3. LEARNING OBJECTIVES
• PATHOGENESIS OF DIABETIC
RETINOPATHY
• CLINICAL FEATURES OF DIABETIC
RETINOPATHY
• INVESTIGATION AND TREATMENT OF
DIABETIC RETINOPATHY
5. PATHOGENESIS OF
DIABETIC RETINOPATHY
• HYPERGLYCEMIA IS CRITICAL
FACTOR
• MICROANGIOPATHY
• THICKING OF BASEMENT
MEMBRANE
• LOSS OF PERICYTES
• RETINAL CAPILLARY NON
PERFUSION
6. PATHOGENESIS OF
DIABETIC RETINOPATHY
• INCREASE LEAKAGE
• RETINAL EDEMA
• EXUDATION
• IRMA(INTRARETINAL
MICROVASCULAR ABNORMALTIES)
• FORMATION OF NEW VESSELS
• RETINAL TRACTIONS
11. MOLECULAR BASIS OF
DIABETIC RETINOPATHY
• POLYOL PATHYWAY
• NONENZYMATIC GLYCATION
OXIDATIVE STRESS
• ACTIVATION OF PROTEIN KINASE
12. RISK FACTORS
• DURATION OF DM
• CONTROL OF DM. WILL NOT
PREVENT BUT DELAY
• HYPERTENSION
• RENAL DISEASE
• PREGNANCY
• OBESITY, HYPERLIPIDAEMIA,
SMOKING, ANAEMIA
13. CLINICAL CLASSIFICATION
OF DIABETIC RETINOPATHY
NON PROLIFERATIVE DIABETIC
MILD, MODERATE,SEVERE
PROLIFERATIVE
LOW RISK
HIGH RISK
END-STAGE DIABETIC EYE DISEASE
14. CLINICAL SIGNIFICANT
MACULAR EDEMA
• RETINAL THICKING WITHIN 1500
MICRON OF FOVEA
• EXUDATION WITHIN 1500 MICRONS
OF FOVEA
• RETINAL THICKING ONE DISC
DIAMETER (1500) OR LARGER ANY
PART OF WHICH IS WITHIN 1500
MICRONS OF FOVEA
29. SCREENING
• NO RETINOPATHY OR MILD NON
PROLIFERATIVE WITH NORMAL
VISION
– SEE YEARLY, OR SOONER IF VISION
DETERIORATES
30. SCREENING
• REFER TO OPHTHALMOLOGIST
– NON PROLIFERATVE DR WITH
MACULAR CHANGES
– NON PROLIFERATVE DR WITH
DECREASE IN VISION
– PRE-PROLIFERATIVE RETINOPATHY
– PROLIFERATIVE RETINOPATHY
35. • VESSELS CAN BE OBSERVED
DIRECTLY.
• HYPERTENSIVE VASCULAR
CHANGES ARE RELATED TO:
• SEVERITY.
• CHRONICITY.
• DURATION OF SYMPTOMS.
• AGE OF THE PATIENTS.
36. Atherosclerosis Arteriosclerosis
• NORMAL AGING PROCESS.
• LOSS OF VESSEL WALL ELASTICITY &
VESSEL WALL THICKENING.
• TWO PATHOLOGICAL PHENOMENON:
ATHEROSCLEROSIS (LIPID
INSUDATION ).
ARTERIOLOSCLEROSIS (COLLAGEN
DEPOSITION).
37.
38. • QUALITY OF THE LIGHT REFLEX
OF VESSEL WALL CHANGES
• THIN LINE OF LIGHT REFLEX WITH
NORMAL COLUMN OF BLOOD.
• DULLER & BROADER REFLEX .
• COPPER WIRE HUE OF RED BROWN
REFLEX.
• SILVER WIRE CHANGES OF
SCLEROSIS OF THE VESSELS WITH
NO APPARENT BLOOD COLUMN.
39.
40.
41. • Changes at arteriolovenous
crossing:
• Arteriolovenous nipping
occurs as the underlying
venules are compressed
(Gunn’s sign).
• Banking of the veins distal to arteriovenus
crossings (Bonnet sign).
• With an increase in sclerosis the arteries & veins,
which normally cross in an acute angle, cross in an
obtuse angle (Salus sign).
42. Vascular leakage
• LOSS OF ENDOTHELIAL CELLS & THE
FORMATION OF TEARS & HOLES IN
THE NECROTIC MUSCLE WALL
RESULTS IN FOCAL LEAKAGE.
• FLAME SHAPED HEMORRHAGES&
RETINAL EDEMA.
• CHRONIC RETINAL EDEMA MAY
RESULT IN THE DEPOSITION OF
HARD EXUDATES AROUND THE
FOVEA IN THE HENLE LAYER WITH A
MACULAR STAR CONFIGURATION.
