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DISEASES OF THE LENS

- CATARACT
- DISPLACEMENT OF THE LENS
(ECTOPIA LENTIS)
- CONGENITAL ANOMALIES
* Coloboma
* Congenital Ectopia lentis
* Congenital Cataract
* Lenticonus
-

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 CATARACT
►Opacity of the lens
Lens Transparency

Factors that play significant roll:

1. Avascularity
2. tightly packed nature of lens
3. semi-permeable character of lens capsule
4. pump mechanism of lens fibres
- regulate electrolyte & water balance
- maintain relative dehydration
5. Auto-oxidation
- ensures integrity of cell mmb. pump

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 CLASSIFICATION OF CATARACT

A. ETIOLOGICAL
B. MORPHOLOGICAL
C. CLINICAL

1.ETIOLOGICAL CLASSIFICATION
A. Congenital cataract
B. Acquired cataract

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2.MORPHOLOGICAL CLASSIFICATION
A. Capsular cataract
→ typically follows uveitis/trauma
B. Subcapsular cataract
(anterior/posterior)

** N>D

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 C. Cortical cataract
D. Nuclear cataract
- results from sclerosis of lens nucleus
- affects distance vision > near
3. CLINICAL CLASSIFICATION
A. Imature cataract
* V/A > 3/60
* transmits red reflex
* allows view of posterior pole
B. Mature cataract
* V/A < 3/60
* doesn’t allow the view of posterior pole

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 CONGENITAL CATARACT
• Occurs due to disturbance in the normal growth of lens
ETIOLOGY
A - Idiopthic(50%)
B - Heredity
C - Maternal factors:
1. mal nutrition during pregnancy
2. maternal infection
- rubella virus(50%)
- cytomegalo virus
- toxoplasmosis
3. drug intake during pregnancy
- Corticosteroids
D. Fetal factors
* deficient oxygenation(anoxia)
* metbolic disorder of the fetus
* birth trauma

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CONGENITAL CATARACT

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 ACQUIRED CATARACT
- occurs due to degeneration of the already
formed normal lens fibres
-exact mechanism of degeneration is not clear

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 TYPES OF ACQUIRED CATARACT
• SENILE CATARACT
• COMPLICATED CATRACT
* Caused by intraocular inflammation
• TRAUMATIC CATARACT
• METABOLIC CATARACT
* Caused by metabolic disorders e.g. DM
• TOXIC CATARACT
* Corticosteroid-induced cataract
• RADIATIONAL CATARACT
• ELECTRIC CATARACT

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 SENILE CATARACT
(AGE-RELATED CATARACT)
• The commonest type
• Affects both sex equally above the age of 50
• Usually bilateral but one eye is affected earlier than the other

ETIOLOGY
1. Heredity
2. Ultraviolet irradiation
3. Diet
* deficient amino acids & vitamins
4. Dehydration crisis
* due to loss of electrolyte
5. Smoking
* Cyanates in smoke causes protein denaturation etc.

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 Mechanism of loss of transparency
*** basically different in nuclear and cortical senile
cataract

with increasing age

(senility)
↓
_______________________________________________________________________________
↓ ↓

Decrease in the function Reduced oxidative reaction

Of active transport pump

mechanism of lens ↓
↓
reversal of Na+/ K+ ratio Deacreased Synthesis of

↓ Protein in Lens fibres

Hydration of lens fibres ↓

↓
_____________________________________________________________________________
↓
Denaturation of Lens proteins
↓
OPacification of Cortical lens fibres

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 . In Nuclear Senile Cataract
--- The usual degenerative changes are:
→ Intensification of nuclear sclerosis
→ Associated with DHN & compaction
of nucleus
→ Formation of hard cataract
→ Brunecent cataract

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 CLINICAL FEATURES OF ARC
SYMPTOMS
1. Glare (intolerance of bright light)
- earliest visual disturbance
- amount vary with the location & size of the opacity
2. Uniocular diplopia/polyopia
- earliest symptom
- caused by irregular refraction of lens
3. Coloured halos
- caused by breaking of white light into colured
spectrum due to presence of water droplets in the lens

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4. Black spot in front of the eye
5. Image blur
6. Refractive change
** Progressive myopia in nuclear cataract
7. Loss of vision
** painless and gradually progressive
** progresses to LP+

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SIGNS
- Opacification of the lens
- ↓V/A
- dim red reflex on retinoscopy
- black shadow against red glow on
ophthalmoscopy etc.

