examination. Instead the term dot haemorrhage/ microaneurysm (H/Ma) is used. 7.3 DIFFUSE CAPILLARY OCCLUSION Progressive capillary occlusion leads to the development of blot haemorrhages, intraretinal microvascular anomalies and venous changes. More extensive capillary occlusion can lead to a featureless retina, followed by neovascularisation. 7.3.1 Blot haemorrhages Where clusters of capillaries occlude, intraretinal blot haemorrhages develop. Such haemorrhages may occur throughout the full thickness of the retina. Blot haemorrhages are considered to represent a deep retinal infarct. The lesion can be seen to be in the outer plexiform layer on fluorescein angiography where it does not mask the overlying capillary bed unlike dot and flame haemorrhages which lie more superficially in the retina. More peripheral, round, large blotch haemorrhage is a common feature of ocular ischaemia. Such patients often develop rubeosis iridis -proliferative iridopathy and consequent neovascular glaucoma. 7.4 COTTON WOOL SPOTS Cotton wool spots are believed to represent the swollen ends of interrupted axons where build-up of axoplasmic flow occurs at the edge of the infarct. Cotton wool spots occur most frequently where the nerve fibre is densest such as the nasal side of the optic nerve. Such features are not exclusive to diabetic retinopathy and do not in themselves appear to increase the risk of new vessel formation. Hence, unless extensive areas 57 affected by cotton wool spots are found they are considered to be a change of no proliferative retinopathy. Cotton wool spots often have abutting looping microvascular anomalies, which are probably a variant of collateral formation, as seen with retinal vein occlusion, rather than the typical IRMA seen with capillary occlusion. 7.5 INTRA-RETINAL MICROVASCULAR ANOMALIES (IRMA) Extensive closure of capillary network between arteriole and venule leads to dilated capillary remnants. These remaining stumps and vascular channels appear as spiky tortuous micro-vascular abnormalities in the areas of capillary occlusion, within retina, the changes are easier to identify on fluorescein angiography. Another possible mechanism for development of IRMA is a variant of collateral formation and may be seen in association with localised arteriolar occlusion and cotton wool spot. In young patients IRMAs may be confused with dilated telangiectatic vessels in the nerve fibre bundles, which reflects state of generalised hyperaemia. In contrast to IRMA, telangiectasia that arise as a consequence of retinal vein occlusion leak fluorescein along their length resulting in retinal oedema and exudate formation. IRMA only leak from their growing tips, are less often associated with exudate and appear to develop endothelial cell tight junctions indicating a probable role in retinal repair. 7.5.1 Venous Beading Where veins run through areas of extensive capillary closure, venous beading occurs. Venous beading may represent foci of venous endothelial cell proliferation that have failed to develop into new vessels. Fluorescein angiography shows vessel wall staining as the vein passes through ischaemic retina and ‘pruning’ where side branches appear occluded shortly after branching from the main vessel. 7.5.2 Venous Reduplication Venous reduplication is rare and usually occurs in conjunction with venous beading. 7.5.3 Venous Loops Venous loops are infrequent and though to develop due to small vessel occlusion and opening of alternative circulation. 7.5.4 Retinal pallor Retinal pallor is a non-specific feature that is best appreciated in hindsight on red-free photographs and on fluorescein angiography, particularly temporal to the macula in patients who appear to have the unexplained presence of new vessels. 58 7.5.5 White lines White lines may represent vessel wall staining or thrombosed arterioles , which often accompany retinal pallor and are similarly found in areas of extensive capillary closure. 7.6 MACULAR CHANGES IN NON-PROLIFERATIVE RETINOPATHY 7.6.1 Macular Oedema Thickening of retina takes place due to accumulation of exudative fluid from damaged outer blood-retina barrier (extracellular oedema) or as a result of hypoxia leading to fluid accumulating within individual retinal cells (intracellular oedema). Both mechanisms are consequences of capillary closure (ischaemia), either indirectly (extracellular) or directly (intracellular). The appearance of macular oedema can be appreciated on stereoscopic examination or inferred by the presence of intraretinal exudate (reference). Leakage from isolated microaneurysms or clusters of microaneurysms may appear as a discrete area of surrounding oedema (focal oedema) radiating out from the leaking microaneurysms. Exudate may delineate the advancing edge of the oedema, much like the tide mark of the sea, Such exudates are usually found in the outer plexiform layer on an OCT scan though the area. The mechanism of more widespread oedema (diffuse oedema) is more complex. In its most simplistic form it may be envisaged to occur as a result of widespread capillary leakage, often from capillary segments with impaired autoregulation rather than discrete microaneurysms. Other mechanisms include retinal pigment epithelium dysfunction or the presence of ischaemia especially that affecting the perifoveal vascular zone. 7.6.2 Macrovascular disease Although classically thought of as a microvascular disorder, some features of a macrovascular origin may be seen in diabetic retinopathy. Arteriolar occlusion, without capillary occlusion, frequently affects the horizontal nerve fibre layer of the retina resulting in flame haemorrhage and cotton wool spot formation. 7.7 OPTIC DISC CHANGES Occasionally swollen optic discs may be seen (diabetic papillopathy) in diabetic patients with poor correlation to retinopathy levels. Diabetic papillopathy would need to be differentiated from ischaemic optic neuropathy and cases with new vessels on the disc (NVD). In patients with diabetic papillopathy, vision is largely not impaired however visual acuity may be affected. 59 7.8 PROLIFERATIVE DIABETIC RETINOPATHY Proliferative diabetic retinopathy (PDR) is the angiogenic