SENILE CATARACT

Also called as ‘age-related cataract’, this is the
commonest type of acquired cataract affecting equally
persons of either sex usually above the age of 50
years. By the age of 70 years, over 90% of the
individuals develop senile cataract. The condition is
usually bilateral, but almost always one eye is affected
earlier than the other.
Morphologically, the senile cataract occurs in two
forms, the cortical (soft cataract) and the nuclear (hard
cataract). The cortical senile cataract may start as
cuneiform (more commonly) or cupuliform cataract.
It is very common to find nuclear and cortical senile
cataracts co-existing in the same eye; and for this
reason it is difficult to give an accurate assessment
of their relative frequency. In general, the predominant
form can be given as cuneiform 70 percent, nuclear 25
percent and cupuliform 5 percent.
Etiology
Senile cataract is essentially an ageing process.
Though its precise etiopathogenesis is not clear, the
various factors implicated are as follows:
A. Factors affecting age of onset, type and
maturation of senile cataract.
1. Heredity. It plays a considerable role in the
incidence, age of onset and maturation of senile
cataract in different families.
2. Ultraviolet irradiations. More exposure to UV
irradiation from sunlight have been implicated for
early onset and maturation of senile cataract in
many epidemiological studies.
3. Dietary factors. Diet deficient in certain proteins,
amino acids, vitamins (riboflavin, vitamin E,
vitamin C), and essential elements have also been
blamed for early onset and maturation of senile
cataract.
4. Dehydrational crisis. An association with prior
episode of severe dehydrational crisis (due to
diarrhoea, cholera etc.) and age of onset and
maturation of cataract is also suggested.
5. Smoking has also been reported to have some
effect on the age of onset of senile cataract.
Smoking causes accumulation of pigmented
molecules—3 hydroxykynurinine and chromophores,
which lead to yellowing. Cyanates in
smoke causes carbamylation and protein
denaturation.
B. Causes of presenile cataract. The term presenile
cataract is used when the cataractous changes similar
to senile cataract occur before 50 years of age. Its
common causes are:
1. Heredity. As mentioned above because of
influence of heredity, the cataractous changes
may occur at an earlier age in successive
generations.

2. Diabetes mellitus. Age-related cataract occurs
earlier in diabetics. Nuclear cataract is more
common and tends to progress rapidly.
3. Myotonic dystrophy is associated with posterior
subcapsular type of presenile cataract.
4. Atopic dermatitis may be associated with presenile
cataract (atopic cataract) in 10% of the
cases.
C. Mechanism of loss of transparency. It is
basically different in nuclear and cortical senile
cataracts.
1. Cortical senile cataract. Its main biochemical
features are decreased levels of total proteins, amino
acids and potassium associated with increased
concentration of sodium and marked hydration of the
lens, followed by coagulation of proteins. The
probable course of events leading to senile
opacification of cortex is as shown in the Figure 8.8.
2. Nuclear senile cataract. In it the usual
degenerative changes are intensification of the agerelated
nuclear sclerosis associated with dehydration
and compaction of the nucleus resulting in a hard
cataract. It is accompanied by a significant increase
in water insoluble proteins. However, the total protein
content and distribution of cations remain normal.
There may or may not be associated deposition of
pigment urochrome and/or melanin derived from the
amino acids in the lens.

Stages of maturation
[A] Maturation of the cortical type of senile
cataract
1. Stage of lamellar separation. The earliest senile
change is demarcation of cortical fibres owing to their
separation by fluid. This phenomenon of lamellar
separation can be demonstrated by slit-lamp
examination only. These changes are reversible.
2. Stage of incipient cataract. In this stage early
detectable opacities with clear areas between them
are seen. Two distinct types of senile cortical
cataracts can be recognised at this stage:
(a) Cuneiform senile cortical cataract. It is
characterised by wedge-shaped opacities with clear
areas in between. These extend from equator towards
centre and in early stages can only be demonstrated
after dilatation of the pupil. They are first seen in the
lower nasal quadrant. These opacities are present
both in anterior and posterior cortex and their apices
slowly progress towards the pupil. On oblique
illumination these present a typical radial spoke-like
pattern of greyish white opacities (Fig. 8.9). On distant
direct ophthalmoscopy, these opacities appear as dark
lines against the red fundal glow.
Since the cuneiform cataract starts at periphery
and extends centrally, the visual disturbances are
noted at a comparatively late stage.
(b) Cupuliform senile cortical cataract. Here a saucershaped
opacity develops just below the capsule

