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  Diabetic Retinopathy  
 

 

  • What is diabetes !! - Diabetes mellitus is the inability of the body to use and store sugar properly, resulting in high blood glucose (sugar) levels
  • Diabetes results in damage to veins, arteries and capillaries throughout the body.
  • Diabetes affecting vision –
    • Increases the likelihood of cataracts
    • Increases the risk glaucoma
    • Risk of developing diabetic retinopathy: damage occurs to the fragile blood vessels of the retina
  • Diabetic retinopathy is a leading cause of new cases of blindness in people aged 20 to 74 years

Etiology

  1. The duration of diabetes:
    • It is the most important factor.
    • In patients diagnosed as having diabetes before the age of 30 years, the incidence of DR :
      • After 10 years is 50%
      • After 30 years is  90%
  2. Glycemic control:
    • Increased severity of diabetic retinopathy is associated with poorer glucose control
  3. Miscellaneous factors:
    • Pregnancy
    • Systemic Hypertension
    • Renal Disease
    • Anaemia.(↓Oxygen )
    • Elevated Serum lipid.
    • Aarotid artery occlusive disease
    • Alcohol
    • Obesity
  4. PVD: degenerative changes in vitreous
  5. High myopia
  6. Removal of cataract

Ophthalmic Features

  1. Microaneurysms
    • Located in the inner nuclear layer.
    • The first clinically detectable lesions.
    • Small round dots .(20-200 μ)
    • Mostly located near and temporal to the macula.
    • When coated with blood they may be indistinguishable from dot haemorrhages.
  2. Haemorrhages : The clinical appearance depending on location
    • 'Dot' and 'Blot':
      • Originating from the venous end of the capillaries.    *located in the compact middle layers of the retina.
    • Flame-shaped:
      • Originate from the more superficial precapillary   arterioles, follow the course of the retinal nerve fibre layer. (liner disribution)
  3. Hard exudates :
    • located between the inner plexiform and inner nuclear layers of the retina. (OPL)
    • They are often distributed in a (circinate pattern).
  4. Retinal edema :
    • Located between the outer plexiform and inner nuclear layers.
    • Later it may involve the inner plexiform and nerve fibre layers, until eventually the entire thickness of the retina may become oedematous.
    • With further accumulation of fluid, the fovea assumes a cystoid appearance .
  5. Cotton-wool spots: (Soft exudates )
    • Nerve fiber layer infarction.
    • Caused by capillary occlusion in the retinal nerve fibre layer.
  6. Intraretinal microvascular abnormalities (lRMA) :
    • Dilated, tortous retinal capillaries that act as a shunt between arterioles and venules.
    • Frequently seen adjacent to areas of capillary closure.
  7.  New Vessels:
    • Unlike IRMA, they arise on the retinal surface and may extend or be pulled into the vitreous cavity.
    • NVD : NV appears on or within one DD of disc margin .
    • NVE : any other location
  8. Fibrous Glial proliferation :
    • Accompained growth of new vessels.
    • It is proliferation between the posterior vitreous gel and the ILM.
    • Derived from retinal glial cells and fibrocytes

                 

 

         

Types of Diabetic Retinopathy

There are two types of diabetic retinopathy:
  1. Nonproliferative diabetic retinopathy (NPDR)
    • Mild - Microaneurysms, retinal hemorrhage and hard exudate
    • Moderate - Mild NPDR plus cotton wool spots .
    • Severe - Moderate NPDR plus one of :
      • Intraretinal Hges in four quadrants .
      • marked venous beading in two or more quadrants
      • IRMA one or more quadrants
  2. Proliferative diabetic retinopathy (PDR)-
    • Early PDR - New vessels and/or fibrous proliferations; or preretinal and/or vitreous hemorrhage
    • PDR with HRC -NVD ≥ 1/3 of DD.
      • less extensive NVD, if vitreous or preretinal hemorrhage is present
      • NVE ≥ half disc area, if vitreous or preretinal hemorrhage is present
    • Advanced PDR -Extensive vitreous hemorrhage precluding grading.
      •  retinal detachment involving the macula.
      •  phthisis bulbi

        

 

        

Investigations

Fluorescein Angiography
  • Not needed to identify CSME or PDR.
  • Useful because
    1. As a guide during CSME treatment.
    2. Identify macular capillary nonperfusion.
    3. Identify subtle areas of NV causing recurrent vitreous hemorrhage despite full PRP

Optical Coherence Tomography (OCT) - In diabetics, OCT can “map” areas of macula edema (“swelling”) thus facilitating fluorescein angiography in guiding laser treatment of the macula.

Treatment

  • Medical Therapy :
    • Glycemic control :
    • Blood pressure control.
    • Blood lipids control.
  • Laser surgery :
    • The treatment of depends on the severity of retinopathy and t   the presence or absence of CSME, which may be present at  any stage .( Focal / Grid / PRP )
  • Drug therapy :
    • Intravitreal (“inside the eye”) drug injections:
    • Triamcinolone (a corticosteroid; mechanism of action unclear)
    • Macugen, Lucentis, & Avastin (drugs primarily used to manage neovascular (“wet”) age-related macular degeneration (reduction in the severity of retinopathy by inhibiting VEGF).
  • Vitrectomy
    • Indications: Vitreous hemorrhage (clear, gel-like substance in middle of eye) fills with non-clearing blood and traction retinal detachment.
    • Performed in the operating room, this microsurgical procedure
    • Involves removing the blood-filled vitreous and removal of
    • Neovascular (new vessel) membranes (fibrovascular proliferation)
    • Improves vision by re-establishing clear vitreous fluids and lowers
    • The probability of future bleeding by removing the neovascular membranes.
    • Removal of scar-like (fibrovascular) membranes results in retinal
    • Reattachment and possible improvement in vision.