Cataract 2.pptx ophthalmology lecture 22

ANATOMY OF THE LENS
 A biconvex structure attached
to the ciliary process by the
zonular fibre, between iris &
vitreous humour
 Non-vascular, colourless and
transparent
 Index of refraction 1.336
 Consists of stiff elongated,
prismatic cells known as lens
fibre, very tightly packed
together
 Divided into nucleus, cortex and
capsule
 The whole lens enclosed within
an
elastic capsule
 Helps to refract incoming light

ANATOMY OF THE LENS
STRUCTURE OF THE
LENS:
 LENS CAPSULE
 ANTERIOR LENS
EPITHELIUM
 LENS FIBER

ANATOMY OF THE LENS
LENS CAPSULE
 Thin transparent,
collagen membrane
 Surrounds
lens
completely
 Elastic in nature but
contain no any
elastic tissue
 Anteriorly secreted
by lens epithelium
and
 posteriorly by basal
cells of elongating

ANATOMY OF THE LENS
ANTERIOR LENS EPITHELIUM
 Single layer below the
lens capsule
 Formed of cuboidal cells
 Become columnar at
equatorial region
LENS FIBER
 The epithelial cells elongated
to form lens fibers which
have a complicated
structural forms.
 Mature lens fibers are
cells which have lost
their nuclei.
 As the lens fibers are formed
throughout the life, these are

ANATOMY OF THE LENS
NUCLEUS
 Its is the central part
containing the oldest fibres.
It consists of different zones,
which are laid down
successively as the
development proceeds.
 Different zones:
I. Embryonic nucleus
II. Fetal nucleus
III. Infantile nucleus
IV. Adult nucleus
CORTEX
 Its is the peripheral part
which compromises the
youngest lens fibres.

LENS TRASPARENCY
 Its transparency is due to the arrangement
of its fibres, internal structure and the
biochemistry of the lens cells and fibres.
 A cataractous lens is when the lens
become
opaque.

CATARACT
WHAT IS CATARACT?
Cataract is a clouding of the lens or any opacity within the lens
which leads to a decrease in vision

INCIDENCE
Incidence of Lens opacities in the “normal”
population with aging.
(Cinotti & Patti, 1968)
AGE GROUP (YEARS) LENS OPACITY (%)
50 – 59 65
60 – 69 83
70 – 79 91
> 80 100

CAUSES
CONGENITA
L
AGE
METABOLIC
 Familial
 Intrauterine infections
 Maternal drug ingestions
 Elderly
 Diabetes
 Hypocalcaemia
 Wilson’s Disease
 Galactosemia

CAUSES
DRUG - INDUCED
TRAUMATIC
AND
INFLAMMATORY
DISEASE
ASSOCIATE
D
 Corticosteroids
 Miotics
 Amiodarone
 Phenothiazines
 Post intra-ocular surgery
 Uveitis
 Down’s Syndrome
 Dystrophia Myotonica
 Lowe’s Syndrome
 Atopic dermatitis

CLASSIFICATION
MORPHOLOGICAL CLASSIFICATION
1. Subcapsular cataract
- Anterior subcapsular cataract
- Posterior subcapsular cataract
2. Nuclear cataract
- Involves the nucleus of lens. Yellow to brown coloration
3. Cortical cataract
- Wedge shaped or radial spoke-like opacities.
4. Polar cataract
- Central posterior part of the lens

CLASSIFICATION
MORPHOLOGICAL CLASSIFICATION

CLASSIFICATION
BASED ON DEGREE OF MATURITY
MATURE IMMATURE
HYPERMATUR
E
MORGAGNIAN
Cataract is a
hypermature cataract in
which liquefaction of
the cortex has allowed
the nucleus to sink
inferiorly
Cataract is shrunken
and wrinkled anterior
capsule due to leakage
of water out of the lens
Cataract is one in which
the lens is completely
opaque.
Cataract is one in which
the lens is partially
opaque.