usually in the central part of posterior cortex (posterior
subcapsular cataract), which gradually extends
outwards. There is usually a definite demarcation
between the cataract and the surrounding clear cortex.
Cupuliform cataract lies right in the pathway of the
axial rays and thus causes an early loss of visual
acuity.
3. Immature senile cataract (ISC). In this stage,
opacification progresses further. The cuneiform (Fig.
8.9) or cupuliform patterns can be recognised till the
advanced stage of ISC when opacification becomes
more diffuse and irregular. The lens appears greyish
white (Fig. 8.10) but clear cortex is still present and so
iris shadow is visible.
In some patients, at this stage, lens may become
swollen due to continued hydration. This condition
is called ‘intumescent cataract'. Intumescence may
persist even in the next stage of maturation. Due to
swollen lens anterior chamber becomes shallow.
4. Mature senile cataract (MSC). In this stage,
opacification becomes complete, i.e., whole of the
cortex is involved. Lens becomes pearly white in
colour. Such a cataract is also labelled as ‘ripe
cataract’ (Fig. 8.11).
5. Hypermature senile cataract (HMSC). When the
mature cataract is left in situ, the stage of
hypermaturity sets in. The hypermature cataract may
occur in any of the two forms:
(a) Morgagnian hypermature cataract: In some
patients, after maturity the whole cortex liquefies
and the lens is converted into a bag of milky
fluid. The small brownish nucleus settles at the
bottom, altering its position with change in the
position of the head. Such a cataract is called
Morgagnian cataract (Fig. 8.12). Sometimes in
this stage, calcium deposits may also be seen
on the lens capsule.

(b) Sclerotic type hypermature cataract:
Sometimes after the stage of maturity, the cortex
becomes disintegrated and the lens becomes
shrunken due to leakage of water. The anterior
capsule is wrinkled and thickened due to
proliferation of anterior cells and a dense white
capsular cataract may be formed in the pupillary
area. Due to shrinkage of lens, anterior chamber
becomes deep and iris becomes tremulous
(iridodonesis).
[B] Maturation of nuclear senile cataract
In it, the sclerotic process renders the lens inelastic
and hard, decreases its ability to accommodate and
obstructs the light rays. These changes begin
centrally (Fig. 8.13) and slowly spread peripherally
almost up to the capsule when it becomes mature;
however, a very thin layer of clear cortex may remain
unaffected.
The nucleus may become diffusely cloudy
(greyish) or tinted (yellow to black) due to deposition
of pigments. In practice, the commonly observed
pigmented nuclear cataracts are either amber, brown
(cataracta brunescens) or black (cataracta nigra)
and rarely reddish (cataracta rubra) in colour
(Fig. 8.14).
Clinical features
Symptoms. An opacity of the lens may be present
without causing any symptoms; and may be
discovered on routine ocular examination. Common
symptoms of cataract are as follows:
1. Glare. One of the earliest visual disturbances
with the cataract is glare or intolerance of bright
light; such as direct sunlight or the headlights of
an oncoming motor vehicle. The amount of glare
or dazzle will vary with the location and size of
the opacity.
2. Uniocular polyopia (i.e., doubling or trebling of
objects): It is also one of the early symptoms. It
occurs due to irregular refraction by the lens
owing to variable refractive index as a result of
cataractous process.
3. Coloured halos. These may be perceived by
some patients owing to breaking of white light
into coloured spectrum due to presence of water
droplets in the lens.
4. Black spots in front of eyes. Stationary black
spots may be perceived by some patients.
5. Image blur, distortion of images and misty vision
may occur in early stages of cataract.
6. Loss of vision. Visual deterioration due to senile
cataract has some typical features. It is painless
and gradually progressive in nature. Paitents with

