Diabetic Retinopathy

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DIABETIC RETINOPATHY

  • Risk factors associated with occurence of DR are:
    • Duration of diabetesis the most important determining factor (MCQ)
      • 50 percent of patients develop DR after 10 years
      • 70 percent after 20 years
      • 90 percent after 30 years of onset of the disease.
    • More in females than males (4:3)
    • Poor metabolic control is less important than duration
    • Heredity.
      • It is transmitted as a recessive trait without sex linkage.
      • The effect of heredity is more on the proliferative retinopathy.
    • Pregnancy
    • Hypertension
    • Other risk factors include smoking, obesity and hyperlipidemia.
  • Pathogenesis.
    • Essentially, it is a microangiopathy affecting retinal precapillary arterioles, capillaries and venules.

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  • Classification
    • Non-proliferative diabetic retinopathy (NPDR)
      • Mild NPDR
      • Moderate NPDR
      • Severe NPDR
      • Very severe NPDR
    • Proliferative diabetic retinopathy (PDR)
    • Diabetic maculopathy
    • Advanced diabetic eye disease (ADED)
  • Non-proliferative diabetic retinopathy (NPDR)
    • Ophthalmoscopic features of NPDR include:
      • Microaneurysmsin the macular area
        • the earliest detectable lesion (MCQ)
      • Retinal haemorrhages
        • deep (dot and blot haemorrhages)
        • superficial haemorrhages (flame-shaped).
      • Hard exudates
        • yellowish-white waxy-looking patches
        • arranged in clumps or in circinate pattern.
        • These are commonly seen in the macular area.
      • Retinal oedema characterized by retinal thickening.
      • Cotton-wool spots (MCQ)
        • if > 8, there is high risk of developing PDR
      • Venous abnormalities
        • beading, looping and dilatation.
      • Intraretinal microvascular abnormalities (IRMA).
      • Dark-blot haemorrhages
        • representing haemorrhagic retinal infarcts.
  • Proliferative diabetic retinopathy (PDR
    • develops in more than 50 percent of cases after about 25 years of the onset of disease.
    • it is more common in patients with juvenile onset diabetes.
    • neovascularisation
      • hallmark of PDR
      • characterised by proliferation of new vessels from the capillaries
        • neovascularisation at the optic disc (NVD)
        • neovascularisation elsewhere (NVE) in the fundus
      • occurs usually along the course of the major temporal retinal vessels.
      • new vessels may proliferate in the plane of retina or spread into the vitreous as vascular fronds.
    • Later on condensation of connective tissue around the new vessels results in formation of fibrovascular epiretinal membrane.
    • Vitreous detachment and vitreous haemorrhage may occur in this stage.
    • Types.
    • On the basis of high risk characteristics (HRCs) described by diabetic retinopathy study (DRS) group, the PDR can be further classified as below:
      • PDR without HRCs (Early PDR)
      • PDR with HRCs (Advanced PDR)
    • High risk characteristics (HRC) of PDR are as follows
      • NVD 1/4 to 1/3 of disc area with or without vitreous haemorrhage (VH) or pre-retinal haemorrhage (PRH)
      • NVD < 1/4 disc area with VH or PRH
      • NVE > 1/2 disc area with VH or PRH
  • Diabetic maculopathy (MCQ)
    • diabetic macular edema
      • Have effect on vision.
      • These changes may be associated with
        • non-proliferative diabetic retinopathy (NPDR) or
        • proliferative diabetic retinopathy (PDR).
      • occurs due to increased permeability of the retinal capillaries.
      • It is termed as clinically significant macular edema (CSME) if one of the following three criteria are present on slit-lamp examination with 90D lens:
        • Thickening of the retina at or within 500 micron of the centre of the fovea.
        • Hard exudate at or within 500 micron of the centre of fovea associated with adjacent retinal thickening.
        • Development of a zone of retinal thickening
          • one disc diameter or larger in size
          • at least a part of which is within one disc diameter of the foveal centre.
  • Advanced diabetic eye disease
    • It is marked by complications such as:
      • Persistent vitreous haemorrhage,
      • Tractional retinal detachment and
      • Neovascular glaucoma.
