LENS-INDUCED (PHACOGENIC) GLAUCOMAS

In this group IOP is raised secondary to some disorder
of the crystalline lens. It includes following subtypes:
1. Phacomorphic glaucoma
Causes. Phacomorphric glaucoma is an acute
secondary angle-closure glaucoma caused by :
Intumescent lens i.e., swollen cataractous lens
due to rapid maturation of cataract or sometimes
following traumatic rupture of capsule is the main
cause of phacomorphic glaucoma.
Anterior subluxation or dislocation of the lens
and spherophakia (congenital small spherical
lens) are other causes of phacomorphic glaucoma.
Pathogenesis. The swollen lens pushes the iris
forward and oblitrates the angle resulting in
secondary acute angle closure-glaucoma. Further,
the increased iridocorneal contact also causes
potential pupillary block and iris bombe formation.
Clinical presentation. Phacomorphic glaucoma
presents as acute congestive glaucoma with features
almost similar to acute primary angle-closure
glaucoma (see page 229) except that the lens in always
cataractous and swollen (Fig. 9.20).
Treatment should be immediate and consists of :
Medical treatment to control IOP by i.v. mannitol,
systemic acetazolamide and topical betablockers.
Cataract extraction with implantation of PCIOL
(which is the main treatment of phacomorphic
glaucoma) should be performed once the eye
becomes quite,
2. Phacolytic glaucoma (Lens protein glaucoma)
Pathogensis. It is a type of secondary open angle
glaucoma, in which trabecular meshwork is clogged
by the lens proteins and macrophages which have
phagocytosed the lens proteins. Leakage of the lens
proteins occurs through an intact capsule in the
hypermature (Morgagnian) cataractous lens.
Clinical features. The condition is characterised by:
Features of congestive glaucoma due to an acute
rise of IOP in an eye having hypermature cataract.
Anterior chamber may become deep and aqueous
may contain fine white protein particles.
Management. It consists of medical therapy to lower
the IOP followed by extraction of the hypermature
cataractous lens with PCIOL implantation.3. Lens particle glaucoma
Pathogenesis. It is a type of secondary open angle
glaucoma, in which trabecular meshwork is blocked
by the lens particles floating in the aqueous humour.
It may occur due to lens particles left after accidental
or planned extracapsular cataract extraction or
following traumatic rupture of the lens.
Clinical features. Raised IOP associated with lens
particles in the anterior chamber.
Management includes medical therapy to lower IOP
and irrigation-aspiration of the lens particles from the
anterior chamber.
4. Glaucoma associated with phacogenic uveitis
Pathogenesis. In this condition IOP is raised due to
inflammatory reaction of the uveal tissue excited by
the lens matter. Basically, it is also a type of secondary
open angle glaucoma where trabecular meshwork is
clogged by both inflammatory cells and the lens
particles.
Management consists of medical therapy to lower
IOP, treatment of iridocyclitis with steroids and
cycloplegics. Irrigation-aspiration of the lens matter
from anterior chamber (if required) should always be
done after proper control of inflammation.
5. Glaucoma associated with phacoanaphylaxis
In this condition, there occurs fulminating acute
inflammatory reaction due to antigen (lens protein) –
antibody reaction. The mechanism of rise in IOP and
its management is similar to that of phacogenic
uveitis.
GLAUCOMAS DUE TO UVEITIS
The IOP can be raised by varied mechanisms in
inflammations of the uveal tissue (iridocyclitis). Even
in other ocular inflammations such as keratitis and
scleritis, the rise in IOP is usually due to secondary
involvement of the anterior uveal tract.
Types. Glaucomas associated with uveitis can be
divided into two main groups:
1. Hypertensive uveitis.
2. Post-inflammatory glaucoma.
1. Hypertensive uveitis
Hypertensive uveitis refers to acute inflammation of
the anterior uvea associated with raised IOP.It includes:
i. Non-specific hypertensive uveitis, and
ii. Specific hypertensive uveitis syndromes
i. Non-specific hypertensive uveitis. It includes all
cases of acute inflammation of the anterior uveal tract
associated with raised IOP, other than the specific
hypertensive uveitis syndromes, but inclusive of
postoperative inflammation.
Mechanisms of rise in IOP. A secondary open-angle
glaucoma occurs due to trabecular clogging (by
inflammatory cells, exudates and turbid aqueous
humour), trabecular oedema (due to associated
trabeculitis), and prostaglandin–induced rise in IOP.
Management. It includes treatment of iridocyclitis and
medical therapy to lower IOP by use of hyperosmotic
agents, acetazolamide and beta- blocker eyedrops
(timolol or betaxolol).
ii. Specific hypertensive uveitis syndromes. These
include:
Fuchs’ uveitis syndrome (see page 160) and
Glaucomatocyclitic crisis (see page 160).
2. Post-inflammatory glaucoma
In it IOP is raised due to after-effects of the
iridocyclitis.
Mechanisms of rise in IOP. include :
Pupillary block due to annular synechiae or
occlusio pupillae,
Secondary angle-closure with pupil block
following iris bombe formation,
Secondary angle-closure without pupil block
due to organisation of the inflammatory debris in
the angle.
Secondary open-angle glaucoma due to
trabecular scarring and obstruction of the
meshwork.
Management. It includes prophylaxis and curative
treatment.
1. Prophylaxis. Acute iridocylitis should be treated
energetically with local steroids and atropine to
prevent formation of synechiae.
2. Curative treatment. It consists of medical therapy
to lower IOP (miotics are contraindicated). Surgical
or laser iridotomy may be useful in pupil block
without angle closure. Filtration surgery may be
performed (with guarded results) in the presence
of angle closure.

Sublaxation And Lens Dislocation

Subluxation
It is partial displacement in which lens is moved
sideways (up, down, medially or laterally), but remains
behind the pupil. It results from partial rupture or
unequal stretching of the zonules (Fig. 8.30 and
8.31A).

