Retina description

1. • PROF MUHAMMAD TARIQ KHAN

2. DIABETES AND THE EYE

3. LEARNING OBJECTIVES
• PATHOGENESIS OF DIABETIC
RETINOPATHY
• CLINICAL FEATURES OF DIABETIC
RETINOPATHY
• INVESTIGATION AND TREATMENT OF
DIABETIC RETINOPATHY

4. PATHOGENESIS

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

7. Pre-proliferative/ sever NPDR
Vascular
tortuosity
Haemorrhage
CWS
Microaneurism

8. Proliferative retinopathy
NVD NVE
Laser burn scars
Pre-retinal
haemorrhage

9. MOLECULAR BASIS OF
DIABETIC RETINOPATHY
• VASCULAR ENDOTHLIAL GROWTH
FACTOR
• PLACENTA GROWTH FACTOR
• PIGMENT EPITHLIUM DERIVED
FACTORS

10. MOLECULAR BASIS OF
DIABETIC RETINOPATHY
• ENDOTHELIUM DERIVED RELAXING
FACTORS
• NITRIC OXIDE
• ENDOTHELIUM DERIVED
CONTRACTING FACTORS
• ENDOTHELIN, CYLO OXYGENASE
PRODUCT

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

15. Diabetic maculopathy
Hard
exudate

16. NON PROLIFERATIVE DIBETIC RETINOPATHY
Blot haemorrhage
Exudate
Microaneurism

17. Pre-proliferative/ sever NPDR
Vascular
tortuosity
Haemorrhage
CWS
Microaneurism

18. Proliferative retinopathy
NVD NVE
Laser burn scars
Pre-retinal
haemorrhage

22. Advanced diabetic eye disease
Preretinal fibrosis and
tractional retinal detachment
Rubeosis iridis

23. End-stage diabetic eye disease
• PHTHISIS
Shrunken, soft eye with
opaque vascularised
cornea and no visual
potential

24. TREATMENT
• LASER: Light
Amplification by the
Stimulated Emission
of Radiation
– Focal
– Grid
– Panretinal
photocoagulation

25. COMPLICATION OF
UNTREATED DIABETIC
RETINOPATHY
• TRACTION RETINAL DETACHMENT
• VITREOUS HEMORRAHGE
• CENTRAL RETINALARTERY
OCCLUSION
• CENTRAL RETINAL VEIN OCCLUSION
• RUBEOTIC GLAUCOMA

26. CAUSES OF SUDDEN LOSS
OF VISION IN DIABETIC
PATIENT
• VITREOUS HEMORRAHGE
• CRVO
• CRAO
• OPTIC NEURITIS
• DIABETIC PAPILLOPATHY

27. HOW DOES LASER WORK
Decreases the No of photorecepters hence low
O2 demand
Converts ischemic retina into infarcted retina
Seales the leaking MA

28. ANTI VEGF

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

31. • THANKYOU

32. HYPERTENSIVE
RETINOPATHY

33. LEARNING OBJECTIVES
• DIAGNOSIS AND TREATMENT OF
HYPERTENSIVE RETINOPATHY
• EYE INVOLVEMENT IN
HYPERTENSION

34. Three distinct categories:
• Hypertensive retinopathy.
• Hypertensive choroidopathy.
• Hypertensive optic neuropathy.

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).

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.

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.

48. Classification of Hypertensive
Retinopathy
• Modified Keith-Wagener-Barker
classification.
• Modified Scheie classification.

49. Modified Keith-Wagener-Barker
Classification:
stage Haemo
rrhage
Exu
date
Disc
edema
A-V
ratio
Light reflex A-V crossing
0 -- -- -- 3:4 Fine yellow
Red
None
1 -- -- -- 1:2 Broad yellow
Red
A-V nipping
Vein depression mild
2 -- -- -- 1:3 Copper wire
Not visible
Vein depression
3 + + -- 1:4 Silver wire
Not visible
Right angle deviation
Distal dilatation
Vein disappearance
4 + + + Fibrous Same Same

51. NEW CLASSIFICATION
• MILD
• MODERATE
• SEVERE

52. Ocular Associations
and Complications
• Branch retinal vein occlusion.
• Central retinal vein occlusion.
• Retinal artery occlusion.
• Retinal artery macro aneurysm.
• Anterior ischemic optic neuropathy.
• Ocular motor nerve palsy.
• Uncontrolled hypertension adversely effect
diabetic retinopathy.

55. INVESTIGATION
• FFA
• OCT
• OCT ANGIO

56. MANAGEMENT
• STRICT CONTROL OF BP
• LIPID PROFILE
• RENAL FUNCTION TEST

57. IMPORTANT SEQ