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.
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
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
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.
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
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