Clinical feautres are as follows
Defective vision occurs due to marked astigmatism
or lenticular myopia.
Uniocular diplopia may result from partial
aphakia.
Anterior chamber becomes deep and irregular.
Iridodonesis is usually present.
Dark edge of the subluxated lens is seen on
distant direct ophthalmoscopy
Complications of subluxated lens include :
Complete dislocation,
Cataractous changes,
Uveitis and
Secondary glaucoma.
Management. Spectacles or contact lens correction
for phakic or aphakic area (whichever is better) is
helpful in many cases. Surgery is controversial and
usually associated with high risk of retinal
detachment. Lensectomy with anterior vitrectomy
may be performed in desperate cases.
II. Dislocation or luxation of the lens
In it all the zonules are severed from the lens. A
dislocated lens may be incarcerated into the pupil or
present in the anterior chamber (Fig. 8.31B), the
vitreous (Fig. 8.31C) (where it may be floating – lens
nutans; or fixed to retina – lens fixata), sub-retinal
space, subscleral space or extruded out of the globe,
partially or completely.
Clinical features of posterior dislocation. These
include: deep anterior chamber, aphakia in pupillary
area, and iridodonesis. Ophthalmoscopic examination
reveals lens in the vitreous cavity.
Clinical features of anterior dislocation are deep
anterior chamber and presence of lens in the anterior
chamber. Clear lens looks like an oil drop in the
aqueous.
Complications associated with dislocated lens are
uveitis and secondary glaucoma.
Management. A lens dislocated in the anterior
chamber and that incarcerated in the pupil should be
removed as early as possible. A dislocated lens from
the vitreous cavity should be removed only if it is
causing uveitis or glaucoma. From the vitreous cavity
lens can be removed after total vitrectomy, either with
the help of an insulated vitreous cryoprobe or by
aspiration facility of vitrectomy probe (only soft
cataract).

After Cataract

After cataract. It is also known as ‘secondary
cataract’. It is the opacity which persists or develops
after extracapsular lens extraction.
Causes. (i) Residual opaque lens matter may persist
as after cataract when it is imprisoned between the
remains of the anterior and posterior capsule,
surrounded by fibrin (following iritis) or blood
(following hyphaema). (ii) Proliferative type of after
cataract may develop from the left-out anterior
epithelial cells. The proliferative hyaline bands may
sweep across the whole posterior capsule.
Clinical types. After cataract may present as
thickened posterior capsule, or dense membranous
after cataract (Fig. 8.28A) or Soemmering’s ring which
refers to a thick ring of after cataract formed behind
the iris, enclosed between the two layers of capsule
(Fig. 8.28B) or Elschnig’s pearls in which the
vacuolated subcapsular epithelial cells are clustered
like soap bubbles along the posterior capsule
(Fig. 8.28C).

Treatment is as follows :
i. Thin membranous after cataract and thickened
posterior capsule are best treated by YAG-laser
capsulotomy or discission with cystitome or
Zeigler’s knife.
ii. Dense membranous after cataract needs surgical
membranectomy.
iii. Soemmering’s ring after cataract with clean central
posterior capsule needs no treatment.
iv. Elschnig’s pearls involving the central part of
the posterior capsule can be treated by YAGlaser
capsulotomy or discission with cystitome.

POSTOPERATIVE MANAGEMENT AFTER CATARACT OPERATION

1. The patient is asked to lie quietly upon the back
for about three hours and advised to take nil
orally.
2. For mild to moderate postoperative pain injection
diclofenac sodium may be given.
3. Next morning bandage is removed and eye is
inspected for any postoperative complication.
4. Antibiotic-steroid eyedrops are used for four
times, three times, two times and then once a day
for 2 weeks each.
5. After 6-8 weeks of operation corneoscleral sutures
are removed (when applied). Now a days most
surgeons are doing sutureless cataract surgery.
6. Final spectacles are prescribed after about 8 weeks
of operation.

INTRAOCULAR LENS IMPLANTATION

Presently, intraocular lens (IOL) implantation is the
method of choice for correcting aphakia. Its
advantages and disadvantages over spectacles and
contact lenses are described in aphakia (see page
31).
The IOL implant history had its beginning on
November 29, 1949, when Harold Ridley, a British
ophthalmologist, performed his first case. Since then
history of IOLs has always been exciting, often
frustrating and finally rewarding and now highly
developed.
Types of intraocular lenses
During the last two decades a large number of
different types and styles of lenses have been
developed. The commonly used material for their
manufacture is polymethylmethacrylate (PMMA).
The major classes of IOLs based on the method of
fixation in the eye are as follows:
1. Anterior chamber IOL. These lenses lie entirely
in front of the iris and are supported in the angle
of anterior chamber (Fig. 8.23). ACIOL can be
inserted after ICCE or ECCE. These are not very
popular due to comparatively higher incidence of
bullous keratopathy. When indicated, ‘Kelman
multiflex’ (Fig. 8.24A) type of ACIOL is used
commonly.

2. Iris-supported lenses. These lenses are fixed on
the iris with the help of sutures, loops or claws.
These lenses are also not very popular due to a
high incidence of postoperative complications.
Example of iris supported lens is Singh and Worst’s
iris claw lens (Figs. 8.24B and 8.25).
3. Posterior chamber lenses. PCIOLs rest entirely
behind the iris (Fig. 8.26). They may be supported by
the ciliary sulcus or the capsular bag. Recent trend is
towards ‘in-the-bag-fixation’. Commonly used model
of PCIOLs is modified C-loop (Fig. 8.24C).
Depending on the material of manufacturing, three
types of PC-IOLs are available :
i. Rigid IOLs. The modern one piece rigid IOLs are
made entirely from PMMA.
ii. Foldable IOLs, to be implanted through a small
incision (3.2 mm) after phacoemulsification are
made of silicone, acrylic, hydrogel and collamer.
iii. Rollable IOLs are ultra thin IOLs. These are
implanted through micro incision (1mm) after
phakonit technique. These are made of hydrogel.
Indications of IOL implantation
Recent trend is to implant an IOL in each and every
case being operated for cataract; unless it is
contraindicated. However, operation for unilateral
cataract should always be followed by an IOL
implantation.

Calculation of IOL power (Biometry)
The most common method of determining IOL power
uses a regression formula called ‘SRK (Sanders,
Retzlaff and Kraff) formula’. The formula is P = A –
2.5L – 0.9K, where:
P is the power of IOL,
A is a constant which is specific for each lens
type.
L is the axial length of the eyeball in mm, which
is determined by A-scan ultrasonography.
K is average corneal curvature, which is
determined by keratometry.
The ultrasound machine equipped with A-scan
and IOL power calculation software is called
‘Biometer’.