IMMATURE CATARACT
Features:
 Opacification becomes more diffuse and irregular.
 Iris shadow still visible.
 Lens is not completely opaque
 Wedge shaped opacities at periphery of the lens
 Progress gradually

IMMATURE CATARACT
IRIS SHADOW IN IMMATURE CATARACT
When there is any clear cortex between the iris and
the opacity (greyish white in immature senile
cataract), the shadow of the iris which falls upon
the opacity, as light is cast upon the eye is visible
through the clear cortex. This is called the ‘iris
shadow’ and is a common sign in immature senile
catarct.

IMMATURE CATARACT
WHAT IS THE IRIS SHADOW?
 Black crescent
 Due to the presence of clear interval between
iris and lens opacity

MATURE CATARACT
 Symptoms
- Usually severe decrease in vision.
 Features
- Complete opacification of the lens capsule, cortex and the
nucleus
- Lens appears pearly white in colour.
 Also known as ripe cataract.
 May progress to hypermature cataract
 May be complicated with phacolytic glaucoma.

MATURE VS IMMATURE
HOW TO DIFFERENTIATE MATURE AND IMMATURE CATARACT?
IMMATURE CATARACT MATURE CATARACT
 Visual acuity is reduced
to counting fingers
 Visual acuity is reduced to
hand movement or
perception of light
 Lens is partially opaque  Lens in totally opaque
 Iris shadow is present  No iris shadow is present
 Fundus may be visible  No fundus details

HYPERMATURE CATARACT
 Which is characterized by wrinkling of the capsule due
to liquefied lens cortex and morgagnian
cataract (sinking of lens nucleus inferiorly within the
capsule)
 This can cause inflammation, eye pain and headache
(if complicated by glaucoma)
 A hypermature cataract is rare and needs removal

MORGAGNIAN CATARACT
 Complete cortex is liquefied and appears milky white in
colour.
 Nucleus settles at the bottom
 Calcium deposits may also be seen on the lens capsule.

PATHOPHYSIOLOG
Y
 The lens is made mostly of water
and
protein fibers.
 Opacity occur when the lens
protein (crystallins) clump together
 Ability for lens to refract lights
reduce which cause reduce visual
acuity.
 Chemical modification of the
lens cause it to be thicken and

PATHOPHYSIOLOG
Y
 It is not fully understood.
 There are three metabolic pathways which
convert glucose in energy (ATP) and other
relevant metabolic molecules. These are:
1. Glycolysis
2. The Pentose Phosphate Shunt
3. The Polyol Route

1. GLYCOLYSIS
Aging Decrease in Hexokinase
concentration
Drop in ATP level
Poor control of
electrolyte balance
Massive influx of water
into the lens
Disorganization of structured
proteins in the lens
Aggregation and precipitation of
protein
CATARACT

2. HMP PATHWAY
Metabolization of 14%
glucose
NADPH + H+ synthesis by
glucose-6-phosphate

3. POLYOL PATHWAY
High glucose level in blood Polyol Pathway
Glucose
Sorbitol
Accumulation of sorbitol in lens Hyper osmotic effect - Influx of excess
water through aquaporin channels
CATARACT
Aldose Reductase
Polyol dehydrogenase has low Km for sorbitol

DIABETES & CATARACT
POLYOL PATHWAY

DIABETES & CATARACT
 Cells use glucose for energy. This normally occurs by
phosphorylation via the enzyme hexokinase.
 However, if large amounts of glucose are present (as in
diabetes mellitus), hexokinase becomes saturated and the
excess glucose enters the polyol pathway when aldose
reductase reduces it to sorbitol.

DIABETES & CATARACT
 Hexokinase can return the molecule to the glycolysis
pathway by phosphorylating fructose to form fructose-6-
phosphate. However, in uncontrolled diabetics that have
high blood glucose - more than the glycolysis pathway can
handle - the reaction's mass balance ultimately favors the
production of sorbitol.

POLYOL PATHWAY
 The retina cells use glucose for energy as normal, and
any glucose not used for energy will enter the polyol
pathway. When blood glucose is normal, this
interchange causes no problems, as aldose reductase
has a low affinity for glucose at normal concentrations.
 In a hyperglycemic state, the affinity of aldose
reductase for glucose rises, causing much sorbitol to
accumulate. This change of affinity is what is meant by
activation of the polyol pathway.

POLYOL PATHWAY
 When sorbitol collects in the lens, it can affect cells and
naturally-occurring proteins, causing the lens to become less
more opaque.
clear and This condition eventually leads to
cataract formation.

