ghazi et al. 2010). The presence of aforementioned features is important in distinguishing post-acute retinal artery occlusion from non-acute optic neuropathy (Ghazi et al. 2010). While retinal thinning occurs with non-acute optic neuropathy, the thinning is limited to nerve fibre and ganglion cell layers, and the thinning is significantly less severe and spares the foveal depression (Ghazi et al. 2010) (Fig. 12.7).

Several studies have documented the temporal change of OCT findings in retinal artery occlusion (Asefzadeh and Ninyo 2008; Leung et al. 2007; Ritter et al. 2012; Saxena et al. 2013).