Primary versus secondary IOL implantation
Primary IOL implantation refers to the use of IOL
during surgery for cataract, while secondary IOL is
implanted to correct aphakia in a previously operated
eye.
Surgical technique of anterior chamber IOL
implantation
Anterior chamber IOL implantation can be carried out
after ICCE and ECCE. After completion of lens
extraction, the pupil is constricted by injecting miotics
(1 percent acetylcholine or pilocarpine without
preservatives) into the anterior chamber. Anterior
chamber is filled with 2 percent methylcellulose or 1
percent sodium hyaluronate (Healon). The IOL, held
by a forceps, is gently slid into the anterior chamber.
Inferior haptic is pushed in the inferior angle at 6
O'clock position and upper haptic is pushed to
engage in the upper angle (Figs. 8.17 G & H).
Technique of posterior chamber IOL implantation
Implantation of rigid intraocular lens. PCIOL is
implanted after ECCE. After completion of ECCE, the
capsular bag and anterior chamber are filled with 2
percent methylcellulose or 1 percent sodium
hyaluronate. The PCIOL (Fig. 8.24C), is grasped by
the optic with the help of IOL holding forceps. The
inferior haptic and optic of IOL is gently inserted into
the capsular bag behind the iris at 6 O'clock position
(Fig. 8.18F). The superior haptic is grasped by its tip,
and is gently pushed down and then released to slide
in the upper part of the capsular bag behind the iris
(Fig. 8.18G). The IOL is then dialled into the horizontal
position (Fig. 8.18H).
Implantation of foldable IOLs is made either with the
help of holder-folder forceps or the foldable IOLs
injector.

PHACOEMULSIFICATION

It is presently the most popular method of
extracapsular cataract extraction. It differs from the
conventional ECCE and manual SICS as follows:
1. Corneoscleral incision required is very small (3
mm). Therefore, sutureless surgery is possible
with self-sealing scleral tunnel or clear corneal
incision made with a 3 mm keratome.
2. Continuous curvilinear capsulorrhexis (CCC) of
4-6 mm is preferred over other methods of anterior
capsulotomy (Fig. 8.20A).
3. Hydrodissection i.e., separation of capsule from
the cortex by injecting fluid exactly between the
two (Fig. 8.20B) is must for phacoemulsification
in SICS. This procedure facilitates nucleus
rotation and manipulation during phacoemulsification.
Some surgeons also perform hydrodelineation
(Fig. 8.20C).

4. Nucleus is emulsified and aspirated by
phacoemulsifier. Phacoemulsifier basically acts
through a hollow 1-mm titanium needle which
vibrates by piezoelectric crystal in its longitudinal
axis at an ultrasonic speed of 40000 times a
second and thus emulsifies the nucleus. Many
different techniques are being used to accomplish
phacoemulsification. A few common names are
‘chip and flip technique’, ‘divide and conquer
technique’ (Figs. 8.20 D&E) ‘stop and chop’ and
‘phaco chop technique’.
5. Remaining cortical lens matter is aspirated with
the help of an irrigation-aspiration technique

6.IOL implantation. A posterior chamber IOL is
implanted in the capsular bag after filling the bag with
viscoelastic substance (Figs. 8.19N, O & P) Foldable IOL is

most ideal with phacoemulsification technique.
7. Removal of viscoelastic material is done
thoroughly from the anterior chamber and capsular
bag with the help of two-way irrigation aspiration
cannula.
8. Wound closure.The anterior chamber is deepened
with balanced salt solution / Ringer's lactate solution
injected through side port entry. This leads to self
sealing of the sclero-corneal tunnel incision due to
valve effect. Rarely a single infinity suture may be
required to seal the wound. The conjunctival flap is
reposited back and is anchored with the help of wet
field cautery (Fig. 8.19Q).

MANUAL SMALL INCISION CATARACT SURGERY

Manual small incision cataract surgery (SICS) is
becoming very popular because of its merits over
conventional ECCE as well as phacoemulsification
technique highlighted above. In this technique ECCE
with intraocular lens implantation is performed
through a sutureless self-sealing valvular sclerocorneo
tunnel incision.

Surgical steps of manual SICS are (Fig. 8.19) :
1. Superior rectus (bridle) suture is passed to fix the
eye in downward gaze (Fig. 8.19A). This is specifically
important in manual SICS where in addition to fixation
of globe, it also provides a countertraction force
during delivery of nucleus and epinucleus.
2. Conjunctival flap and exposure of sclera (Fig.
8.19B). A small fornix based conjunctival flap is made
with the help of sharp-tipped scissors along the
limbus from 10 to 2 O’clock positions. Conjunctiva
and the Tenon's capsule are dissected, seperated from
the underlying sclera and retracted to expose about 4
mm strip of sclera along the entire incision length.
3. Haemostasis is achieved by applying gentle and
just adequate wet field cautery.
4. Sclero-corneal tunnel incision. A self-sealing
sclero-corneal tunnel incision is made in manual SICS.
It consists of following components:
i. External scleral incision. A one-third to halfthickness
external scleral groove is made about
1.5 to 2mm behind the limbus. It varies from 5.5
mm to 7.5 mm in length depending upon the
hardness of nucleus. It may be straight, frown
shaped or chevron in configuration (Figs. 18.19C,
D & E).
ii. Sclero-corneal tunnel. It is made with the help of
a crescent knife. It usually extends 1-1.5 mm into
the clear cornea (Fig. 8.19F).
iii. Internal corneal incision. It is made with the
help of a sharp 3.2 mm angled keratome
(Fig. 8.19G).
5. Side-port entry of about 1.5-mm valvular corneal
incision is made at 9 o'clock position (Fig. 8.19H).
This helps in aspiration of the sub-incisional cortex
and deepening the anterior chamber at the end of
surgery.
6. Anterior capsulotomy. As described in
conventional ECCE, the capsulotomy in manual SICS
can be either a canopner, or envelope or CCC.
However, a large sized CCC is preferred (Fig. 8.19I).
7. Hydrodissection. As described in ECCE
hydrodissection (Fig. 8.19J) is essential to separate
corticonuclear mass from the posterior capsule in
SICS.
8. Nuclear management. It consists of following
manoeuvres :
i. Prolapse of nucleus out of the capsular bag into
the anterior chamber is usually initiated during
hydrodissection and completed by rotating the
nucleus with Sinskey's hook (Fig. 8.19K).
ii. Delivery of the nucleus outside through the
corneo-scleral tunnel can be done by any of the
following methods:
Irrigating wire vectis method (Fig. 8.19L). (It is
the most commonly used method).
Blumenthal's technique,
Phacosandwitch technique,
Phacofracture technique, and
Fishhook technique.
9. Aspiration of cortex. The remaining cortex is
aspirated out using a two-way irrigation and
aspiration cannula (Fig. 8.19M) from the main incision
and/or side port entry.
10. IOL implantation. A posterior chamber IOL is
implanted in the capsular bag after filling the bag with
viscoelastic substance (Figs. 8.19N, O & P)
11. Removal of viscoelastic material is done
thoroughly from the anterior chamber and capsular
bag with the help of two-way irrigation aspiration
cannula.
12. Wound closure.The anterior chamber is deepened
with balanced salt solution / Ringer's lactate solution
injected through side port entry. This leads to self
sealing of the sclero-corneal tunnel incision due to
valve effect. Rarely a single infinity suture may be
required to seal the wound. The conjunctival flap is
reposited back and is anchored with the help of wet
field cautery

