CATARACT

• Blindness due to cataract is an enormours

problem in terms of human morbidity but also
economic loss & social burden.
• The WHO /NCPB survey shows backlog
22millions blind in India
• Annual incidence of catarac blindness is 3.8
millions
• Level of performance is under 1.6 to 1.9
millions
 LENS

• It is crystalline ,transparent , biconvex structure

placed between iris and vitreous in saucer shaped
depression the patellar fossa.
• Its diameter is 9-10mm and thickness 3.5mm-5mm.
• Its weight is 135mg
• It has two surface, anterior surface is less convex
( radius of curvature 10mm) than posterior surface
(radius 6mm).
• Its refractive index 1.39 and total dioptric power is
18 D.
 STRUCTURE
• It consists of
• Lens capsule- thin transparent hyaline membrane
• Anterior epithelium
• Lens fiber- it is divided in central part nucleus which
consists of oldest fibres and peripheral part cortex
which consists of younger fibres.
• Suspensory ligaments of lens – it consists of fibres
passing from ciliary body to lens .They hold lens in
position and enable ciliary muscle to act on it.
• Lens fibres – the epithelial cells elongate to form lens fibres
• Mature lens fibres are cells which have lost their nuclei
• They are formed throughout the life and are arranged
compactly as
• Nucleus- it is central part containing the oldest fibres. It
consists of different zones
• Embryonic nucleus- inner part of nucleus that corresponds
lens upto 3 months of gestation age
• Fetal nucleus- it lies around embryonic nucleus and
corresponds to lens from 3 month of gestation age till birth.
• Infantile nucleus- corresponds to lens from birth to puberty
• Adult nucleus- lens fibres formed after puberty to rest of life
• Cortex – peripheral part that comprises of youngest lens fibres
• A cataract begins when proteins in eye forms
clumps that prevents lens from sending clear
images to retina.
• The retina then converts light into signals
• It then sends the signal to output nerve which
then carries to brain
• The brain then analyses signal in occipital lobe
 DEFINITION
• Cataract is defined as loss in transparency of lens due
to its opacification leading to impairment of vision
• It has chronic visual loss

CLASSIFICATION
A. Etiological classification
a. Congenital and developmental cataract
b. Acquired cataract
 CLASSIFICATION OF
CATARACT

ETIOLOGICAL MORPHOLOGICAL

1. CAPSULAR 4. SUPRANUCLEAR
CONGENITAL &
ACQUIRED 2. SUBCAPSULAR 5. NUCLEAR
DEVELOPMENTAL
3. CORTICAL 6. POLAR
 B . Morphological classification
a. Capsular cataract- it may be anterior or posterior
capsular cataract
b. Subcapsular cataract- it involves the superficial part
of cortex. It may be anterior or posterior.
c. Cortical cataract- it involves major part of cataract
d. Supranuclear cataract- it involves deeper part of
cortex just outside the nucleus
e. Nuclear cataract- nucleus of crystalline lens
f. Polar cataract- capsule and superficial part of cortex
at polar region. It is also anterior or posterior.
 ACQUIRED CATARACT [age related cataract]
• In this cataract opacification occurs due to
degeneration of already formed normal
transparent fibers.
• It is also called senile cataract or age related
cataract
• It is most commonly found acquired cataract.
• It is usually bilateral.
• Mainly it is of two forms cortical (soft) and
nuclear (hard) cataract.
 ETIOLOGY
• AGE- usually above 50 years of age.
• SEX- equally affects both sex
• HEREDITY- age of onset & maturation
• UV RADIATION- early onset & maturation of senile cataract
• DIETARY FACTORS- diet deficient in certain proteins, amino
acid, vitamin E, C, Riboflavin.
• DEHYDRATION-severe cases of diarrhea, cholera
• SMOKING- associated with nuclear cataract
• DIABETES MELLITUS-nuclear cataract common and
progress rapidly
• ATOPIC DERMATITIS- pre senile cataract
 MECHANISM OF LOSS OF TRANSPARENCY
1. Cortical senile cataract-
• Decreased levels of total proteins and amino
acids
• Cogulation of proteinS
• Increasedd sodium level and decreased
potassium level
• Hydration of lens
 NUCLEAR SENILE CATARACT
• Due degenerative changes there is nuclear
sclerosis
• Associated dehydration
• Compact nucleus or hard nucleus
 STAGES OF MATURATION OF
CORTICAL TYPE SENILE CATARACT
1. Stage of lamellar separation-
• Demarcation of cortical fibers due
to their separation by fluid
• These changes are reversible
2. Stages of incipient cataract
• early opacities with clear areas
between them are seen
• Only seen in dilated pupil
• Irregularities in refraction , polyopia
• Two types of cataract are seen
0
Cuneiform senile cortical cataract – wedge
shaped opacities with clear areas between
• Visual disturbances are noted at later stages

