UG

1. METABOLIC DISORDERS
OF EYE
Farra
035

2. DIABETIC RETINOPATHY
• Retinal changes in patients with
diabetes mellitus
• Leading cause of blindness
RISK FACTORS
1)DURATION OF DIABETES
• After 10 years – 20% type 1 & 25% type
2
• After 20 years – 90% type 1 & 60% type
2
• After 30 years – 95% both type 1 & type
2
will develops retinopathy

3. 2) AGE OF ONSET OF DIABETES
• In a child – negligible for first 10 years
• Start after onset of puberty
3)SEX - More in females (4:3)
4)POOR METABOLIC CONTROL
5)HEREDITY – recessive trait
6)PREGNANCY
7)HYPERTENSION
8)OTHER – smoking, obesity, hyperlipidemia

4. PATHOGENESIS
HYPERGLYCEMIA
MICROANGIOPATHY
Microvascular
occlusion
Microaneurys
m
Capillary leakage
and haemorrhage

5. RETINAL
ISCHEMIC
Retinal
edema
Hard
exudate
Av shunt
formation
Neovascularaza
tion

6. CELLULAR DAMAGE
Sorbitol accumulation
Advanced glycation end
(AGE) product accumulates
Activation of protein kinase
C isoforms
Excessive oxidative stress
HEMATOLOGICAL &
BIOCHEMICAL CHANGES
+ Platelet adhesiveness
+ Blood viscosity
RBC deformation, Rouleaux
formation
+ Fibrinolysis

7. Classification - ETDRS
• Non proliferative diabetic retinopathy (NPDR)
– Mild NPDR
– Moderate NPDR
– Severe NPDR
– Very severe NPDR
• Proliferative diabetic retinopathy (PDR)
– Without high risk
– With high risk
• Diabetic maculopathy
– CSME
– Non-CSME
• Advanced diabetic eye disease (ADED)

8. EARLY TREATMENT DIABETIC RETINOPATHY STUDY (ETDRS)
CLASSIFICATION
• Mild NPDR
– One microaneurysm present
• Moderate NPDR
– Microaneurysm / intraretinal hemorrhage in 2-3 quadrants
– Early mild IRMA
– Hard/soft exudates (+/-)
• Severe NPDR (any one of 4-2-1 Rule)
– Four quadrants of microaneurysm / extensive intraretinal
hemorrhage
– Two quadrants of venous beading
– One quadrant of IRMA changes
• Very severe NPDR
– Any two of 4-2-1 Rule

9. 1) NON PROLIFERATIVE DIABETIC
RETINOPATHY (NPDR)
Ophthalmoscopic features
• Microaneurysms
• Retinal hemorrhage
• Retinal edema
• Hard exudates
• Cotton wool spots
• Venous abnormalities
• Intraretinal microvascular abnormalities
• Dark-blot hemorrhages

14. Scattered
hyperfluoresc
ent
Microaneurysms
may leak plasma
constituent into
retina

15. 2) PROLIFERATIVE DIABETIC
RETINOPATHY (PDR)
• Develops in more than
50% of cases after 25
years of onset of disease.
• Hallmark – occurrence of
neovascularization at
optic disc (NVD) and/or
elsewhere (NVE)
• Later findings:
– Fibrovascular epiretinal
membrane formation
– Vitreous detachment &
vitreous hemorrhage
Vitreous
hemorrhage
Vitreous

16. TYPES (by DRS group)
• Early NVD or NVE PDR
without HRCs
• PDR with HRCs
*High risk characteristics
(HRC)
• NVD 1/4 to 1/3 of disc
area with/without
vitreous hemorrhage (VH)
• NVD <1/4 disc area with
VH
• NVE >1/2 disc area with
VH

17. 3) DIABETIC MACULOPATHY
• Changes in macular region
• Diabetic macular edema (DME) – occurs due
to increase permeability of retinal capillaries
Clinically significant macular edema (CSME)
Three criteria:
• 1) thickening of retina within 500μ of centre
of fovea
• 2) 1 + hard exudates
• 3) Development of a zone of retinal
thickening one disc diameter or larger in size

19. Signs & Symptoms
• Blurred or distorted vision or
difficulty reading
• Partial or total loss of vision
– a shadow or veil across patient’s
visual field
• Eye pain

20. Management
• Investigations (urine, glucose, lipid,
HbA1C, fundus fluorescein angiography)
• Control sugar, lipid, renal function,
anaemia and hypertension
• Change of lifestyle
• Intravitreal anti-VEGF (bevacizumab
1.25mg, ranibizumab 0.5mg)
• Intravitreal steroids (triamcinolone
acetonide 20mg)
• Laser therapy
• Surgical treatment

21. DIABETIC CATARACT
• Early age & progresses rapidly
• True diabetic cataract
– Rare and in young people
blood sugar >200mg/ml
– Excess glucose is sorbitol
– Accumulate in fibre and cause osmotic imbalance
– Snowflake / snowstorm cataract

22. GALACTOSEMIC CATARACT
• Rare, congenital , in infant
• Bilateral cataract
• Typical “oil drop cataract”
• Inborn error of galactosaemia, occurs in two
forms
• Reversible by elimination of milk and milk
products in early stage

23. THYROID EYE DISEASE
• Denotes typical ocular changes – lid
retraction, lid lag & proptosis
Etiopathogenesis
• Associated with hyperthyroidism (90%),
hypothyroidism (4%), euthyroidism (6%)
Risk factors
• Female (4-6 times more common)
• Smoking
• Middle age
• Autoimmune thyroid disease

24. PATHOGENESIS
Infiltration with lymphocytes, plasma cells,
macrophages, mast cells
Increased acid mucopolysaccharide in orbital soft
tissue
Extraocular muscles enlarged due to edema,
infiltration with round cells
Stimulate adipogenesis, fibroblast proliferation,
glycosaminoglycans synthesis
Activated T-cell act on fibroblast-adipocyte lineage

25. Clinical features
• Lid signs
– Retraction of upper lids
(Dalrymple’s sign)
– Lid lag (von Graefe’s sign)
– Fullness of eyelids
(Enroth’s sign)
– Difficult eversion of upper
lid (Gifford’s sign)
– Infrequent blinking
(Stellwag’s sign)
• Conjunctival signs
– Deep injection
– Chemosis

26. • Ocular motility defects
– Convergence weakness
(Mobius’s sign)
– Elevator palsy
• Exophthalmos
(proptosis)
• Lacrimation
• Photophobia

27. MARFAN SYNDROME
• Autosomal dominant
mesodermal dysplasia
• Lens is displaced
upwards and temporally
(bilateral symmetrical)
due to weakend zonules
• Myopia
• Blurred vision

28. HOMOCYSTINURIA
• Autosomal recessive, inborn error metabolism
• Eye anomalies:
• Ectopia lentis – in contrast to Marfan syndrome which
features upward ectopia lentis, downward dislocation
is the typical finding of
homocystinuria or subluxation of lens
• Myopia (short sightedness)
• Glaucoma
• Optic atrophy
• Retinal detachment
• Cataracts

29. WILSON DISEASE
• Autosomal recessive
condition where copper
build up in the body
• Kayser–Fleischer rings (KF
rings),
a pathognomonic sign
• Copper accumulation at the
Descemet’s membrane
• Sunflower cataract –
accumulation of copper
under posterior capsule of
lens
• Golden plaques deposition
at the posterior pole