CONVENTIONAL EXTRACAPSULAR CATARACT EXTRACTION

Surgical steps of conventional ECCE are :
1. Superior rectus (bridle) suture is passed to fix the
eye in downward gaze (Fig. 8.17A).
2. Conjunctival flap (fornix based) is prepared to
expose the limbus (Fig. 8.17B) and haemostasis is
achieved by wet field cautery. Many surgeons do
not make conjunctival flap.
3. Partial thickness groove or gutter is made through
about two-thirds depth of anterior limbal area from 10
to 2 O’clock (120o) with the help of a razor blade knife
(Fig. 8.17C).
4. Corneoscleral section. The anterior chamber is
opened with the razor blade knife or with 3.2-mm
keratome.
5. Injection of viscoelastic substance in anterior
chamber. A viscoelastic substance such as 2%
methylcellulose or 1% sodium hyaluronate is injected
into the anterior chamber. This maintains the anterior
chamber and protects the endothelium.
6. Anterior capsulotomy. It can be performed by any
of the following methods:
i. Can-opener's technique. In it, an irrigating
cystitome (or simply a 26 gauge needle, bent at
its tip) is introduced into the anterior chamber
and multiple small radial cuts are made in the
anterior capsule for 360o (Fig. 8.18A).
ii. Linear capsulotomy (Envelope technique). Here
a straight incision is made in the anterior capsule
(in the upper part) from 2-10 O'clock position.
The rest of the capsulotomy is completed in the
end after removal of nucleus and cortex.
iii. Continuous circular capsulorrhexis (CCC).
Recently this is the most commonly performed
procedure. In this the anterior capsule is torn in
a circular fashion either with the help of an
irrigating bent-needle cystitome or with a
capsulorrhexis forceps (Fig. 8.20B).
7. Removal of anterior capsule. It is removed with
the help of a Kelman-McPherson forceps (Fig. 8.18B).
8. Completion of corneoscleral section. It is
completed from 10 to 2 O’ clock position either with
the help of corneo-scleral section enlarging scissors
or 5.2-mm blunt keratome (Fig. 8.18C).
9. Hydrodissection. After the anterior capsulotomy,
the balanced salt solution (BSS) is injected under the
peripheral part of the anterior capsule. This
manoeuvre separates the corticonuclear mass from
the capsule.
10. Removal of nucleus. After hydrodissection the
nucleus can be removed by any of the following
techniques:
i. Pressure and counter-pressure method. In it the
posterior pressure is applied at 12 O’clock
position with corneal forceps or lens spatula and
the nucleus is expressed out by counter-pressure
exerted at 6 O'clock position with a lens hook
(Fig. 8.18D).
ii. Irrigating wire vectis technique. In this method,
loop of an irrigating wire vectis is gently passed
below the nucleus, which is then lifted out of the
eye.
11. Aspiration of the cortex. The remaining cortex is
aspirated out using a two-way irrigation and
aspiration cannula (Fig. 8.18E).
12. Implantation of IOL. The PMMA posterior
chamber IOL is implanted in the capsular bag after
inflating the bag with viscoelastic substance (Figs.
8.18 G & H).
13. Closure of the incision is done by a total of 3 to
5 interrupted 10-0 nylon sutures or continuous sutures
(Fig. 8.18I).
14. Removal of viscoelastic substance. Before tying
the last suture the visco-elastic material is aspirated
out with 2 way cannula and anterior chamber is filled
with BSS.
15. Conjunctival flap is reposited and secured by
wet field cautery.
16. Subconjunctival injection of dexamethasone 0.25
ml and gentamicin 0.5 ml is given.
17. Patching of eye is done with a pad and sticking
plaster or a bandage is applied.

INTRACAPSULAR CATARACT EXTRACTION

Presently, the technique of intracapsular cataract
extraction (ICCE) is obsolete and sparingly performed
world wide. However, the surgical steps are described
in detail as a mark of respect to the technique which
has been widely employed for about 50 years over
the world and also to care for the emotions of few
elderly surgeons who are still performing this
operation (though unethical) at some places in
developing countries.
Surgical steps of the ICCE technique are as follows:
1. Superior rectus (bridle) suture is passed to fix the
eye in downward gaze (Fig. 8.17A).
2. Conjunctival flap (fornix based) is prepared to
expose the limbus (Fig. 8.17B) and haemostasis is
achieved by wet field or heat cautery. All surgeons
do not make conjunctival flap.
3. Partial thickness groove or gutter is made through
about two-thirds depth of anterior limbal area from
9.30 to 2.30 O'clock (150o) with the help of a razor
blade knife (Fig. 8.17C).
4. Corneoscleral section. The anterior chamber is
opened with the razor blade knife or with 3.2mm
keratome (Fig. 8.17D).
5. Iridectomy (Fig. 8.17E). A peripheral iridectomy
may be performed by using iris forceps and de
Wecker's scissors to prevent postoperative pupil
block glaucoma.
6. Methods of lens delivery. In ICCE the lens can be
delivered by any of the following methods:
i. Indian smith method. Here the lens is delivered
with tumbling technique by applying pressure on
limbus at 6 O'clock position with lens expressor
and counterpressure at 12 O’clock with the lens
spatula. With this method lower pole is delivered
first.
ii. Cryoextraction. In this technique, cornea is lifted
up, lens surface is dried with a swab, iris is
retracted up and tip of the cryoprobe is applied
on the anterior surface of the lens in the upper
quadrant. Freezing is activated (–40oC) to create
adhesions between the lens and the probe. The
zonules are ruptured by gentle rotatory
movements and the lens is then extracted out by
sliding movements. In this technique, upper pole
of the lens is delivered first (Fig. 8.17F).
iii. Capsule forceps method. The Arruga's capsule
holding forceps is introduced close into the
anterior chamber and the anterior capsule of the
lens is caught at 6 O'clock position. The lens is
lifted slightly and its zonules are ruptured by
gentle sideways movements. Then the lens is
extracted with gentle sliding movements by the
forceps assisted by a pressure at 6 O'clock
position on the limbus by the lens expressor.
iv. Irisophake method. This technique is obsolete
and thus not in much use.
v. Wire vectis method. It is employed in cases with
subluxated or dislocated lens only. In this method
the loop of the wire vectis is slide gently below
the subluxated lens, which is then lifted out of
the eye.
7. Formation of anterior chamber. After the delivery
of lens, iris is reposited into the anterior chamber with
the help of iris repositor and chamber is formed by
injecting sterile air or balanced salt solution.
8. Implantation of anterior chamber (ACIOL) (Figs.
8.17 G & H). For details see page 197.
9. Closure of incision is done with 5 to 7 interrupted
sutures (8-0, 9-0 or 10-0 nylon) (Fig. 8.17I).
10. Conjunctival flap is reposited and secured by
wet-field cauery.
11. Subconjunctival injection of dexamethasone 0.25
ml and gentamicin 0.5 ml is given.
12. Patching of eye is done with a pad and sticking
plaster or a bandage is applied.