Cupuliform senile cortical cataract

• Saucer shaped opacity develop below the
capsule central part of posterior cortex
• Early loss of visual activity
3. IMMATURE SENILE CATARACT
• opacification progresses further
• Lens appears greyish white
• Iris shadow visible
• Intumescent cataract -Sometimes lens
become swollen due to hydration
• Ant chamber becomes shallow
4. MATURE SENILE CATARACT
• Opacification becomes complete
• Lens pearly white color
5. HYPERMATURE SENILE CATARACT
When mature cataract is left as it is then
hypermaturity sets in. It is of two forms

a) Morgagnian hypermature cataract

b) Sclerotic hypermature cataract

a) Morgagnian hypermature cataract

• whole cortex liquifies , lens is converted into

bag of milky fluid
• The brownish nucleus settles at bottom`
b) Sclerotic hypermature cataract
• Sometimes the cortex becomes disintegrated ,
the lens becomes shrunken due to leakage of
water
• The anterior capsule is thickened and wrinkled
• Ant chamber becomes deep
• Iridodonesis
• Dense white capsular cataract
MATURATION OF NUCLEAR SENILE CATARACT
• As cataract progress the lens becomes
inelastic and hard, decreases its ability too
accommodate and obstruct the light rays
• The change start centrally and spread
peripherally
• The nucleus becomes amber, brown, or black
in colour
 SYMPTOMS
1. Symptomless found on routine examination
2. Glare and intolerance of bright light
3. Uniocular polyopia
4. Coloured halos
5. Black spots stationary
6. Blurred vision, distortion of image
7. Loss of vision- painless and gradually
progressive
• Patient with central opacity early loss of
vision i.e cupuliform
• In patients with peripheral opacity visual loss
is delayed i.e cuneiform
• In nuclear sclerosis distant vision deteriorates
Patient is able to see near objects without
presbyopia glasses. This is called second sight.
• As opacification progresses vision diminishes
until PL , PR is positive.
 SIGNS
1 Visual acuity testing ranging from 6/9 to just
PL+
2 oblique illumination examination reveals
colour of lens
3 test for iris shadow seen in immature cataract
4 Distant direct opthalmoscopic examination –
Black shadow against red glow
5 Slit lamp examination in fully dilated pupil
CONGENITAL AND DEVELOPMENTAL CATARACT
• They occur due to some disturbances in
normal growth of lens.
• Congenital cataract -when disturbance occurs
before birth . So cataract is limited to
embryonic or fetal nucleus.
• Developmental cataract- occurs from infancy
to adolescence. Infantile and adult nucleus are
affected
• Etiology – exactly not known.
• I. Heredity-
• II. Maternal factors
1. Malnutrition during pregnancy
2. Infections- Maternal infections like rubella
are associated with cataract in 50 percent of
cases, cytomegalo virus, Toxoplasmosis etc
3. Drugs ingestion- during pregnancy (e.g.,
thalidomide, corticosteroids).
4. Radiation
III. Foetal or infantile factors
1. Deficient oxygenation (anoxia) owing to placental
haemorrhage.
2. Birth trauma
3. Metabolic disorders of the foetus or infant such as
galactosemia, galactokinase deficiency and neonatal
hypoglycemia.
4. Cataracts associated with other congenital anomalies
e.g., as seen in Lowe's syndrome
5. Malnutrition in early infancy.
6. Ocular disease associated with cataract e.g
retinopathy off premaurity.
7. Idiopathic
 METABOLIC CATARACT
• Caused due to endocrine disorder
