Def

Risk factor
Aging

Cataract
Classificati
on

LENS CHANGES
Normal senescent changes occurring in lens, usually after presbyopia
(4) Age, UV, Nicotine, Substances (meds)
Slow increase in sagittal width and convexity;
Lens yellowing;
Decreased transmission of blue light
Any opacification of lens with some influence on vision
Based on anatomical location, cause of cataract or appearance

CATARACT CLASSIFICATION
1. Congenital/developmental cataracts
Presentatio
Non progressive
n
2/3 bilateral (Cause more likely to be established > common = genetic
mutation)
Unilateral aet less clear
Morph
Whitish-blue tinge (Cerulian cataract)
Association
Maternal infection (rubella, toxoplasmosis, CMV, varicella)
Chromosomal abnormalities (Downs)
Metabolic disorders (Galactosemia)
2. Presenile,
Aetiology

Drugs

Cortic
al

secondary cataracts (aetiology)

Penetrating and blunt trauma; metallic FB
Chronic uveitis
Long standing retinal detachments (without treatment > metabolism
changed > effect on lens metabolism)
Drugs
Steroids (10-20mg/year systemically)
Phenothiazines (anti-psychotic)
Phospholine
Iodides (insect killer spray)

3. Age related cataracts (senescent/senile) - Different types (according to morph)

Location
Spokes begin at equator; early spokes only seen with dilation
Often found infra-nasal initially
May involve anterior, posterior or equatorial cortex
Aetiology
Due to electrolyte imbalance
Normally: low sodium and high potassium ion
Cortical = opposite > hydration of cortex > vacuoles > clefts >
radial/spoke like appearance
Slow progression
Clinical
Advanced spokes > difficult to view peripheral retina
Sx > glare, decreased night vision and acuity
Secondary changes occur in capsule permeability > unpredictable
effects on acuity
More easily seen with retroillumination or direct ophthalmoscope
Prevalence
Most common
65+
Stages
Incipient
Vacuoles, water clefts, spokes

Nuclea
r

Pathogene
sis

Clinical
signs

Test
Prevalence

Capsul
ar

Intumesce
Lens swells > pupillary block danger
nt
Mature
Milky cortex + lens dehydration
Hypermat
Danger of phaco-anaphylactic uveitis and glaucoma
ure
Morgagnia
Liquefied cortex > nucleus moves freely in lens
n
1. Modification of lens fibre proteins into high molecular weight
proteins
2. increased lens density
3. gradual shift in myopia, affecting distance vision more than near
4. Senopia/second sight
Increased spherical aberration
Acccentuation of normal yellowing = cataract when it impacts vision
Temporary increase in acuity
Slow progression
Optic section + cobalt filter
Common
65+

Anterior

Location
Association

Lie directly under lens capsule

Associated with fibrous metaplasia of anterior
epithelium of lens

Posterior

Location
Association
Symptoms

Lies on visual axis closer to nodal point

Associated with significant reduction in acuity
Decreased contrast sensitivity and night vision
Near vision affected more than distance
Aberrant migration of lens epithelial cells from
equator secrete basement membrane > plaque
formation inside capsule
Granular aggregation > dirty smear on visual axis
Earlier onset 50y

Pathogenes
is

Pesentatio
n
Diabet
ic

(Any age) Sorbitol > osmotic pressure gradient > hydration and
opacification

Comparison table for age related cataracts:

Cataract
Nuclear sclerotic
cataract

Clinical appearance
Progressive yellowing
of lens nucleus

Pathogenesis
Increasing high
molecular weight
proteins

Cortical cataract

Vacuoles
Spokes
Milky clouding
Granular
Beaten copper
Posterior capsular

Alternating capsule
permeability
Hydration of cortex
Aberrant migration of
epithelial cells to
posterior subcapsular

Posterior subcapsular
cataract

Clinical features
Decreased distance
vision
Senopia
Slow progression
Unpredictable VA loss
Slow progression
Obscured fundus view
Decreased near VA
Younger
Dramatic vision loss

zone

pole

Process of cataract development:

In lens cortex
Due to electrolyte
imbalance.

