This document discusses diabetic retinopathy, which is a microvascular complication of longstanding diabetes mellitus that causes damage to the blood vessels in the retina. It is the most severe ocular complication of diabetes and the most common cause of blindness between ages 20-65. The risk and progression of diabetic retinopathy increases with longer duration of diabetes, poor blood sugar control, pregnancy, hypertension, nephropathy, and other factors. The document describes the pathogenesis, classification, signs, and treatment options for diabetic retinopathy.
2. Diabetic retinopathy
The most severe of ocular complications of diabetes
Caused by damage to blood vessels of the retina,
leads to retinal damage
Microvascular complication of longstanding diabetes
mellitus
Most prevalence cause of legal blindness between
the ages of 20 and 65 years
Common in DM type 1 > type 2
3.
4. Duration of diabetes
Most important factor
Patient diagnosed before age 30 year
50% DR after 10 yrs
90% DR after 30 yrs
Poor metabolic control
Relevant to development and progression of DR
HbA1c associated with risk
Pregnancy
Associated with rapid progression of DR
Risk factors
5. Hypertension
Very common in patients with DM type 2
Should strictly control (<140/80 mmHg)
Nephropathy
Associated with worsening of DR
Others
Obesity, increased BMI, high waist-to-hip ratio
Hyperlipidemia
Anemia
Risk factors
10. Microaneurysm
Retinal hemorrhage
“Dot or Blot” Spot
“Flame or Splinter shape” hemorrhage
Hard exudate
Cotton wool Spot
Venous beading
Intra-retinal microvascular abnormalities (IRMA)
Signs of NPDR
11. The earliest signs of DR
Localized saccular outpouchings of capillary
wall red dots
Focal dilatation of capillary wall where
pericytes are absent
Fusion of 2 arms of capillary loop
Microaneurysm
13. Capillary or microaneurysm is weakened
rupture intraretinal hemorrhages
Dot & blot hemorrhages
Usually round or oval
Flame-shape or splinter hemorrhages
More superficial - in nerve fiber layer
Absorbed slowly after several weeks
Retinal Hemorrhage
17. Yellow deposits of lipid and protein within the
retina
Accumulations of lipids leak from
surrounding capillaries and microaneurysms
Hyperlipidemia may correlate with the
development of hard exudates
Hard exudate
18.
19.
20.
21. Non-proliferative diabetic retinopathy
Right eye: Microaneurysm, few flame-shaped and dot-blot hemorrhages and hard
exudate [with hard exudate in macula area] - moderate non proliferative diabetic
retinopathy
Left eye: Microaneurysm, numerous flame-shaped and dot-blot hemorrhage [more than
20 dots in 4 quadrant], hard exudate [with hard exudate in macula area] - severe non
proliferative diabetic retinopathy
22. 5% of DM pt.
Findings
Neovascularization : NVD (Neovascularization of
disc), NVE (Neovascularization of Elsewhere)
Vitreous changes
Advanced diabetic eye disease
Final stage of Uncontrolled PRD
Glaucoma (neovascularization)
Blindness from persistent vitreous hemorrhage
Proliferative diabetic retinopathy
Angiogenic facors from hypoxic retina
Has an adjunctive role.
VEGF:VEGF-A,VEGF-B,PIGF VEGF receptor 1 and 2(both r unequally distributed in R and C).
Ranibizumab0.5mg/0.05ml(Antibody Fab fragment_recombinant humanised) neutralises/inhibit/bind all isoform of VEGF A
Aflibercept(Fusion protein recombinant composed of an Fc domain) neutralises/inhibit/bind all isoform of VEGF A,VEGF B and PIGF,has longer hallf life and much higher affinity to VEGF
Bevacizumab1.25mg/0.05ml(complete Ab,very much cheaper,A larger molecule than Ranibizumab,serious sys adverse event is slightly higher)
Func of VEGF 1.promotion of angiogenesis 2.increase vas permeability 3.Dilation of BV