Conventional ECCE versus SICS

Conventional large incision ECCE, though still being
performed by many surgeons, is being largely replaced
by small incision cataract surgery (SICS) techniques.
Merits of conventional ECCE over SICS. The only
merit of conventional ECCE over SICS is that it is a
simple technique to master with short learning curve.

Dermerits of conventional ECCE over SICS include:
Long incision (10 to 12 mm).
Multiple sutures are required.
Open chamber surgery with high risk of vitreous
prolapse, operative hard eye and expulsive
choroidal haemorrhage.
High incidence of post-operative astigmatism.
Postoperative suture-related problems like irritation
and suture abscess etc.
Postoperative wound-related problems such as
wound leak, shallowing of anterior chamber and
iris prolapse.
Needs suture removal, during which infection
may occur.

SICS vs phacoemulsification

Merits of manual SICS over phacoemulsification
1. Universal applicability i.e., all types of cataracts
including hard cataracts (grade IV and V) can be
operated by this technique.
2. Learning curve. This procedure is much easier to
learn as compared to phacoemulsification.
3. Not machine dependent. The biggest advantage
of manual SICS is that it is not machine dependent
and thus can be practised anywhere.
4. Less surgical complications. Disastrous
complication like nuclear drop into vitreous cavity
is much less than phacoemulsification technique.
5. Operating time in manual SICS is less than that
of phocoemulsification, especially in hard cataract.
Therefore, it is ideal for mass surgery.
6. Cost effective. With manual SICS, the expenses
are vastly reduced as compared to considerable
expenses in acquiring and maintaining phaco
machine. There is no need to spend on
consumable items like the phacotip, sleeves,
tubing and probe. Further, in SICS always PMMA
IOLs are used which are much cheeper than
foldable IOLs.
Demerits of manual SICS over phacoemulsification
1. Conjunctival congestion persists for 5-7 days at
the site of conjunctival flap.
2. Mild tenderness sometime may be present owing
to scleral incision.
3. Postoperative hyphaema may be noted
sometimes.
4. Surgical induced astigmatism is more as the
incision in SICS is large (about 6 mm) as compared
to phacoemulsification (about 3.2 mm).
Merits of phacoemulsification over manual SICS
1. Topical anaesthesia may be sufficient for
phacoemulsification in expert hands.
2. Postoperative congestion is minimal after
phacoemulsification, as phaco is usually
performed through a clear corneal incision.
3. Small incision. The chief advantage of
phacoemulsification over manual SICS is that it
can be performed through a smaller (3.2 mm)
incision.
4. Less corneal complications. Phacoemulsification
can be performed in the posterior chamber
without prolapsing the nucleus into the anterior
chamber, thereby minimising the risk of corneal
complications.
5. Visual rehablitation is comparetively quicker in
phacoemulsification as compared to manual SICS.
6. Postoperative astigmatism is comparatively less
when foldable IOLs are implanted through a
smaller incision (3.2 mm).
Demerits of phacoemulsification vis-a-vis manual
SICS
1. Learning curve for phacoemulsification is more
painful both for the surgeons and patients.
2. Complications encountered during phacoemulsification
like nuclear drop are unforgiving.
3. Machine dependent. This procedure is solely
machine dependent and in the event of an
unfortunate machine failure in the middle of
surgery one has to shift to conventional ECCE.
4. High cost. Cost of this technique is very high
because of expensive machine, accessories and
maintenance.
5. Limitations. It is very difficult to deal with hard
cataracts (grade IV and V) with this technique,
and also there is high risk of serious corneal
complications due to more use of phaco energy
in such cases.
Conclusion. Inspite of the demerits listed above
the phacoemulsification has become the preferred
method of cataract extraction world wide because
the complication rate in the expert hands is minimal
and the technique provides an almost quiet eye
early postoperatively and an early visual
rehabilitation. However, for the masses, especially
in developing countries, the manual SICS offers the
advantages of sutureless cataract surgery as a low
cost alternative to phacoemulsification with the
added advantages of having wider applicability and
an easier learning curve.

ECCE vs ICCE

Advantages of ECCE over ICCE
1. ECCE is a universal operation and can be
performed at all ages, except when zonules are
not intact; whereas ICCE cannot be performed
below 40 years of age.
2. Posterior chamber IOL can be implanted after
ECCE, while it cannot be implanted after ICCE.
3. Postoperative vitreous related problems (such as
herniation in anterior chamber, pupillary block
and vitreous touch syndrome) associated with
ICCE are not seen after ECCE.
4. Incidence of postoperative complications such
as endophthalmitis, cystoid macular oedema and
retinal detachment are much less after ECCE as
compared to that after ICCE.
5. Postoperative astigmatism is less, as the incision
is smaller.
Advantages of ICCE over ECCE
1. The technique of ICCE, as compared to ECCE, is
simple, cheap, easy and does not need
sophisticated microinstruments.
2. Postoperative opacification of posterior capsule
is seen in a significant number of cases after
ECCE. No such problem is known with ICCE.
3. ICCE is less time consuming and hence more
useful than ECCE for mass scale operations in
eye camps.