• Senile cataract in diabetes appears at early
age
• Classical diabetic cataract is called snowflake
cataract, usually occurs in young patients
GLACTACTOSAEIC CATARACT
• Caused due to error in glactose metabolism
• Bilateral cataract (oil droplet central lens
opacities)
• Lens change is reversible if milk & milk
poducts eliminated diet
CATARACT DUE TO COPPER METABOLISM
• Wilson’s disease
• Sunflower cataract yellowish brown dots
 COMPLICATED CATARACT
• Opacification of the lens secondary to other
intraocular disease.
• Any condition in which the ocular circulation is
disturbed or in which inflammatory toxin are
formed disturbs nutrition of lens
• Causes- inflammatory condition iridocylitis,
hypopyon corneal ulcer, endopthalmitis
• Degenerative causes- retinitis pigmentosa, etc
• Retinal detachment
• Glaucoma
• Intraocular tumours - retinoblastoma
 CLINICAL FEATURES
• Posterior subcapsular cataract
• Opacities bread crumb appearance
• Polychromatic lustre
DRUG INDUCED CATARACT
• Posterior subcapsular cataract
• Prolong use of steroids
• Children more prone
• Steroids substituted by NSAID
ATOPIC DERMATITIS
 RADIATIONAL CATARACT
• Damage to the lens epithelium
• Posterior subcapsular opacities
• Glass worker cataract
• exposure to x rays
 MANAGEMENT OF CATARACT IN ADULTS
A] Non surgical measures
1. Treatment of cause of catarct may stop
progression
• E g Adequate control diabetes mellitus
• Removal of steroids
• Removal of irradiation
• Early diagnosis and treatment of ocular
disease
2. topical preparation containing iodide salts of
potassium and calcium e.g catagon drops
 3. measures to improve vision during incipient
and immature cataract
• Refraction
• Arrangement of illumination
• Use of dark goggles
• Mydriatics – small axial cataract
B. SURGICAL MANAGEMENT
INDICATIONS
1. Visual improvement
2. Medical indications
Lens induced glaucoma
R D , diabetic retinopathy
3. Cosmetic indications
• PREOPERATIVE EVALUATION
1. General medical examination of patients
• Exclude systemic disease , cardiac , lung disorders, ,
source of infection septic gums, UTI, etc.
2. Ocular examination
a. Visual acuity
• Perception of light- its absence indicates nil visual
prognosis
• Perception of rays- test of peripheral retina
• -ve PRPL denotes RD , visual pathway defect, indicates
poor prognosis
• Dense cataract PLPR may be inaccurate but good visual
prognosis
b. Pupil – light reactions, RAPD, ability of pupil
to dilate
c. Anterior segment evaluation
• Cornea
• Cataractous lens- morphology , maturity of
lens, grade of nuclear sclerosis for phaco
• Posterior synechiae, pseudo exfoliation,
iridodonosis, pigments, anterior chamber
depth.
d. Intraocular pressure
e. Examination of lids , conjunctiva, and lacrimal
apparatus
• Local source of infection
• Lacrimal syringing
• If no patency than DCR or DCT
e. Fundus examination- macula, rule out other
causes of decreased vision
f. A - scan- to calculate power of intraocular lens
SURGICAL TECHNIQUES FOR CATARACT
EXTRACTION
A. Intracapsular cataract extraction [ICCE]-
entire cataractous lens along with intact
capsule.
B. Extracapsular cataract extraction [ECCE]-
anterior capsule , nucleus, cortex is removed
posterior capsule is kept intact.
a. Conventional ECCE
b. Small incision cataract surgery
c. Phacoemulsification
 SURGICAL
TECHNIQUE FOR
CATARACT
EXTRACTION