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CLINICAL EXAMINATION
- V/A
- IOP
- Optic nerve & retina function test
* pupillary reflex
* perception & projection of light
* Red-Green colour discrimination

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 COMPLICATION OF CATARACT
• Dislocation/subluxation of lens
• Lens-induced uveitis
- due to leakage of lens protein into A/C
- in hyper mature cataract stage
- the protein act as antigen and induce
antigen-antibody reaction → uveitis
• Lens-induced glaucoma
* three types:
A. Phacolytic glaucoma
- due to leakage of lens protein

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B. Phacomorphic glaucoma
- caused by intumescent lens which results
pupillary block & secondary angle closure
C. Lens-particle glaucoma
- caused by blockage of TMW by retained
cortical material

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 MGT OF CATARACT
■ Non- surgical
■ Surgical
A. Non-Surgical Mgt
1. Treatment of cause
--- to prevent progression
* control of DM
* removal of drugs
* early Rx of ocular diseases like uveitis
* removal of irradiation

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 2. Measure to improve vision
--- in immature cataract stage
* Refraction → but needs frequent correction
* use of dark goggle for patients with central opacity
B. Surgical Mgt
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1. Visual improvement
- the most common indication
- depends upon individual needs
2. Medical indication
A. if it causes complications
*** Lens-induced uveitis /glaucoma
B. if Rx of retinal disease is hampered by lens opacity
3. Cosmetic

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 SURGICAL TECHNIQUES FOR CATARACT
EXTRACTION

• INTRACAPSULAR CATARACT EXTRACTION

* lens is removed along the capsule followed by:
1. eye glass/contact lens correction or
2. anterior chamber lens implantation

• EXTRACAPSULAR CATARACT EXTRACTION

* nucleus & anterior capsule are removed leaving the posterior
capsule in place
* followed by posterior chamber lens implantation

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Immature cataract

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Matured Cortical Cataract

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 Ocular manifestations of HIV/AIDS
• Microvasculopathy
• Tumours
• Neurophthalmology
• Opportunistic infections

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 GLAUCOMA
• is a group of ocular disorder characterised by:
*** progressive optic nerve damage resulting in a
characteristic appearance of optic disc &
irreversible visual field defect

• Frequently associated with raised IOP

N.B IOP is the most common risk factor for
the development of Glaucoma

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OCULAR HYPERTENSION
*** raised IOP without any associated glaucomatous
damage
- only 1% of cases will develop visual field loss each year
- treatment is indicated if IOP is >30mmhg;retinal nerve fibre
defect and para papillary change

NORMAL / LOW TENSION GLAUCOMA

*** typical cupping of the disc and/or visual field defects
associated with a normal or low IOP

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 Pathogenesis Of Glaucomatous Ocular Damage

●All types of glaucoma are characterised by:

- a progressive optic neuropathy result from the death of retinal
ganglion cell (RGCs)
Etiological Factors Of RGCs Death
1. Raised IOP(mechanical theory)
- causes mechanical stretch leading to axonal deformation and
ischemia by altering capillary blood flow
2. Pressure Independent Factors
( Vascular insufficiency Theory)
- factors affecting vascular perfusion of optic nerve head in the
absence of raised IOP
- common in normal tension glaucoma

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 Factors Affecting IOP
* Normal range --- 10-21mmhg

1. Local
2.General
A. Local Factors
1. rate of aqueous secretion
2. resistant to aqueous out flow drainage)
- most of the resistance is at TMW
3. increased episcleral venous pressure

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B. General Factors
1. Heredity
2. Age
- usually after the age of 40
- due to reduced facility of aqueous out flow
3. Sex
- F>M
4. Diurnal Variation
* Normal eyes - <5mmhg
* Glaucomatous eye - >8mmhg

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 CLASSIFICATION OF GLAUCOMA

A. CONGENITAL GLAUCOMA
B. PRIMARY ADULT GLAUCOMA
1. Primary Open Angle Glaucoma (POAG)

2. Primary Angle Closure Glaucoma (PACG)

C. SECONDARY GLAUCOMA
** A rise of IOP is associated with some primary ocular or
systemic disease

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 CONGENITAL GLAUCOMA
• Results due to developmental abnormalities of the angle of
the A/C
→obstructing the drainage of Aq. H → ↑IOP
CLASSIFICATION
A. True Congenital Glaucoma
- IOP is raised during intrautrine life
- the child is born with ocular engorgement
→Buphthalmos (Bull-like eyes)
- occurs in 40% of cases