MANAGEMENT OF CATARACT IN ADULTS

Treatment of cataract essentially consists of its
surgical removal. However, certain non-surgical
measures may be of help, in peculiar circumstances,
till surgery is taken up.
A. Non-surgical measures
1. Treatment of cause of cataract. In acquired
cataracts, thorough search should be made to find
out the cause of cataract. Treatment of the causative
disease, many a time, may stop progression and
sometimes in early stages may cause even regression
of cataractous changes and thus defer the surgical
treatment. Some common examples include:
Adequate control of diabetes mellitus, when
discovered.
Removal of cataractogenic drugs such as
corticosteroids, phenothiazenes and strong
miotics, may delay or prevent cataractogenesis.
Removal of irradiation (infrared or X-rays) may
also delay or prevent cataract formation.
Early and adequate treatment of ocular diseases
like uveitis may prevent occurrence of complicated
cataract.
2. Measures to delay progression. Many commercially
available preparations containing iodide salts of
calcium and potassium are being prescribed in
abundance in early stages of cataract (especially in
senile cataract) in a bid to delay its progression.
However, till date no conclusive results about their
role are available. Role of vitamin E and aspirin in
delaying the process of cataractogenesis is also
mentioned.
3. Measures to improve vision in the presence of
incipient and immature cataract may be of great
solace to the patient. These include:
Refraction, which often changes with considerable
rapidity, should be corrected at frequent intervals.
Arrangement of illumination. Patients with
peripheral opacities (pupillary area still free), may
be instructed to use brilliant illumination.
Conversely, in the presence of central opacities,
a dull light placed beside and slightly behind the
patient’s head will give the best result.
Use of dark goggles in patients with central
opacities is of great value and comfort when
worn outdoors.
Mydriatics. The patients with a small axial cataract,
frequently may benefit from pupillary dilatation.
This allows the clear paraxial lens to participate
in light transmission, image formation and
focussing. Mydriatics such as 5 percent
phenylephrine or 1 percent tropicamide; 1 drop
b.i.d. in the affected eye may clarify vision.
B. Surgical management
Indications
1. Visual improvement. This is by far the most
common indication. When surgery should be advised
for visual improvement varies from person to person
depending upon the individual visual needs. So, an
individual should be operated for cataract, when the
visual handicap becomes a significant deterrent to
the maintenance of his or her usual life-style.
2. Medical indications. Sometimes patients may be
comfortable from the visual point (due to useful vision
from the other eye or otherwise) but may be advised
cataract surgery due to medical grounds such as
Lens induced glaucoma,
Phacoanaphylactic endophthalmitis and
Retinal diseases like diabetic retinopathy or retinal
detachment, treatment of which is being hampered
by the presence of lens opacities.
3. Cosmetic indication. Sometimes patient with
mature cataract may insist for cataract extraction (even
with no hope of getting useful vision), in order to
obtain a black pupil.
Preoperative evaluation
Once it has been decided to operate for cataract, a
thorough preoperative evaluation should be carried
out before contemplating surgery. This should
include:
I. General medical examination of the patient to
exclude the presence of serious systemic diseases
especially: diabetes mellitus; hypertension and
cardiac problems; obstructive lung disorders and any
potential source of infection in the body such as
septic gums, urinary tract infection etc.
II. Ocular examination. A thorough examination of
eyes including slit-lamp biomicroscopy is desirable
in all cases. The following useful information is
essential before the patient is considered for surgery:

be explored since, if it is defective, operation will be
valueless, and patient must be warned of the
prognosis, to avoid unnecessary disappointment and
medicolegal problems. A few important retinal function
tests are considered here.
1. Light perception (PL). Many sophisticated retinal
function tests have been developed, but light
perception must be present, if there is to be any
potential for useful vision.
2. A test for Marcus-Gunn pupillary response
(indicative of afferent pathway defect) should be
made routinely. If present, it is a poor prognostic
sign.
3. Projection of rays (PR). It is a crude but an
important and easy test for function of the
peripheral retina. It is tested in a semi-dark room
with the opposite eye covered. A thin beam of
light is thrown in the patient's eye from four
directions (up, down, medial and lateral) and the
patient is asked to look straight ahead and point
out the direction from which the light seems to
come.
4. Two-light discrimination test. It gives information
about macular function. The patient is asked to
look through an opaque disc perforated with two
pin-holes behind which a light is held. The holes
are 2 inches apart and kept about 2 feet away
from the eye. If the patient can perceive two
lights, it indicates normal macular function.
5. Maddox rod test. The patient is asked to look at
a distant bright light through a Maddox rod. An
accurate perception of red line indicates normal
function.
6. Colour perception. It indicates that some macular
function is present and optic nerve is relatively
normal.
7. Entoptic visualisation. It is evaluated by rubbing
a point source of light (such as bare lighted bulb
of torch) against the closed eyelids. If the patient
perceives the retinal vascular pattern in black
outline, it is favourable indication of retinal
function. Being subjective in nature, the
importance of negative test can be considered if
the patient can perceive the pattern with the
opposite eye.
8. Laser interferometry. It is a very good test for
measuring the macular potential for visual acuity
in the presence of opaque media.
9. Objective tests for evaluating retina are required
if some retinal pathology is suspected. These
tests includes ultrasonic evaluation of posterior
segment of the eye; electrophysiological studies
such as ERG (electroretinogram), EOG
(electrooculogram) and VER (visually-evoked
response); and indirect ophthalmoscopy if
possible.
B. Search for local source of infection should be
made by ruling out conjunctival infections,
meibomitis, blepharitis and lacrimal sac infection.
Lacrimal sac should receive special attention. Lacrimal
syringing should be carried out in each patient with
history of watering from the eyes. In cases where
chronic dacryocystitis is discovered, either DCR
(dacryocystorhinostomy) or DCT (dacryocystectomy)
operation should be performed, before the
cataract surgery.
C. Anterior segment evaluation by slit-lamp
examination. It is of utmost importance. Presence of
keratic precipitates at the back of cornea, in a case of
complicated cataract, suggests management for subtle
uveitis before the cataract surgery. Similarly,
information about corneal endothelial condition is also
very important, especially if intraocular lens
implantation is planned.
D. Intraocular pressure (IOP) measurement.
Preoperative evaluation is incomplete without the
measurement of IOP. The presence of raised IOP
needs a priority management.
Preoperative medications and preparations
1. Topical antibiotics such as tobramycin or
gentamicin or ciprofloxacin QID for 3 days just
before surgery is advisable as prophylaxis against
endophthalmitis.
2. Preparation of the eye to be operated. Eyelashes
of upper lid should be trimmed at night and the
eye to be operated should be marked.
3. An informed and detailed consent should be
obtained.
4. Scrub bath and care of hair. Each patient should
be instructed to have a scrub bath including face
and hair wash with soap and water. Male patients
must get their beard cleaned and hair trimmed.
Female patients should comb their hair properly.

