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Diabetic Retinopathy

Introduction

Diabetic retinopathy is a common microvascular complication of diabetes and remains the leading cause of blindness in people less than 65 years old worldwide. It affects 30-40% of patients with diabetes and is associated with an increased risk of life-threatening vascular complications, including acute coronary syndrome, congestive heart failure and stroke.

Risk Factors that increase the likelihood of developing/exacerbating retinopathy in diabetics include:

  1. Prolonged duration of diabetes
  2. Poor long-term control of diabetes
  3. Recent good control of diabetes (hypoglycaemia exacerbates retinopathy)
  4. Ethnic origin (Hispanics, South Asians)
  5. Pregnancy
  6. Puberty
  7. Co-existing hypertension
  8. Co-existing hyperlipidaemia (especially hypertriglyceridaemia and low HDL levels)
  9. Co-existing nephropathy
  10. Recent cataract surgery (increased inflammation exacerbates retinopathy)

Pathogenesis

Diabetic retinopathy is predominantly a hyperglycaemia-mediated microangiopathy.

1. Intramural pericyte loss

  • Loss of autoregulation of retinal capillaries à weakening of the capillary wall à  microaneurysm formation
  • If microaneurysms rupture, they form small intraretinal bleeds called dot and blot haemorrhages

2. Vascular endothelial function

  • Increased permeability of the retinal vessels à leakage of fluid and proteinaceous material à retinal oedema and hard exudates

3. Progressive retinal ischaemia

  • Elaboration of vasoproliferative substances (e.g. vascular endothelial growth factor / VEGF) à pre-retinal neovascularization à vitreous or subhyaloid haemorrhage

Fundus findings

  • Intra-retinal haemorrhages: usually visually insignificant
  • Hard exudates: lipoproteins following partial / complete resorption of retinal oedema
  • Cotton wool spots: focal areas of ischaemic infarcts
  • Intra-retinal microvascular abnormalities (IRMA): pre-neovascularization retinal vascular abnormalities

Classification system

The most commonly used classification system is the International Clinical Disease Severity Scale for Diabetic Retinopathy:

  • No retinopathy
    No microvascular lesions
  • Mild non-proliferative diabetic retinopathy
    Microaneurysms only
  • Moderate non-proliferative diabetic retinopathy
    Microaneurysms and other microvascular lesions, but not to the level of severe non-proliferative diabetic retinopathy
  • Severe non-proliferative diabetic retinopathy
    More than 20 intra-retinal haemorrhages in four quadrants of the retina, or venous beading in at least two quadrants, or intra-retinal microvascular abnormalities in at least one quadrant. There must be no evidence of proliferative disease
  • Proliferative diabetic retinopathy
    Neovascularization of the retina, subhyaloid haemorrhage, vitreous haemorrhage, tractional retinal detachment, neovascularization of the iris and angle

Management

Systemic therapy

It is important to remember that diabetic retinopathy is an ocular manifestation of an underlying systemic disease. Therefore systemic treatment forms the mainstay of management in diabetics.

1. Glycaemic control

Tight blood glucose control reduces risk of development and progression of diabetic retinopathy in both type 1 and type 2 diabetes. A 1% decrease in HbA1c equates to a 40% decrease in diabetic retinopathy risk and a 15% reduction in risk of blindness. There is a small risk of initial worsening of retinopathy at the onset of therapy. However, the long-term benefits far outweighs this short-term problem. It is important however to be aware that over-aggressive control of blood glucose increases mortality risk. Thus a balance must be reached between preventing long-term hyperglycaemia and avoiding hypoglycaemic episodes.

Long-term blood glucose control is determined using 3-monthly blood HbA1c measurements. A goal of 5.5-6.0% is ideal but may be difficulty to achieve.

2. Blood pressure control

Hypertension exacerbates diabetic retinopathy through increased blood flow and mechanical damage of vascular endothelial cells. A 10mmHg decrease in systolic blood pressure equates to a 35% decrease in diabetic retinopathy risk and a 50% reduction in risk of blindness. Again, it is important to be aware that over-aggressive blood pressure control also increases mortality risk.

3. Lipid-lowering therapy

Dyslipidaemia is associated with increased risk of diabetic retinopathy. Importantly, aggressive lipid control has not been shown to increase mortality risk.

Ocular Therapy

Diabetic retinopathy carries a risk of vision loss that can be prevented or minimized with timely ocular therapy. 

1. Laser Photocoagulation

a) Panretinal photocoagulation for proliferative retinopathy (Indirect laser)

This is the mainstay of treatment for proliferative diabetic retinopathy without vitreous haemorrhage or tractional retinal detachment. Goal of therapy is to stop progression and encourage regression of retinal neovascularization. The laser is used to burn and create scars on the peripheral retina, thereby reducing overall oxygen demand. 

b) Macula laser photocoagulation for diabetic macula oedema

This is the mainstay of treatment for diabetic macula oedema. Goal of therapy is to encourage reabsorption of macula oedema by the retinal pigment epithelium. However, macula laser treatments carry significant risk of visual loss, therefore the fovea and its surroundings should be avoided.

As laser therapy remains a destructive form of treatment, macula laser is gradually being replaced by treatment courses involving intra-vitreal injection of anti-VEGF. 

2. Surgical Intervention

This is the mainstay of treatment for proliferative diabetic retinopathy with vitreous haemorrhage and/or tractional retinal detachment. Goal of surgery is to remove blood (vitreous haemorrhage) and traction membranes from the retinal surface and to place laser photocoagulation treatment (direct laser). Additional intraocular gas or silicone oil may be needed to reattach the retina in cases of tractional retinal detachment.

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