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Dr. Atul Kumar Anand
Senior Resident
AIIMS Patna
Any opacity of lens or its capsule, whether
developmental or acquired, is called
cataract
 In general,
develomental
opacities are partial &
stationary, acquired
opacities progress
until entire lens
involved, but
exceptions are well
known in both types.
Lens transparency is maintained by
regular arrangement of lens fibres which
are devoid of organelles, avascularity,
pump mechanism of lens fibres,
maintaining relative dehydration
Cataract is caused by degeneration &
opacification of lens fibres
Loss of transparency occurs because of
abnormalities of lens protein & consequent
disorganization of lens fibres
Reasons for degeneration of lens fibres &
consequent loss of transparency are not
yet clear & probably vary in different cases.
Any factor physical or chemical which
disturb the critical intra & extracellular
equilibrium of water & electrolytes or
deranges colloidal system within fibres
tend to bring about opacification.
By Anatomic Location
Cortical
Nuclear
Subcapsular
Anterior
Posterior
Polar
Mixed
• Acquired :-
• Senile or age-related
• Electric cataract
• Traumatic
• Associated with intraocular
diseases(complicated)
• Associated with systemic diseases
(metabolic)
• Caused by noxious agents(radiation)
• Toxic cataract(drugs, Fe, Cu)
• Dermatogenic
• Miscellaneous syndrome & disease
 Congenital or
developmental
By Etiology
1. Immature(IMC)
2. Mature(MC)
3. Hyper-mature(HMC) :
Morgagnian &
Sclerotic(shrunken)cataract
Cataract centralis pulverulenta
Lamellar cataract
Sutural cataract
Anterior polar cataract
Posterior polar cataract
Coronary cataract
Punctate cataract
Total congenital cataract
Congenital membranous cataract
Commonest type of acquired cataract, occurs
equally in male & female, usually bilateral,
but earlier in one eye than other
 Rare in persons under 50 yrs of age(presenile), unless
A/W metabolic or other systemic problems
 Considerable genetic influence in its incidence.
 In hereditary cases, may appear at an earlier age in
successive generations, phenomenon K/A history of
Anticipation
1. Subcapsular Cataract
A. Anterior Subcapsular
Cataract
Lies Directly Under the
anterior Lens Capsule
B. Posterior Subcapsular
Cataract
• Lies just in front of the posterior
lens capsule
• More Profound effect on vision
than a comparable nuclear or
cortical cataract
• Near vision is frequently impaired
more than the distance vision
Slow sclerosis in the nucleus – Essential
feature
Starts as an exaggeration of the normal
ageing changes involving the lens nucleus
Characterized in its early stage by its
yellowish hue
When advanced , the nucleus appears
brown
 Classical signs of
hydration
followed by
coagulation of
proteins appear primarily
in the cortex
 May involve anterior, posterior or equatorial cortex
 Both Cortical and Subcapsular cataracts are grayish white on
oblique illumination and appear black in the red background of
the fundus on retro-illumination
• Age – most patients over 50 years of age have
some degree of lens opacification.
• Family history of cataract/Hereditary
• Chronic ultraviolet light exposure (sunlight)
• Trauma
• Cigarette smoking
• Alcohol abuse
• Diabetes mellitus
• Myotonic dystrophy
• Radiation exposure
• Dehydration crisis(diarrhoea)
• Chronic corticosteroid use
• Uveitis
An Immature Cataract :
• Lens is partially opaque(Greyish white),iris shadow
visible
A Mature Cataract :
• Lens is completely opaque(Pearly white), iris shadow
not visible(also not visible in clear lens)
A Hypermature Cataract :
• When mature cataract is left in situ, stage of
hypermaturity sets in(Milky white), may occur in two
forms
Morgagnian Cataract:
• A Hypermature Cataract in which total liquefaction of
the cortex has allowed the nucleus to sink inferiorly
Sclerotic type:
cortex becomes disintegrated & lens becomes
shrunken due to leakage of water. Anterior capsule is
wrinkled & thickened
Immature Mature
Hypermature Morgagnian
 Two main processes are involved in senile
cataract:
• Hydration
• Sclerosis
 Hydration
Lamellar separation and
collection of protein
fluid between lens fibers.
scattering of light and loss of
transparency.
 Mechanisms of increased hydration are:
• Failure of active pump mechanism
• Increased leakage across posterior or
anterior capsule
• Increased Osmotic pressure
Sclerosis
compaction of lens proteins
and fibers
aggregates of very high
molecular weight proteins
scattering of light and loss of
transparency.