5. To lower IOP, acetazolamide 500 mg stat 2 hours
before surgery and glycerol 60 ml mixed with
equal amount of water or lemon juice, 1 hour
before surgery, or intravenous mannitol 1 gm/kg
body weight half an hour before surgery may be
used.
6. To sustain dilated pupil (especially in
extracapsular cataract extraction) the
antiprostaglandin eyedrops such as indomethacin
or flurbiprofen should be instilled three times one
day before surgery and half hourly for two hours
immediately before surgery. Adequate dilation of
pupil can be achieved by instillation of 1 percent
tropicamide and 5 percent or 10 percent
phenylephrine eyedrops every ten minutes, one
hour before surgery.
Anaesthesia
Cataract extraction can be performed under general
or local anaesthesia. Local anaesthesia is preferred
whenever possible (see page 571-573).
Types and choice of surgical techniques
I. Intracapsular cataract extraction (ICCE) . In this
technique, the entire cataractous lens along with the
intact capsule is removed. Therefore, weak and
degenerated zonules are a pre-requisite for this
method. Because of this reason, this technique
cannot be employed in younger patients where
zonules are strong. ICCE can be performed between
40-50 years of age by use of the enzyme alphachymotrypsin
(which will dissolve the zonules).
Beyond 50 years of age usually there is no need of
this enzyme.
Indications. ICCE has stood the test of time and has
been widely employed for about 50 years over the
world. Now (for the last 25 years) it has been almost
entirely replaced by planned extracapsular technique.
At present the only indications of ICCE is markedly
subluxated and dislocated lens.
II. Extracapsular cataract extraction (ECCE). In
this technique, major portion of anterior capsule with
epithelium, nucleus and cortex are removed; leaving
behind intact posterior capsule.
Indications. Presently, extracapsular cataract
extraction technique is the surgery of choice for
almost all types of adulthood as well as childhood
cataracts unless contraindicated.
Contraindications. The only absolute contraindication
for ECCE is markedly subluxated or
dislocated lens.

Types of extracapsular cataract extraction
The surgical techniques of ECCE presently in vogue
are:
Conventional extracapsular cataract extraction
(ECCE),
Manual small incision cataract surgery (SICS),
Phacoemulsification

COMPLICATED CATARACT

It refers to opacification of the lens secondary to
some other intraocular disease. Some authors use the
term secondary cataract for the complicated cataract.
Many authors use the term secondary cataract to
denote after cataract. Therefore, to avoid confusion
and controversy, preferably, the term secondary
cataract should be discarded.
Etiology
The lens depends for its nutrition on intraocular
fluids. Therefore, any condition in which the ocular
circulation is disturbed or in which inflammatory
toxins are formed, will disturb nutrition of the
crystalline lens, resulting in development of
complicated cataract. Some important ocular
conditions giving rise to complicated cataract are listed
here.
1. Inflammatory conditions. These include uveal
inflammations (like iridocyclitis, parsplanitis,
choroiditis), hypopyon corneal ulcer and
endophthalmitis.
2. Degenerative conditions such as retinitis
pigmentosa and other pigmentary retinal dystrophies
and myopic chorioretinal degeneration.

3. Retinal detachment. Complicated cataract may
occur in long-standing cases.
4. Glaucoma (primary or secondary) may sometimes
result in complicated cataract. The underlying
cause here is probably the embarrassment to the
intraocular circulation, consequent to the raised
pressure.
5. Intraocular tumours such as retinoblastoma or
melanoma may give rise to complicated cataract
in late stages.
Clinical features
Typically the complicated cataract starts as posterior
cortical cataract. Lens changes appear typically in
front of the posterior capsule. The opacity is irregular
in outline and variable in density. In the beam of slitlamp
the opacities have an appearance like ‘breadcrumb’.
A very characteristic sign is the appearance
of iridescent coloured particles the so-called
‘polychromatic lustre’ of reds, greens and blues. A
diffuse yellow-haze is seen in the adjoining cortex.
Slowly the opacity spreads in the rest of the cortex,
and finally the entire lens becomes opaque, giving
chalky white appearance. Deposition of calcium is
common in the later stages.

Diabetic cataract

Diabetes is associated with two types of cataracts:
1. Senile cataract in diabetics appears at an early
age and progresses rapidly.
2. True diabetic cataract. It is also called ‘snow flake
cataract’ or ‘snow-storm cataract’. It is a rare
condition, usually occurring in young adults due to
osmotic over-hydration of the lens. Initially a large
number of fluid vacuoles appear underneath the
anterior and posterior capsules, which is soon
followed by appearance of bilateral snowflake-like
white opacities in the cortex.

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

CONGENITAL AND DEVELOPMENTAL CATARACTS

These occur due to some disturbance in the normal
growth of the lens. When the disturbance occurs
before birth, the child is born with a congenital
cataract. Therefore, in congenital cataract the opacity
is limited to either embryonic or foetal nucleus.
Developmental cataract may occur from infancy to
adolescence. Therefore, such opacities may involve
infantile or adult nucleus, deeper parts of cortex or
capsule. Developmental cataract typically affects the
particular zone which is being formed when this
process is disturbed. The fibres laid down previously
and subsequently are often normally formed and
remain clear. Congenital and developmental opacities
assume most variegated appearance and minute
opacities (without visual disturbance) are very
common in normal population. These are detected
with the beam of slit lamp under full mydriasis.

