Diabetic Retinopathy Flashcards
What is at the pathophysiology of diabetic retinopathy?
Hyperglycaemia causes increased retinal blood flow and abnormal metabolism in the retinal vessel walls.
This precipitates damage to endothelial cells and pericytes,
Endothelial dysfunction leads to increased vascular permeability causing characteristic exudates seen on fundoscopy.
Pericyte dysfunction predisposes to the formation of micro aneurysms.
Neovascularisation is thought to be caused by the production of growth factors in response to retinal ischaemia.
What structural changes can occur?
Ischaemia can cause new vessels forming on the iris (rubeosis) If these block aqueous humour drainage, glaucoma may result.
Formation of age related cataract is accelerated in DM.
Typically this is premature senile cataract.
Describe the pathogenesis.
Microangiopathy in capillaries causes:
1 Vascular occlusion causing ischaemia with new vessel formation (i.e. proliferative retinopathy) which heightens the risk fo retinal detachment.
Occlusion also causes cotton wool spots (ischaemic nerve fibres)
2 Vascular leakage as pericytes are lost, capillaries bulge (microaneurysms) and there is oedema and hard exudates (lipoprotein and lipid filled macrophages)
Rupture of micro aneurysms at the nerve fibre level causes flame-shaped haemorrhages.
When deep in the retina, blot haemorrhages form.
What are the types of diabetic retinopathy?
Non-proliferative retinopathy and proliferative retinopathy
Describe non-proliferative retinopathy.
Mild:
1 or more microaneursms (dots)
Moderate: Microaneurysms Blot haemorrhages Hard exudates (yellow patches) Cotton wool spots (ischaemic nerve fibres)
Severe:
Large Blot haemorrhages and micro aneurysms in 4 quadrants
Venous beading in at least 2
NPDR can progress to proliferative retinopathy
Describe proliferative retinopathy
Retinal neovascularisation - may lead to vitreous haemorrhage
Fibrous tissue forming anterior to retinal disc
More common in T1DM
Describe maculopathy
Leakage from vessels close to the macula cause oedema and can threaten vision.
Based on location
Hard exudates and other background changes on macula: micro aneurysms (dots) Blot haemorrhages
More common in T2DM
Who should you refer?
Maculopathy
Severe NPDR
Proliferative retinopathy
For urgent assessment and treatment to prrotect vision
Describe screening
DM 1 and 2 should have eyes screened at diagnosis and at least annually after.
Screening is by dilated fundus photography
Lesions are mostly at the posterior pole
Describe management of DR
Ensure target BP is < 140/80 or <130/80 if end-organ damage
Lens may have a higher refractive index producing myopia On treatment the refractive index reduces and vision is more hypermetropic so do not correct refractive errors until good DM control.
Pregnancy, dyslipidaemia, raised BP, renal disease, smoking, anaemia and poor DM control accelerates DR
Photocoagulation by laser is used to treat maculopathy and proliferative retinopathy - peripheral retina which is not receiving adequate blood flow treated to remove the stimulus driving the neovascular process
NB does not improve vision - prevents blindness
May cause loss of peripheral, colour and night vision
Intravitreal triamcinolone and anti-VEGF drugs areused with laser to treat macular oedema.
What are CNS effects of DR?
Ocular palsies 3 and 6 may occur
May be pupil sparing in 3rd nerve palsy as pupillary fibres run peripherally in the nerve and receive blood supply from dial vessels