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 B. Infantile Glaucoma
- occur at the age of 1-3 years
- occurs in 50% of cases
C. Juvenile Glaucoma
- occurs between 3-16 years
- 10% of cases
CLINICAL FEATURES
1. Photophobia
2. Lacrimation
3. Raised IOP

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4. Corneal signs
A. Corneal edema
B. Corneal enlargement  Buphthalmos
C. Breaks in Descemet’s membrane
* because it is less elastic than corneal stroma
5. Scleral sign
* it becomes thin and appears blue
6. Deep Anterior Chamber
7. Flat iris
* due to stretching of zonules
8. Optic disc cupping

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 TREATMENT
- Surgical mgt after IOP is lowered by drugs
* Goniotomy / Trabeculotomy

PRIMARY OPEN ANGLE GLAUCOMA

( CHRONIC SIMPLE GLAUCOMA)
- commonly occurs after 65 years
- no obvious systemic/ocular cause of rise in IOP
- characterised by:
1. slowly progressive raised IOP(>21mmhg)
2. optic disc cupping
3. visual field defect
- etiopathogenesis is not exactly known

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 RISK FACTORS POAG
1. Rise in IOP
- due to increased resistance to aqueous out flow caused by age
related thickening of Trabeculae
2. Heredity
3. Age
4. Race
* common in Blacks than Whites
5. Diabetics
6. Cigarette smoking

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CLINICAL FEATURE OF POAG
SYMPTOMS
- Asymptomatic until it has caused a significant loss of
visual field
- Reading and close work difficulties
* caused by accomodative failure due to constant
pressure on ciliary muscle and its nerve supply
- Delayed dark adaptation

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 SIGNS
1. Anterior segment sign
- normal anterior segment
- in late stage:
* sluggish pupil reflex
* slightly hazy cornea
2. IOP change
- exaggeration of the normal diurnal variation
3. Optic disc change
- Cupping due to loss of neural rim tissue
- optic disc haemorrhage
4. Visual field defect etc.

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Clinical Investigation of POAG
1. V/A
2. Tonometry
3. Gonioscopy
4. Slit-lamp examination
5. Posterior segment examination
6. Visual field test

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 MANAGEMENT OF POAG
• The aim of Rx is to lower IOP to a level where further visual loss doesn’t
occur
A. Medical Therapy
** lowers IOP by:
1. reducing aqueous secretion
- Timolol
- Betaxolol
- Brimonidine
- Acetazolamide etc.
2. increasing aqueous outflow
- pilocarpine
- latanoprost
B. Filtration surgery
** Trabeculectomy

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 PRIMARY ANGLE CLOSURE GLAUCOMA
(PACG)
• No obvious systemic/ocular cause
• Rise in IOP occurs due to:
- blockage of the aqueous humour by closure of
narrow angle of the anterior chamber
RISK FACTORS OF PACG
1. Hyper metropic eyes with shallow A/C
2. Age
3. Sex --- F>m
4. Family history
5. Race
** Common in South-East Asias , Eskimos & Chinese
** Uncommon in Blacks

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CLINICAL CLASSIFICATION OF PACG
A. Latent PACG
B. Sub acute (Intermittent) PACG
C. Acute PACG
D. Chronic PACG
E. Absolute glaucoma

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 ACUTE PACG
• Occurs due to a sudden total angle closure leading to severe
rise in IOP
• Sight threatening emergency
CLINICAL FEATURE
SYMPTOMS
- Pain
- Nausea & vomiting
- Rapidly progressive impairment of vision
- Haloes

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 SIGNS
- Markedly elevated IOP (40-70 mmhg)
- Ciliary flush
- Oedematous cornea
- Shallow anterior chamber
- Semi dilated & fixed pupil
- Oedematous & hyperaemic optic disc
MGT
- essentially surgical
*** Medical therapy before the eye is ready for operation

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 ABSOLUTE PACG
• The final phase
CLINICAL FEATURES
1. Painful blind eye( NLP)
2. High IOP (stony hard eye ball)
3. Ciliary flush
4. Corneal edema
5. Shallow A/C
6. Fixed & dilated pupil
7. Optic disc shows glaucomatous optic atrophy
MGT
A. Retrobulbar alcohol injection
B. Enucleation of the eye ball
** if pain is not relieved by the above mgt

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Peripheral Iridectomy

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