CLINICAL PRESENTATION
Decreased visual acuity
 is the commonest complaint.
- Progressive and painless
- Worse in bright light
 There may be complaint of glare and monocular diplopia if the
cataract splits the visual axis
 A myopic shift in the refraction with progression of cataract may
also be noted
 Some complain of a white reflex in the pupil
PRESENTING COMPLAINTS AND HISTORY

CLINICAL PRESENTATION
PAST MEDICAL HISTORY
 May reveal risk factors such as
- Trauma
- Intrauterine infections
- Diabetes or other metabolic
disorders
 Cataract may have occurred in other members of
the family in the hereditary variants.
FAMILY HISTORY

PE FINDINGS
 Visual acuity is impaired for both distance and near
and
patient may even be blind.
 Opacity in the lens
 Ocular adnexia and intraocular structures when
examined may reveal lesions that may point at
- The cause, type and eventual visual prognosis
 If RAPD positive, this indicates an optic nerve disease
or
extensive macular lesions
- Visual prognosis guarded in such cases

VISUAL
ACUITY
Blurred vision due to scattering of light on the retina

LENS OPACITY
Normal eye – Good
red reflex
Cataractous eye – Poor red
reflex

TREATMEN
T
The treatment of cataracts is :
1. Glasses
2. Better lighting
3. Surgery
a. Phacoemulsification
b. ECCE
c. ICCE (not performed now)
Sometimes a cataract should be removed even if it doesn't
cause major problems with vision, if it is preventing the
treatment of another eye problem, such as age-related
macular degeneration, diabetic retinopathy or retinal
detachment

TREATMEN
T
The aim of treatment is:
1. Improve vision
2. Increase mobility and independence
3. Relief from the fear of going blind

INDICATION
S
1. Work or lifestyle is affected by vision problems caused by the cataract.
2. Glare caused by bright lights is a problem.
3. Cannot pass a vision test
4. Have double vision.
5. Notice a big difference in vision when you compare one eye to the
other.
6. Have another vision-threatening eye disease, such as diabetic
retinopathy or macular degeneration.

SURGERY: ICCE
 Intracapsular cataract extraction
 Involves extraction of the entire lens, including the
posterior capsule and zonules
 Weak and degenerated zonules are a pre-requisite for this
method
 This is the surgery of choice if there is markedly
subluxated or dislocated lens
 This technique of surgery has largely been replaced by
ECCE

SURGERY: ECCE
 Extracapsular cataract extraction
 An 5 mm to 6 mm incision is made in the eye where the
clear front covering of the eye (cornea) meets the
white of the eye (sclera).
 Another small incision is made into the front portion of
the lens capsule. The lens is removed, along with any
remaining lens material.
 An IOL may then be placed inside the lens capsule.
And
the incision is closed.
*it is usually done if the cataract is too large to be destroyed
by ultrasound

COMPLICATION
S
1. Infection in the eye (endophthalmitis).
1. Swelling and fluid in the center of the nerve layer (cystoid
macular edema).
1. Swelling of the clear covering of the eye (corneal edema).
1. Bleeding in the front of the eye (hyphema).
1. Detachment of the nerve layer at the back of the eye (retinal
detachment).

ICCE VS ECCE
ECCE ICCE
Small incision 5-6mm Large incision 10-12mm
Posterior lens conserved Removal entire lens
No stiches required, self healing Required stiches, long
rehabilitation
time
IOL implant Aphakic eye
Post operative complication
minimal
Added risk for retinal
detachment, corneal edema
and vitreous loss

PHARMACOEMULSIFICATION
 Two small incisions are made in the eye where the clear front covering
(cornea) meets the white of the eye (sclera).
 A circular opening is created on the lens surface (capsule)
 A small surgical instrument (phaco probe) is inserted into the eye.
 Sound waves (ultrasound) are used to break the cataract into small pieces.
Sometimes a laser is used too. The cataract and lens pieces are removed
from the eye using suction.
 An intraocular lens implant (IOL) may then be placed inside the lens
capsule.
 Usually, the incisions seal themselves without stitches.

Cataract 2.pptx ophthalmology lecture 22

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