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CATARACTAUDI ADIBAH | AFFAN SYAFIQI | AMANINA NASIR | NURUL HIDAYU | NIK NOR LIYANA | ARINA ZAHARI
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
and focus it onto the retina
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 fibers
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
arranged compactly as nucleus
& cortex of the lens.
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
Cataract is a clouding of the lens or any opacity within the lens
which leads to a decrease in vision
WHAT IS CATARACT?
CATARACT
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
CONGENITAL
AGE
METABOLIC
 Familial
 Intrauterine infections
 Maternal drug ingestions
 Elderly
 Diabetes
 Hypocalcaemia
 Wilson’s Disease
 Galactosemia
CAUSES
DRUG - INDUCED
TRAUMATIC AND
INFLAMMATORY
DISEASE
ASSOCIATED
 Corticosteroids
 Miotics
 Amiodarone
 Phenothiazines
 Post intra-ocular surgery
 Uveitis
 Down’s Syndrome
 Dystrophia Myotonica
 Lowe’s Syndrome
 Atopic dermatitis
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
MORPHOLOGICAL CLASSIFICATION
CLASSIFICATION
MORPHOLOGICAL CLASSIFICATION
CLASSIFICATION
MORPHOLOGICAL CLASSIFICATION
CLASSIFICATION
CLASSIFICATION
BASED ON DEGREE OF MATURITY
HYPERMATURE MORGAGNIAN
Cataract is shrunken
and wrinkled anterior
capsule due to leakage
of water out of the lens
Cataract is a
hypermature cataract in
which liquefaction of
the cortex has allowed
the nucleus to sink
inferiorly
MATURE IMMATURE
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
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.
IRIS SHADOW IN IMMATURE CATARACT
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 CATARACT
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
HYPERMATURE CATARACT
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.
PATHOPHYSIOLOGY
OF CATARACT
PATHOPHYSIOLOGY
 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 harden
PATHOPHYSIOLOGY
 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
GlucoseSorbitol
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
clear and more opaque. 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
VISUAL ACUITY
VISUAL ACUITY
LENS OPACITY
Normal eye – Good
red reflex
Cataractous eye – Poor red
reflex
MANAGEMENT
TREATMENT
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
TREATMENT
The aim of treatment is:
1. Improve vision
2. Increase mobility and independence
3. Relief from the fear of going blind
INDICATIONS
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
SURGERY: ECCE
COMPLICATIONS
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.
PHARMACOEMULSIFICATION
COMPARISON
MASTITIS
THANK YOU

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Cataract

  • 1. CATARACTAUDI ADIBAH | AFFAN SYAFIQI | AMANINA NASIR | NURUL HIDAYU | NIK NOR LIYANA | ARINA ZAHARI
  • 2. 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 and focus it onto the retina
  • 3. ANATOMY OF THE LENS STRUCTURE OF THE LENS:  LENS CAPSULE  ANTERIOR LENS EPITHELIUM  LENS FIBER
  • 4. 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 fibers
  • 5. 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 arranged compactly as nucleus & cortex of the lens.
  • 6. 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.
  • 7. 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.
  • 8. CATARACT Cataract is a clouding of the lens or any opacity within the lens which leads to a decrease in vision WHAT IS CATARACT?
  • 10. 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
  • 11. CAUSES CONGENITAL AGE METABOLIC  Familial  Intrauterine infections  Maternal drug ingestions  Elderly  Diabetes  Hypocalcaemia  Wilson’s Disease  Galactosemia
  • 12. CAUSES DRUG - INDUCED TRAUMATIC AND INFLAMMATORY DISEASE ASSOCIATED  Corticosteroids  Miotics  Amiodarone  Phenothiazines  Post intra-ocular surgery  Uveitis  Down’s Syndrome  Dystrophia Myotonica  Lowe’s Syndrome  Atopic dermatitis
  • 13. 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 MORPHOLOGICAL CLASSIFICATION
  • 17. CLASSIFICATION BASED ON DEGREE OF MATURITY HYPERMATURE MORGAGNIAN Cataract is shrunken and wrinkled anterior capsule due to leakage of water out of the lens Cataract is a hypermature cataract in which liquefaction of the cortex has allowed the nucleus to sink inferiorly MATURE IMMATURE Cataract is one in which the lens is completely opaque. Cataract is one in which the lens is partially opaque.
  • 18. 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
  • 19. 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. IRIS SHADOW IN IMMATURE CATARACT
  • 20. IMMATURE CATARACT WHAT IS THE IRIS SHADOW?  Black crescent  Due to the presence of clear interval between iris and lens opacity
  • 21. 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.
  • 23. 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
  • 24. 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
  • 26. 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.
  • 28. PATHOPHYSIOLOGY  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 harden
  • 29. PATHOPHYSIOLOGY  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
  • 30. 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
  • 31. 2. HMP PATHWAY Metabolization of 14% glucose NADPH + H+ synthesis by glucose-6-phosphate
  • 32. 3. POLYOL PATHWAY High glucose level in blood Polyol Pathway GlucoseSorbitol 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
  • 34. 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.
  • 35. 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.
  • 36. 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.
  • 37. POLYOL PATHWAY  When sorbitol collects in the lens, it can affect cells and naturally-occurring proteins, causing the lens to become less clear and more opaque. This condition eventually leads to cataract formation.
  • 38. 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
  • 39. 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
  • 40. 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
  • 41. VISUAL ACUITY Blurred vision due to scattering of light on the retina
  • 44. LENS OPACITY Normal eye – Good red reflex Cataractous eye – Poor red reflex
  • 46. TREATMENT 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
  • 47. TREATMENT The aim of treatment is: 1. Improve vision 2. Increase mobility and independence 3. Relief from the fear of going blind
  • 48. INDICATIONS 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.
  • 49. 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
  • 50. 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
  • 52. COMPLICATIONS 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).
  • 53. 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
  • 54. 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.