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Diabetic Retinopathy
Presented By
Dr. Md. Rezwanul Hasan
Jr. Consultant, Vitreo-Retina Dept.,
Deep Eye Care Foundation & Eye Hospital
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
 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
 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
 Microvascular occlusion
 Microvascular leakage
Pathogenesis
Microvascular leakage
Degeneration and loss of pericytes
Plasma leakage
Intraretinal hemorrhage
Hard exudate
(Circinate pattern)
Capillary wall weakening
microaneurysm
Retinal edema
Microvascular occlusion
Neovascularization
and fibrovascular proliferation
VEGF
Increased plasma viscosity
Deformation of RBC
Increased platelets stickiness
Decreased capillary blood flow
and perfusion
Endothelial cell damage and proliferation
Capillary basement membrane thickening
Retinal hypoxia
A-V shunt
IRMA*
*intraretinal microvascular abnormalities
Proliferative
retinopathy
Rubeosis iridis
Classification
 Non-proliferative diabetic retinopathy (NPDR)
 Mild NPDR
 Moderate NPDR
 Severe NPDR
 Proliferative diabetic retinopathy (PDR)
 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
 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
Microaneurysm
 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
Dot Spot VS Flame Shape
Dot Spot VS Flame Shape
Hemorrhage
 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
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
 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
Neovascularization of disc
NVE
Venous
beading
IRMA
New vessels of the disc (advanced)
Retinal detachment
Vitreous hemorrhage
 Prevention
 Treat underlying conditions
 Control blood sugar – HbA1c < 7
 Control blood pressure – SBP < 130 mmHg
 Control lipid profile – TG, LDL
 Correct anemia
 Control diabetic nephropathy
 Pregnancy makes DR worsen
Medical therapy
Laser Photocoagulation
Vitreoretinal surgery
Intravitreal triamcinolone acetonide
Anti-VEGF
Treatment
Thank You

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Screening of Diabetic Retinopathy

  • 1. Diabetic Retinopathy Presented By Dr. Md. Rezwanul Hasan Jr. Consultant, Vitreo-Retina Dept., Deep Eye Care Foundation & Eye Hospital
  • 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
  • 6.  Microvascular occlusion  Microvascular leakage Pathogenesis
  • 7. Microvascular leakage Degeneration and loss of pericytes Plasma leakage Intraretinal hemorrhage Hard exudate (Circinate pattern) Capillary wall weakening microaneurysm Retinal edema
  • 8. Microvascular occlusion Neovascularization and fibrovascular proliferation VEGF Increased plasma viscosity Deformation of RBC Increased platelets stickiness Decreased capillary blood flow and perfusion Endothelial cell damage and proliferation Capillary basement membrane thickening Retinal hypoxia A-V shunt IRMA* *intraretinal microvascular abnormalities Proliferative retinopathy Rubeosis iridis
  • 9. Classification  Non-proliferative diabetic retinopathy (NPDR)  Mild NPDR  Moderate NPDR  Severe NPDR  Proliferative diabetic retinopathy (PDR)
  • 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
  • 14. Dot Spot VS Flame Shape
  • 15. Dot Spot VS Flame Shape
  • 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
  • 23.
  • 26. New vessels of the disc (advanced)
  • 28.
  • 29.  Prevention  Treat underlying conditions  Control blood sugar – HbA1c < 7  Control blood pressure – SBP < 130 mmHg  Control lipid profile – TG, LDL  Correct anemia  Control diabetic nephropathy  Pregnancy makes DR worsen Medical therapy
  • 30. Laser Photocoagulation Vitreoretinal surgery Intravitreal triamcinolone acetonide Anti-VEGF Treatment

Hinweis der Redaktion

  1. 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