INTRACAPSULAR EXTRACAPSULAR
CATARACT CATARACT
EXTRACTION EXTRACTION
ICCE ECCE

SMALL INCISION
CATARACT PHACO
SURGERY EMULSIFICATION
SICS
PREOPERATIVE MEDICATIONS AND PREPERATION
1. Consent
2. Scrub bath, care of hair and marking of eye
3. Preoperative antibiotics and disinfection
a. topical antibiotics- moxifloxacin 0.3% q.i.d 3 days before
surgery
b. povidine iodine
4. I O P lowering – digital massage or by IOP lowering drugs.
5. Mydriasis – tropicamide plus[ tropicamide 1% + phenylephrine
2.5%] every 15 minutes
6. Flubiprofen 0.3% or keterolac 0.5 % t.i.d
7. ANAESTHESIA
General or local anaesthesia or topical anaesthesia
7. ANAESTHESIA
General or local anaesthesia or topical anaesthesia
PERIBULBAR BLOCK
• Davis and Mandel in 1986
• Injection of 6 to 7ml of anaesthetic solution [mixture of 2%
lignocaine, and 0.5 to 0.75 % bupivacaine 2 : 1 with
hyaluronidase 5 IU /ml and adrenaline one in one lac in
peripheral space of orbit
• It diffuses into muscle cone and lids leading to globe and
orbicularis akinesia and anaesthesia
• First injunction through upper lid junction of medial one third
lateral two third
• Second through lower lid junction of lateral one third and
medial two third
• Orbital compression 10 to 15 minutes
 SURGICAL STEPS OF MANUAL SICS
1. Universal speculum is inserted to keep the eyelids apart.
Superior rectus suture- fixes the eye in downward gaze.
2. Conjunctival flap and exposure of sclera- 10 to 2 clock
position with sharp edge scissor. Conjunctiva is cut and
sclera is exposed along entire incision length.
3. Haemostasis –cautery
4. External scleral incision- 1/3 to ½ thickness scleral
groove is made about 2mm behind limbus. Incision is
straight or curved.
5. Sclero–corneal tunnel- made by crescent knife. It
extends 1-1.5mm into cornea.
6. Internal corneal incision is made with help of keratome
CONJUNCTIVAL FLAP
MEASUREMENT WITH VERNIER DE CALLIPER
EXTERNAL SCLERAL INCISION
TUNNEL FORMATION & INTERNAL CORNEAL
INCISION
SIDE PORT ENTRY
CONTINOUS CIRCULAR CAPSULORRHEXIS [CCC]
DELIVERY OF NUCLEUS
IOL IMPLANTATION
7. Side-port corneal incision is made at 9’O clock position.
8. Anterior capsulotomy – It is done by continuous circular
capsulorrhexis [CCC] . Here the anterior capsule is torn in
circular fashion with help of irrigating bent needle
cystitome.
9. Hydrodissection – RL is injected under peripheral part
of anterior capsule. This separates the corticonuclear
mass from the posterior capsule.
10. Nuclear management
a. Prolapse of nucleus from capsular bag into anterior
chamber.
b. Delivery of nucleus outside through corneal scleral
tunnel is done by wire vectis method.
11. Aspiration of cortex is done by two way
irrigation and aspiration cannula.
12. A posterior chamber IOL is implanted in
capsular bag after filling bag with viscoelastic
material.
13. Removal of viscoelastic material with help two
way cannula.
14. The ant chamber is formed by RL solution
injected through side port. This also seals sclero-
corneal tunnel
15. The conjunctival flap is reposited back and
anchored with cautery.
 PHACOEMULSIFICATIN
• Corneal incision (3mm) is taken with keratome.
• CCC is done for anterior capsulotomy.
• Hydrodissection
• Phacoemulsifier is (1mm titatium needle that vibrat
ultrasonic speed of4000times)used used to emulsifi
the nucleus by divide and conquer technique.
• Cortical lens matter is aspirated with irrigation and
aspiration technique.
• Foldable IOL is implanted.
• Next step same as SICS.
POST OPERATIVE MANAGEMENT
• Patient is made to lie down and take nil orally
• Injection diclofenac for mild pain
• Next morning bandage is removed
• Antibiotic steroid eye drop eg Apdrop PD 1
hrly initially, afterwards taper the dose
• Topical NSAID eye drop 3times / day used for 4
weeks
• Topical cycloplegic drug eg homide
• Oral antibiotic and analgesic
PREOPERATIVE COMPLICATIONS
1. Anxiety – anxiolytic drugs
2. Nausea and gastritis due to acetozolamide.
Prescribe antacids
3. Corneal abrasion due to tonometry
4. Complication due to local anaesthesia
a. Oculocardiac reflex
b. Perforation of globe
c. Subconjunctival injection
d.Spontaneous dislocation of lens
OPERATIVE COMPLICATIONS
1. Superior rectus musclee laceraion
2. Excessive bleeding
3. Incision related
a. button holing of anterior wall of tunnel caused due to
superficial dissection of scleral flap.
b. Premature entry into anterior chamber
c. Scleral disinsertion
2. Injury to cornea [descemets detachment]
3. Iridodialysis
4. Nuclear drop common in phaco.
5. Posterior capsular rupture PCR
6. Vitreous loss
POSTOPERATIVE COMPLICATIONS
7. Hyphaema
8. Iris prolapse
9. Striate keratopathy- mild corneal odema with
descement’s fold due to endothelial damage.
10. Flat anterior chamber
11.Postoperative anterior uvetis
12. Endopthalmitis
13. Malposition of IOL
14. Toxic anterior segment sndrome
15. Bullous keratopathy- postoperative corneal
oedema.
16.Cystoid macular oedema
17. Retinal detachment
18. After cataract