Cortical cataract
Due to electrolyte
imbalance

Nuclear
Due to modification of
lens fibre proteins

Low sodium and high

potassium ion
content

High sodium and low

potassium ion content

Results in high
molecular weight
proteins

Diabetic cataract
Sorbitol causes
osmotic pressure
gradient
Leads to hydration and
opacification

VISUAL SYMPTOMS WITH CATARACTS

1. Glare
2. Decreased night vision
3. Decreased contrast sensitivity
4. Decreased acuity
5. Monocular diplopia/ghosting images

EVALUATION OF PX WITH CATARACT

Listen to px
Common complaints:
1. Glasses dont work
2. Present glasses frustrating
3. Glasses seem dirty
4. Photophobia
5. Outside vision worse
Procedure:
Visual
analysis

Ocular health
tests

Refer

1.
2.
3.
4.
5.

Best refraction and VA (distance and near; dark and bright)

DDx with PH (with nuclear cataracts, dont reduce plus at near too much)
Consider aniseikonia effects
Glare testing and contrast sensitivity
Demonstrate Purkinje effects using +9D lens with bright background
(indicates good macular function if observed)
1. Check for alternative reason for reduced acuity (Dont assume reduced VA
is solely due to opacities)
2. Ophthalmoscopy should indicate VA (if macula is okay)
3. Pupils no APD
4. Macular integrity: photostress test, PAM or interferometer
Presurgical tests:
1. Keratometry > Willis keratopathy (vascular formation on lens)
2. A and B-scan ultrasound
3. Specular microscopy > corneal endothelial integrity (significant guttata
imposes increased risk for bullous keratopathy > long standing oedema)

POST OPERATIVE COMPLICATIONS

A. Early complications
1. Eyelids
1. Ptosis
2. Lid oedema
3. Damage to levator from lid speculum
4. Ecchymosis
2. Conjuncti
1. Injection
2. Subconjunctival haemorrhage
va
3. Chemosis (rule out discharge, i.e. mucus = infection)
3. EO
Vertical or horizontal diplopia, esp if retrobulbar injection with
muscles
anaesthetic
4. Wound
1. High astigmatism (up to 3D WRA acceptable, and will decrease
with healing)
2. Leak
3. Dehiscence (poor wound suturing of secondary trauma)
4. Flat or shallow anterior chamber
5. Positive Seidel sign
6. Hypotony (6mmHg>)
7. Bleb formation
8. Iris prolapse into woundd
9. Peaked pupil or iris damage from surgery
5. Cornea
1. Epithelial basement membrane disturbances
2. Abrasion
3. Superficial punctate keratitis
4. Oedema
5. Secondary surgical trauma which generally resolves the first
week (if later, worry about bullous keratopathy)
6. Descemets membrane detachment > rolls towards anterior
chamber and if large enough, can cause endothelium
dysfunction
7. Endothelial ddeposits
8. Iris pigment
9. Keratic precipitates
6. Anterior
1. Mild iritis (secondary to surgical trauma)
2. Hypotony (secondary to ciliary shutdown or wound leak)
chamber
3. Increased IOP (DT viscoelastic material, steroids, hyphaema, IOL
pupillary block) > if hyphaema found, refer px back to surgeon
4. Retained cortex (increases risk of infection)
5. Worst case = hypopion/endophthalmitis
7. Iris
Atrophy
Sphincter damage > traumatic mydriasis or pupillary distortion

B. Late complications:
1. Wound
Included astigmatism > tight sutures cause steepening along that
meridian
Steeper vertical = minus cyl axis 180
Loose/exposed sutures > FB or GPC
2. Cornea
Biggest corneal complication = bullous keratopathy > endothelial
decompensation
Epithelial down-growth: corneal or conjunctival epithelial cells grow
down through wound and cover endothelium, iris and trabecular
meshwork
3. Capsule
Wrinkled capsule
After cataracts (Elschnig pearls = residual epithelial cells which grow
on capsule)
Remediation with YAG (laser) capsulotomy
Displaced IOL and pupillary capture
4. Retina
Cystsoid macular oedema
6 weeks to months post-op (confirm with Fang)
Mostly resolves without treatment
Can lead to permanent vision loss with or without macular hole
Increased risk of retinal detachment due to vitreous traction
Tends to occur within year post op
Risk less with ECCE
Common complaints/effects (even when op has gone well):
1. Glare
2. Reflections
3. Sparkles
4. Fusional problems
5. Eyes more tender/sensitive with IOL

WHY IS CATARACT SURGERY CONSIDERED TO BE A TYPE OF REFRACTIVE SURGERY?

