Progression of Retinopathy


In patients with diabetes, the majority of lesions of retinopathy are asymptomatic, i.e. without visual symptoms. Macular oedema however, often causes slow and insidious loss of visual function. Proliferative retinopathy, by itself, causes no visual loss, however, its complications usually lead to acute and profound visual loss. Thus, it is crucial to identify the earliest signs of retinopathy (Figure 1).

Figure 1. Early signs of diabetic retinopathy

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The appearance of retinopathy depends on the lesion itself. With progressive capillary occlusion, more microaneurysms, retinal haemorrhages and early cotton wool spots (micro-infarcts in the nerve fibre layer) develop (Figure 2). This is still regarded as non-proliferative retinopathy.

Figure 2. Progressive capillary occlusion

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With more extensive capillary occlusion and features such as IRMA (IntraRetinal Microvascular Abnormalities) and venous beading develop and are visible (Figure 3). Large ‘devoid’ areas can also be seen; these are ischaemic.

Figure 3. More extensive capillary occlusion

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As peripheral retinal ischaemia progresses, the eye may generate very fine abnormal new vessels or ‘neovascularisation’. This is termed proliferative retinopathy (Figure 4). Proliferative retinopathy is the result of large-scale retinal ischaemia where the retinal periphery has a compromised blood supply and the eye develops new vessels in an attempt to re-nourish itself. While new vessels do not usually cause visual symptoms, they are extremely fragile and can break, causing vitreous or pre-retinal haemorrhage and acute and profound visual loss. Retinal laser photocoagulation is the indicated treatment for proliferative retinopathy.

Figure4. Proliferative retinopathy

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As the new vessels continue to grow, they develop a ‘scaffold’ of fibrous tissue, attached to both the back of the vitreous and to the retina (Figure 6). Shrinkage or contraction of the fibrous tissue can cause detachment of the retinal layers and acute visual loss. Urgent vitreoretinal surgery with additional endolaser photocoagulation may be the only effective treatment.

Figure 5. ‘Scaffold’ of fibrous tissue built during the progressive retinopathy phase

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With progressive capillary leakage in the macular region, deposits of lipid hard exudates can be seen, often very close to the fovea (Figure 6). This is Clinically Significant Macular Oedema (CSMO), which is associated with increased retinal thickening and usually causes progressive visual loss. Macular oedema occurs when the perifoveal area becomes swollen due to accumulation of either plasma or lipid in the middle retinal layers. With stereoscopic viewing of photographs centred on the macular, the extent and apparent thickness of the macular region can be assessed to diagnose and quantify macular oedema.

Figure 6. Clinically significant macular oedema

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Retinopathy Level allocation
Following the assessment of lesions, a summarising Retinopathy Level is assigned per eye (Table 1, Figure 7).

Table 1. Retinopathy Level allocation

Level

Description

10

No retinopathy

20, 35

Mild-to-moderate non-proliferative diabetic retinopathy

43, 47

Moderate-to-severe non-proliferative diabetic retinopathy

53

Very severe non-proliferative diabetic retinopathy

61+

Proliferative diabetic retinopathy

Figure 7. Example retinopathy lesions

figure 8-1
figure 8-2
figure 8-3
Microaneurysms
Haemorrages and  microaneurysms
Microaneurysms and hard exudate
Level 20
Level 35
Level 35
figure 8-4
figure 8-5
figure 8-6
Haemorrages and  microaneurysms, cotton wool spots or intraretinal microvascular abnormalities
Haemorrages and  microaneurysms, beading and intraretinal microvascular abnormalities
Proliferative
Levels 43-47
Level 53
Levels 61+