Stages
1. Lamellar separation: earliest change, revesible
2. Incipient Cataract
3. Immature
1. Cuneiform Cataract
2. Cupuliform Cataract
4. Intumescent cataract
5. Mature &
6. Hypermature cataract
1.Liquefactive or Morgagnian Type
2.Sclerotic Cataract
• Lamellar Separation :
 Demarcation of the lens fibres owing to
their separation by fluid
 Can only be seen with slit lamp; invisible
ophthalmoscopically
 Incipient Stage
• Lens Striae:
 Wedge shaped spokes of
opacity with clear areas
between them in the periphery of the
lens cortex
 Some in front of and some behind the
nucleus
• Preceded by sectoral alterations in the
refractive indices of the lens fibres thus
producing irregularities in the refraction,
some visual deterioration & Polyopia
• The bases of the wedge shaped opacities (Cuneiform
opacities)are peripheral & they are most common in
lower nasal quadrant.
• At first they can only be seen with the
pupil dilated; but as they develop, their
apices appear within the normal
pupillary margin.
• Seen With ophthalmoscope, or slit lamp
in retroillumination,they are black
against red background of fundus
 As they approach the axial area the
vision becomes seriously disturbed
 Fig:- cortical spoke like opacities
. Intumescent Cataract:
• Opacification becomes more diffuse & irregular
• Cortex becomes cloudy & eventually uniformly white &
opaque
• Progressive hydration of the cortical layers may cause a
swelling of the lens, thus making the anterior chamber
shallow
. Ripe / Mature Cataract:
• The entire cortex
becomes opaque, the
swelling subsides
 As long as there is any clear lens substance
b/w the pupillary margin of the iris & the
opacity, the iris throws a shadow upon the
grey opacity when the light is cast upon the
eye from one side.
 When the cortex is completely opaque, the
iris throws no shadow and the cataract is
said to be mature.
. The stage of Hypermaturity :
• Cortex becomes disintegrated
• The lens becomes more & more inspissated
and shrunken , sometimes yellow in appearance
• The anterior capsule becomes thickened by the
proliferation of the anterior cubical cells so that a dense
white capsular cataract is formed in the pupillary area
• Owing to the shrinkage of the lens, iris become tremulous
& the ant. chamber deep, & finally, degeneration of the
suspensory ligament may lead to luxation of the lens.
 Sometimes, at the stage of
maturity, the cortex becomes fluid
and nucleus may sink to the
bottom of the lens.
 The liquefied cortex is milky,
the nucleus appearing as a brown
mass limited above by a
semicircular line, altering its
position with changes in position
of the head.
Another Common type of Cortical Senile
Cataract
Consists of a dense aggregation of opacities
just beneath the capsule; usually in the
posterior cortex
Difficult to see with Ophthalmoscope but can
be seen as a dark shadow on distant direct
ophthal, appears in the beam of the slit lamp
as a yellow layer, best seen in
retroillumination
• Urochrome or melanin pigment deposition
may take place giving nucleus a typical
color:
 Yellow
 Red (Cataracta rubra)
 Brown(Cataracta brunescnence)
 Black (Cataracta nigra)
 Decrease in visual acuity
• Gradual, painless, progressive
 Glare - intolerance of bright light
• More common in PSCC
 Decrease in contrast sensitivity
• Blurr image, misty vision
 Myopic shift – nuclear sclerosis
 Color halos – incipient cataract
• Breaking of white light into colored spectrum
 Mono-ocular Diplopia or Polyopia- cuneiform cat.
• Irregular refraction of lens-variable refractive index
Normal aging change
Excessive amount of sclerosis
Associated with myopia-increase in refractive
index- 2nd sight for age
Yellowish hue-due to urochrome
Advanced- brunescent
 Progress is usually Very slow & hyper-maturity
generally doesn’t occur
Nuclear cataract
• Exaggeration of normal nuclear
ageing change
• Causes increasing myopia
• Increasing nuclear opacification
• Initially yellow then brown
Progression
Opacities start as clefts and vacuole between
lens fibres due to hydration of cortex
Loss of vision –location in visual axis
 glare-vary in rate of progression
Cuneiform or radial spoke-like opacities
Cupliform cat.(central opacities)- better vision in
dim light evening(dilated pupil)- day blindness
Oblique illumination-white
Retroillumination-black
Cortical cataract
Initially vacuoles and clefts Progressive radial spoke-like opacities
Progression
Anterior-
directly under lens capsule
Posterior-
seen in younger
just in front of posterior capsule,
intense glare,
decrease vision in bright light, miosis
Cause-
trauma,steroid, inflammation
Subcapsular cataract
Anterior Posterior
To be continued …..