    • Management
      • Screening for diabetic retinopathy (MCQ)
        • Every year, till there is no diabetic retinopathy or there is mild NPDR.
        • Every 6 months, in moderate NPDR.
        • Every 3 months, in severe NPDR.
        • Every 2 months, in PDR with no high risk characteristic.
    • Medical treatment.
      • Role of pharmacological modulation.(MCQ)
        • Protein kinase C (PKC) inhbitors,
        • Vascular endothelial growth factors (VEGF) inhibitors(MCQ)
        • Aldose reductase and ACE inhibitors
        • Antioxidants such as vitamin E
      • Role of intravitreal steroids in reducing diabetic macular oedema
        • Flucinolone acetonide intravitreal implant and
        • Intravitreal injection of triamcinolone
    • Photocoagulation. (MCQ)
      • It remains the mainstay in the treatment of diabetic retinopathy and maculopathy.
      • Either argon or diode laser can be used.
    • Macular photocoagulation.
      • Macula is treated by laser only if there is clinically significant macular oedema (CSME).
      • Laser treatment is contraindicated in ischaemic diabetic maculopathy.
      • In patients with PDR associated with CSME, macular photo-coagulation should be considered first i.e., before PRP since the PRP may worsen macular oedema. (MCQ)
      • Macular photocoagulation includes two techniques:
        • Focal treatment
          • done with argon laser (MCQ)
          • carried out for all lesions (microaneurysms, IRMA or short capillary segments) 500-3000 microns from the centre of the macula
          • Spot size of 100-200 μm of 0.1 second duration is used.
        • Grid treatment.
          • Grid pattern laser burns are applied in the macular area for diffuse diabetic macular oedema
    • Panretinal photocoagulation (PRP) or scatter laser
      • consists of 1200-1600 spots
      • each 500 μm in size and 0.1 sec. duration.
      • Laser burns are applied 2-3 disc areas from the centre of the macula extending peripherally to the equator
      • In PRP, temporal quadrant of retina is first coagulated. (MCQ)
      • PRP produces destruction of ischaemic retina which is responsible for the production of vasoformative factors.
      • Indications for PRP are:
        • PDR with HRCs
        • Neovascularization of iris (NVI),
        • Severe NPDR associated with:
          • Poor compliance for follow up,
          • Before cataract surgery/YAG capsulotomy,
          • Renal failure,
          • One-eyed patient
          • Pregnancy
    • Surgical treatment.
      • It is required in advanced cases of PDR.
      • Pars plana vitrectomyis indicated for
        • dense persistent vitreous haemorrhage
        • tractional retinal detachment
        • epiretinal membranes.
  • HYPERTENSIVE RETINOPATHY
    • Grading of hypertensive retinopathy
      • Keith and Wegner (1939) have classified hypertensive retinopathy changes into following four grades:
        • Grade I
          • mild generalized arteriolar attenuation, particularly of small branches
          • broadening of the arteriolar light reflex
          • vein concealment.
        • Grade II  
          • marked generalized narrowing and focal attenuation of arterioles
          • associated with deflection of veins at arteriovenous crossings (Salus’ sign).
        • Grade III  
          • This consists of Grade II changes plus
            • copper-wiring of arterioles
            • banking of veins distal to arteriovenous crossings (Bonnet sign)
            • tapering of veins on either side of the crossings (Gunn sign)
            • right-angle deflection of veins (Salu’ s sign).
            • Flame-shaped haemorrhages
            • cotton-wool spots
            • hard exudates
        • Grade IV
          • This consists of all changes of Grade III plus
            • silver-wiring of arterioles
            • papilloedema.
    • Arteriosclerotic changes
      • manifest as changes in arteriolar reflex and A-V nipping
      • esult from thickening of the vessel wall
      • are a reflection of the duration of hypertension.
    • Increased vascular permeability
      • results from hypoxia
      • responsible for haemorrhages, exudates and focal retinal oedema.

Animation: Diabetic Retinopathy

Understanding Proliferative Diabetic Retinopathy

Diabetes and the Eye

Diabetic Retinopathy

Diabetic Retinopathy

Understanding Nonproliferative Diabetic Retinopathy