A. IOL in terms of CTL possibilities:
May be spherical, toric, multifocal
Toric IOL: Ideally will compensate for corneal toricity as lenticular astigmatism will be
removed with cataract.
B. Artificial accommodation:
1. Monovision:
- Considered in px with previous successful adaptation to monovision or
anisometropic px
- Low success rate > due to aim of pseudophakic px having clear distance vision
predominantly
2. Bifocal/multifocal IOL:
a. Concentric power rings like CTL:
- central dominance for distance and peripheral near
- 30/10% area for near dominance
b. Pseudo-accommodating IOL:
- Softer siliconematerial
- Allows 1.75D accommodation
- Pushes on vitreous > pushes lens forward > increase plus through effective power
- Doesnt change shape, only positioning
- Attached to zonules
c. Aspheric IOL (new)
- Power decreases towards periphery > reduce spherical aberration
C. Corneal modification:
Cuts on peripheral cornea > change shape > reduce corneal astig
Laser modification of cornea: carves concentric rings into cornea > inbuilt multifocal
scleral expansion rings
D.

Options for correction/modification of residual power after cataract op:

Refit with correct IOL
Give px CTL or specs over and above
Excimer laser for over and above (residual power/cyl)
Piggyback IOL
- One in bag and second in aqueous or sulcus
- Alternate technique when capsule tears or in extremely high hyperopes who need
+35D lens
- Max power available = 29D, thus hyperope needs +6D in sulcus/aqueous

E.
1.
2.
3.
4.

How to do retinoscopy on px with multifocal lens:

Record unaided VA > px should get 6/6 (surgeon will aim for +0.25)
Measure K > use as starting point; if residual astig exists, it should be corneal
Ret in dark room to enlarge pupils over distance portion with dim light (dilate if necessary)
Add > put on lights for constricted pupils

OTHER ABNORMALITIES OF THE LENS

Posterior lenticonus:
Prevalence:
- Not common
- Most common type of acquired, unilateral cataract in children
- Begins at any age up to mid-teens
- Rarely detected in early infancy
Aetiology:
- Cause unknown
- Trauma, traction from hyaloid system and inflammation suggested
Presentation:
- Usually unilateral an sporadic; bilateral and familial cases reported
- Posterior protrusion > generalized, not cone > posterior lentiglobus
- Back surface of lens undergoes progressive posterior bowing
- Do not progress/remains stationary for years or decades
Clinical:
1. Starts as transparent protrusion in posterior lens capsule
2. Protrusion usually axial, round and well circumscribed; found in normal sized eye
3. Usually in central part of lens or just nasal to it
4. Protrusion initially clear
5. Red reflex through protrusion is distorted, but reflex around it is not = oil droplet
appearance with ophthalmoscopy + pathognomonic scissors movement on ret
6. Opacification in protrusion: vision reduced by few lines > optics around opacity not
distorted
7. Opacification slowly moves anterior to involve rest of cortex
8. Cataracts develop in most severe cases, beginning with opacification of posterior
cortex > obscures underlying defect
- Posterior lenticonus sometimes not recognized until surgery has removed total
cataract anterior to posterior capsule, allowing defect in posterior capsule to be
seen
Signs:
1. Axial refraction markedly myopic and peripheral error hyperopic
2. If it starts in early childhood > anisometropia/optical distortion > amblyopia > poor
vision
3. Strabismus

Anterior lenticonus
Bilateral axial projection into anterior chamber
Eg. Alport syndrome
Microspherophakia
Definition: Lens is small and spherical
Prevalence:
- Commonly associated with Weill-Marchesani syndrome
Lens is displaced superior temporally
Small stature
Deafness
High myopia
Management:
- Gonioscopy > determine presence of peripheral anterior synechiae
- Peripheral laser irodotomy > prevent repeated attacks of pupillary block glaucoma
and progressive closure of filtration angle by peripheral anterior synechiae
- Surery > surgeon should be prepared to suture intraocular lens to iris or sclera
- Anterior chamber lens usually contraindicated due to peripheral anterior synechiae
Presentation:
- Zonules loose > lens may eventually dis-insert > dislocation
Lens

coloboma
Characterized by segmental notching/agenesis at inferior equator
Absence of lens zonules in that area
May be associated with iris or fundus coloboma