central opacities (e.g., cupuliform cataract) have
early loss of vision. These patients see better
when pupil is dilated due to dim light in the
evening (day blindness). In patients with
peripheral opacities (e.g. cuneiform cataract) visual
loss is delayed and the vision is improved in
bright light when pupil is contracted. In patients
with nuclear sclerosis, distant vision deteriorates
due to progressive index myopia. Such patients
may be able to read without presbyopic glasses.
This improvement in near vision is referred to as
‘second sight'. As opacification progresses,
vision steadily diminishes, until only perception
of light and accurate projection of rays remains
in stage of mature cataract.
Signs. Following examination should be carried out
to look for different signs of cataract:
1. Visual acuity testing. Depending upon the
location and maturation of cataract, the visual
acuity may range from 6/9 to just PL + (Table 8.1).
2. Oblique illumination examination. It reveals
colour of the lens in pupillary area which varies
in different types of cataracts (Table 8.1).
3. Test for iris shadow. When an oblique beam of
light is thrown on the pupil, a crescentric shadow
of pupillary margin of the iris will be formed on
the greyish opacity of the lens, as long as clear
cortex is present between the opacity and the

pupillary margin (Fig. 8.15). When lens is
completely transparent or completely opaque, no
iris shadow is formed. Hence, presence of iris
shadow is a sign of immature cataract.
4. Distant direct ophthalmoscopic examination (for
procedure see page 564). A reddish yellow fundal
glow is observed in the absence of any opacity
in the media. Partial cataractous lens shows black
shadow against the red glow in the area of
cataract. Complete cataractous lens does not even
reveal red glow (Table 8.1).

5. Slit-lamp examination should be performed with
a fully-dilated pupil. The examination reveals
complete morphology of opacity (site, size, shape,
colour pattern and hardness of the nucleus).

Differential diagnosis
1. Immature senile cataract (ISC) can be
differentiated from nuclear sclerosis without any
cataract as shown in Table 8.3.
Table 8.3 : Immature senile cataract versus
nuclear sclerosis
ISC Nuclear sclerosis
1. Painless progressive 1. Painless progressive
loss of vision loss of vision
2. Greyish colour of lens 2. Greyish colour of lens
3. Iris shadow is present 3. Iris shadow is absent
4. Black spots against red 4. No black spots are
glow are observed on seen against red glow
distant direct ophthalmoscopy
5. Slit-lamp examination 5. Slit-lamp examination
reveals area of reveals clear lens
cataractous cortex
6. Visual acuity does not 6. Visual acuity usually
improve on pin-hole improves on pin-hole
testing testing
II. Mature senile cataract can be differentiated from
other causes of white pupillary reflex (leukocoria) as
shown in Table 8.4.
Table 8.4 : Differences between mature senile
cataract and leukocoria
MSC Leukocoria
1. White reflex in pupillary White reflex in pupillary
area area
2. Size of pupil usually Pupil usually semidilanormal
ted
3. Fourth Purkinje image is Fourth Purkinje image
absent is present
4. Slit-lamp examination Slit-lamp examination
shows cataractous shows transparent
lens lens with white reflex
behind the lens
5. Ultrasonography normal Ultrasonography
reveals opacity in the
vitreous cavity

Complications
1. Phacoanaphylactic uveitis.A hypermature cataract
may leak lens proteins into anterior chamber. These
proteins may act as antigens and induce antigenantibody
reaction leading to uveitis.
2. Lens-induced glaucoma. It may occur by different
mechanisms e.g., due to intumescent lens
(phacomorphic glaucoma) and leakage of proteins
into the anterior chamber from a hypermature cataract
(phacolytic glaucoma).
3. Subluxation or dislocation of lens. It may occur
due to degeneration of zonules in hypermature