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CATARACT 1.pptx

  • 1. Dr. Atul Kumar Anand Senior Resident AIIMS Patna
  • 2. Any opacity of lens or its capsule, whether developmental or acquired, is called cataract
  • 3.  In general, develomental opacities are partial & stationary, acquired opacities progress until entire lens involved, but exceptions are well known in both types.
  • 4. Lens transparency is maintained by regular arrangement of lens fibres which are devoid of organelles, avascularity, pump mechanism of lens fibres, maintaining relative dehydration Cataract is caused by degeneration & opacification of lens fibres Loss of transparency occurs because of abnormalities of lens protein & consequent disorganization of lens fibres
  • 5. Reasons for degeneration of lens fibres & consequent loss of transparency are not yet clear & probably vary in different cases. Any factor physical or chemical which disturb the critical intra & extracellular equilibrium of water & electrolytes or deranges colloidal system within fibres tend to bring about opacification.
  • 7. • Acquired :- • Senile or age-related • Electric cataract • Traumatic • Associated with intraocular diseases(complicated) • Associated with systemic diseases (metabolic) • Caused by noxious agents(radiation) • Toxic cataract(drugs, Fe, Cu) • Dermatogenic • Miscellaneous syndrome & disease  Congenital or developmental By Etiology
  • 8. 1. Immature(IMC) 2. Mature(MC) 3. Hyper-mature(HMC) : Morgagnian & Sclerotic(shrunken)cataract
  • 9. Cataract centralis pulverulenta Lamellar cataract Sutural cataract Anterior polar cataract Posterior polar cataract Coronary cataract Punctate cataract Total congenital cataract Congenital membranous cataract
  • 10.
  • 11. Commonest type of acquired cataract, occurs equally in male & female, usually bilateral, but earlier in one eye than other  Rare in persons under 50 yrs of age(presenile), unless A/W metabolic or other systemic problems  Considerable genetic influence in its incidence.  In hereditary cases, may appear at an earlier age in successive generations, phenomenon K/A history of Anticipation
  • 12. 1. Subcapsular Cataract A. Anterior Subcapsular Cataract Lies Directly Under the anterior Lens Capsule
  • 13. B. Posterior Subcapsular Cataract • Lies just in front of the posterior lens capsule • More Profound effect on vision than a comparable nuclear or cortical cataract • Near vision is frequently impaired more than the distance vision
  • 14. Slow sclerosis in the nucleus – Essential feature Starts as an exaggeration of the normal ageing changes involving the lens nucleus Characterized in its early stage by its yellowish hue When advanced , the nucleus appears brown
  • 15.  Classical signs of hydration followed by coagulation of proteins appear primarily in the cortex  May involve anterior, posterior or equatorial cortex  Both Cortical and Subcapsular cataracts are grayish white on oblique illumination and appear black in the red background of the fundus on retro-illumination
  • 16. • Age – most patients over 50 years of age have some degree of lens opacification. • Family history of cataract/Hereditary • Chronic ultraviolet light exposure (sunlight) • Trauma • Cigarette smoking • Alcohol abuse • Diabetes mellitus • Myotonic dystrophy • Radiation exposure • Dehydration crisis(diarrhoea) • Chronic corticosteroid use • Uveitis
  • 17. An Immature Cataract : • Lens is partially opaque(Greyish white),iris shadow visible A Mature Cataract : • Lens is completely opaque(Pearly white), iris shadow not visible(also not visible in clear lens) A Hypermature Cataract : • When mature cataract is left in situ, stage of hypermaturity sets in(Milky white), may occur in two forms
  • 18. Morgagnian Cataract: • A Hypermature Cataract in which total liquefaction of the cortex has allowed the nucleus to sink inferiorly Sclerotic type: cortex becomes disintegrated & lens becomes shrunken due to leakage of water. Anterior capsule is wrinkled & thickened
  • 20.
  • 21.
  • 22.  Two main processes are involved in senile cataract: • Hydration • Sclerosis
  • 23.  Hydration Lamellar separation and collection of protein fluid between lens fibers. scattering of light and loss of transparency.
  • 24.  Mechanisms of increased hydration are: • Failure of active pump mechanism • Increased leakage across posterior or anterior capsule • Increased Osmotic pressure
  • 25. Sclerosis compaction of lens proteins and fibers aggregates of very high molecular weight proteins scattering of light and loss of transparency.
