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Creado por Anna Walker
hace más de 9 años
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Pregunta | Respuesta |
What are the risk factors for diabetic retinopathy? | Long duration of diabetes (key factor). Poor metabolic control. Pregnancy. HTN. Renal disease. Other adjustable factors (obesity, hyperlipidaemia, smoking, anaemia). |
What is the first sign of diabetic retinopathy? | Microaneurysms. |
Describe the initial pathogenesis of diabetic retinopathy. | Hyperglycaemia leads to an abnormal exression of type IV collagen - and this is turn leads to further changes that increase hypoxia (bleeds, infarcts etc). There is basement membrane thickening of the enothelial cells. Endothelial cell damage. RBC changes such as increasingly rigid walls. Platelets become more sticky. These 4 changes all predispose to the formation of microemboli in the capillaries. The arterial side is affected as these microemboli lead to occlusion and ischaemia. The venous side is affected as cells called pericytes (that work to strengthen the venules) are lost - this weakens the walls and there are outpouchings (microaneurysms) and eventually leakage of plasma. |
What pathology is the direct result of this leakage of plasma? | The plasma that leaks out is scavenged and engulfed by macrophages, which leads to the appearance of hard exudates on the retina. |
What are the consequences of chronic retinal ischaemia? | Initially, there is opening of pre-existing AV shunts as a result of the ischaemia. Subsequently a vasoformative substance is released from the retina (VEGF-like factors) which produces abnormal new vessels. These new vessels are very fragile and often rupture on the retina. As a result we may see rubeosis iridis and proliferative retinopathy. |
What are the classifications of diabetic retinpathy? | Background retinopathy, Pre-proliferative, Proliferative, Diabetic Maculopathy (not a sequential stage but denotes any involvement of the macula). |
Describe the pathologies seen in background diabetic retinopathy. | Microaneurysms. Haemorrhages (dot, blot and flame-shaped). Exudates. Normal vision if macula not involved. Microaneurysms are usually seen on the temporal side of the fovea. Usually affect those who are younger and have T1DM. Flame-shaped haemorrhages are very superficial (in nerve fibre layer). Treatment is not needed at this stage but monitor for proliferative changes. |
Describe the pathologies seen in pre-proliferative diabetic retinopathy. | Cotton-wool spots (caused by axon infarctions), venous changes (beading, loops), arterial narrowing, dark (therefore deeper) blot haemorrhages, intraretinal microvascular abnormalities (IRMA - opening of pre-existing channels in response to hypoxia between arteries and veins - 80% usually sprout from a vein). |
What is meant by the 4-2-1 rule of pre-proliferative diabetic retinopathy? | Developed from the Early Treatment Diabetic Retinopathy Study (ETDRS). Retinal abnormalities in pre-proliferative diabetic retinopathy are subdivided as "mild", "moderate", "severe" or "very severe". Retinal hemorrhages in all four quadrants, intraretinal microvascular abnormalities (IRMA) in two quadrants, or venous abnormalities in any part of the retina constitute "severe NPDR" and indicate high risk of progression to proliferative diabetic retinopathy. |
Describe the pathologies seen in proliferative diabetic retinopathy. | Affects 5-10% of diabetics. Characterised by neovascularisation - flat or elevated. The severity is determined by comparing with the area of the disc. If the new vessels are appearing on the disc or within one diameter, it is classed as NVD. If it is anywhere else on the retina, it is classed as NVE (neovascularisation elseswhere), can even be on the iris. Those with T1DM are at increased risk and 60% of them are affected 30 years post-diagnosis. Also these patients may have haemorrhages (vitreous or pre-retinal). They will have normal vision unless they haemorrhage or there is macular involvement. |
What is the appropriate treatment for proliferative diabetic retinopathy? | Panretinal Laser Photocoagulation. Initial treatment is 2000-3000 burns. Start peripherally where there are mostly rod photoreceptors - sacrifice these preferentially over the cones. The idea is that you are decreasing the demand for oxygen so therefore removing the stimulus for VEGF to be released. Most patients stabilise after their first few treatments. If they dont, may have to move in more centrally. If stable, you will see good involution of the vessels, pallor of the disc and residual 'ghost vessels' If poor involution and progressive proliferation - vitreoretinal surgery. |
Describe the pathology seen in diabetic maculopathy. | More common in T2DM. Can be focal, diffuse or ischaemic (where macula appears normal but acuity is poor). Ischaemic tends to affect those who are smokers, are obese or who have poorly controlled disease. There will be a large area seen that is not perfused on FA - treatment not appropriate. Diffuse = diffuse retinal thickening. Focal = mainly treated with laser aimed at the leaking microaneurysm. Hard exudates clear up and they may achieve near normal vision. It is a gentle laser treatment to stimulate the RPE layer - opens up pores into the choroid. Now this gentle laser treatment is combined with injection of anti-VEGF. |
When does NPDR usually manifest? | At around 8-10 years duration of DM |
Describe the appearance of exudates. | Yellowish-white deposits with well defined edges; represent precipitation of leaked lipoproteins from diseased retinal vasculature |
Describe the appearance of cotton wool spots. | Greyish white, poorly defined fluffy edged lesions in the nerve fibre layer; represent axoplasmic accumulations adjacent to retinal nerve fibre micro infarcts. |
What are some late complications of PDR? | Retinal fibrosis Traction retinal detachment Iris neovascularisation (rubeosis iridis) and neovascular glaucoma |
What is focal diabetic maculopathy? | focal leakage from microaneurysms or dilated capillaries resulting in focal retinal thickening and surrounding exudates |
What is diffuse diabetic maculopathy? | diffuse leak from dilated capillaries resulting in diffuse retinal oedema which may be associated with some retinal haemorrhages but usually no exudates |
What is ischaemic diabetic maculopathy? | Due to closure of the perifoveal capillary network; manifests as diffuse oedema plus associated dark haemorrhages. Fluorescein angiography is important in confirming ischaemia |
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