  • 26. Stages 1. Lamellar separation: earliest change, revesible 2. Incipient Cataract 3. Immature 1. Cuneiform Cataract 2. Cupuliform Cataract 4. Intumescent cataract 5. Mature & 6. Hypermature cataract 1.Liquefactive or Morgagnian Type 2.Sclerotic Cataract
  • 27. • Lamellar Separation :  Demarcation of the lens fibres owing to their separation by fluid  Can only be seen with slit lamp; invisible ophthalmoscopically
  • 28.  Incipient Stage • Lens Striae:  Wedge shaped spokes of opacity with clear areas between them in the periphery of the lens cortex  Some in front of and some behind the nucleus
  • 29. • Preceded by sectoral alterations in the refractive indices of the lens fibres thus producing irregularities in the refraction, some visual deterioration & Polyopia • The bases of the wedge shaped opacities (Cuneiform opacities)are peripheral & they are most common in lower nasal quadrant.
  • 30. • At first they can only be seen with the pupil dilated; but as they develop, their apices appear within the normal pupillary margin. • Seen With ophthalmoscope, or slit lamp in retroillumination,they are black against red background of fundus  As they approach the axial area the vision becomes seriously disturbed  Fig:- cortical spoke like opacities
  • 31. . Intumescent Cataract: • Opacification becomes more diffuse & irregular • Cortex becomes cloudy & eventually uniformly white & opaque • Progressive hydration of the cortical layers may cause a swelling of the lens, thus making the anterior chamber shallow
  • 32. . Ripe / Mature Cataract: • The entire cortex becomes opaque, the swelling subsides
  • 33.  As long as there is any clear lens substance b/w the pupillary margin of the iris & the opacity, the iris throws a shadow upon the grey opacity when the light is cast upon the eye from one side.  When the cortex is completely opaque, the iris throws no shadow and the cataract is said to be mature.
  • 34. . The stage of Hypermaturity : • Cortex becomes disintegrated • The lens becomes more & more inspissated and shrunken , sometimes yellow in appearance • The anterior capsule becomes thickened by the proliferation of the anterior cubical cells so that a dense white capsular cataract is formed in the pupillary area • Owing to the shrinkage of the lens, iris become tremulous & the ant. chamber deep, & finally, degeneration of the suspensory ligament may lead to luxation of the lens.
  • 35.  Sometimes, at the stage of maturity, the cortex becomes fluid and nucleus may sink to the bottom of the lens.  The liquefied cortex is milky, the nucleus appearing as a brown mass limited above by a semicircular line, altering its position with changes in position of the head.
  • 36. Another Common type of Cortical Senile Cataract Consists of a dense aggregation of opacities just beneath the capsule; usually in the posterior cortex Difficult to see with Ophthalmoscope but can be seen as a dark shadow on distant direct ophthal, appears in the beam of the slit lamp as a yellow layer, best seen in retroillumination
  • 37. • Urochrome or melanin pigment deposition may take place giving nucleus a typical color:  Yellow  Red (Cataracta rubra)  Brown(Cataracta brunescnence)  Black (Cataracta nigra)
  • 38.  Decrease in visual acuity • Gradual, painless, progressive  Glare - intolerance of bright light • More common in PSCC  Decrease in contrast sensitivity • Blurr image, misty vision  Myopic shift – nuclear sclerosis  Color halos – incipient cataract • Breaking of white light into colored spectrum  Mono-ocular Diplopia or Polyopia- cuneiform cat. • Irregular refraction of lens-variable refractive index
  • 39. Normal aging change Excessive amount of sclerosis Associated with myopia-increase in refractive index- 2nd sight for age Yellowish hue-due to urochrome Advanced- brunescent  Progress is usually Very slow & hyper-maturity generally doesn’t occur
  • 40. Nuclear cataract • Exaggeration of normal nuclear ageing change • Causes increasing myopia • Increasing nuclear opacification • Initially yellow then brown Progression
  • 41. Opacities start as clefts and vacuole between lens fibres due to hydration of cortex Loss of vision –location in visual axis  glare-vary in rate of progression Cuneiform or radial spoke-like opacities Cupliform cat.(central opacities)- better vision in dim light evening(dilated pupil)- day blindness Oblique illumination-white Retroillumination-black
  • 42. Cortical cataract Initially vacuoles and clefts Progressive radial spoke-like opacities Progression
  • 43. Anterior- directly under lens capsule Posterior- seen in younger just in front of posterior capsule, intense glare, decrease vision in bright light, miosis Cause- trauma,steroid, inflammation