Etiology
Exact etiology is not known. Some factors which have
been associated with certain types of cataracts are
described below:
I. Heredity. Genetically-determined cataract is due to
an anomaly in the chromosomal pattern of the
individual. About one-third of all congenital cataracts
are hereditary. The mode of inheritance is usually
dominant. Common familial cataracts include:
cataracta pulverulenta, zonular cataract (also occurs
as non-familial), coronary cataract and total soft
cataract (may also occur due to rubella).
II. Maternal factors
1. Malnutrition during pregnancy has been
associated with non-familial zonular cataract.
2. Infections. Maternal infections like rubella are
associated with cataract in 50 percent of cases.
Other maternal infections associated with
congenital cataract include toxoplasmosis and
cytomegalo-inclusion disease.
3. Drugs ingestion. Congenital cataracts have also
been reported in the children of mothers who
have taken certain drugs during pregnancy (e.g.,
thalidomide, corticosteroids).
4. Radiation. Maternal exposure to radiation during
pregnancy may cause congenital cataracts.
III. Foetal or infantile factors
1. Deficient oxygenation (anoxia) owing to placental
haemorrhage.
2. Metabolic disorders of the foetus or infant
such as galactosemia, galactokinase deficiency
and neonatal hypoglycemia.
3. Cataracts associated with other congenital
anomalies e.g., as seen in Lowe's syndrome,
myotonia dystrophica and congenital icthyosis.
4. Birth trauma.
5. Malnutrition in early infancy may also
cause developmental cataract.
IV. Idiopathic. About 50 percent cases are sporadic
and of unknown etiology.
Clinical types
Congenital and developmental cataracts have been
variously classified. A simple morphological
classification of congenital and developmental
cataract is as under :
I. Congenital capsular cataracts
1. Anterior capsular cataract
2. Posterior capsular cataract
II. Polar cataracts
1. Anterior polar cataract
2. Posterior polar cataract
III. Nuclear cataract
IV. Lamellar cataract
V. Sutural and axial cataracts
1. Floriform cataract
2. Coralliform cataract
3. Spear-shaped cataract
4. Anterior axial embryonic cataract
VI. Generalized cataracts
1. Coronary cataract
2. Blue dot cataract
3. Total congenital cataract
4. Congenital membranous cataract
I. Congenital capsular cataracts
1. Anterior capsular cataracts are nonaxial,
stationary and visually insignificant.
2. Posterior capsular cataracts are rare and can be
associated with persistent hyaloid artery remnants.
II. Polar cataracts
1. Anterior polar cataract. It involves the central
part of the anterior capsule and the adjoining
superficial-most cortex. It may arise in the following
ways:
i. Due to delayed development of anterior chamber.
In this case the opacity is congenital usually
bilateral, stationary and visually insignificant.
ii. Due to corneal perforation. Such cataracts may
also be acquired in infantile stage and follow
contact of the lens capsule with the back of
cornea, usually after perforation due to ophthalmia
neonatorum or any other cause.
Morphological types: Anterior polar cataracts may
occur as any of the following morphological patterns:
i. Thickened white plaque in the centre of capsule.
ii. Anterior pyramidal cataract. In it the thickened
capsular opacity is cone-shaped with its apex
towards cornea.
iii. Reduplicated cataract (double cataract).
Sometimes along with thickening of central point
of anterior capsule, lens fibres lying immediately
beneath it also become opaque and are
subsequently separated from the capsule by
laying of transparent fibres in between. The
burried opacity is called ‘imprint’ and the two
together constitute reduplicated cataract.

2. Posterior polar cataract. It is a very common lens
anomaly and consists of a small circular circumscribed
opacity involving the posterior pole.
Associations. Posterior polar cataract may be
associated with :
Persistent hyaloid artery remnants (Mittendorf dot),
Posterior lenticonus, and
Persistent hyperplastic primary vitreous (PHPV).
Types. Posterior polar cataract occurs in two forms:
Stationary form and
Progressive form which progresses after birth.
III. Nuclear cataracts
i. Cataracta centralis pulverulenta (Embryonic
nuclear cataract). It has dominant genetic trait and
occurs due to inhibition of the lens development at a
very early stage and thus, involves the embryonic
nucleus. The condition is bilateral and is characterised
by a small rounded opacity lying exactly in the centre
of the lens. The opacity has a powdery appearance
(pulverulenta) and usually does not affect the vision.
ii. Total nuclear cataract. It usually involves the
embryonic and fetal nucleus and sometimes infantile
nucleus as well. It is characterized by a dense chalky
white central opacity seriously impairing vision. The
opacities are usually bilateral and non progressive.
IV. Lamellar cataract
Lamellar or Zonular cataract refer to the developmental
cataract in which the opacity occupies a discrete zone
in the lens. It is the most common type of congenital
cataract presenting with visual impairment. It
accounts for about 40 percent of the cases.
Etiology. It may be either genetic or environmental
in origin.
Genetic pattern is usually of dominant variety.
Environmental form is associated with deficiency
of vitamin D.
Sometimes maternal rubella infection contracted
between 7th and 8th week of gestation may also
cause lamellar cataract.
Characteristic features. Typically, this cataract occurs
in a zone of foetal nucleus surrounding the embryonic
nucleus (Fig. 8.5).
Occasionally two such rings of opacity are seen.
The main mass of the lens internal and external
to the zone of cataract is clear, except for small
linear opacities like spokes of a wheel (riders)
which may be seen towards the equator.
It is usually bilateral and frequently causes severe
visual defects.
V. Sutural and axial cataracts
Sutural cataracts are comparatively of common
occurrence and consist of a series of punctate
opacities scattered around the anterior and posterior
Y-sutures. Such cataracts are usually static, bilateral
and do not have much effect on the vision. The
individual opacities vary in size and shape and have
different patterns and thus are named accordingly as
under:
1. Floriform cataract. Here the opacities are
arranged like the petals of a flower.
2. Coralliform cataract. Here the opacities are
arranged in the form of a coral.

3. Spear-shaped cataract. The lenticular opacities
are in the form of scattered heaps of shining
crystalline needles.
4. Anterior axial embryonic cataract occurs as fine
dots near the anterior Y-suture.
VI. Generalized cataracts
1. Coronary cataract (Fig. 8.6). It is an extremely
common form of developmental cataract occurring
about puberty; thus involving either the adolescent
nucleus or deeper layer of the cortex. The opacities
are often many hundreds in number and have a regular
radial distribution in the periphery of lens (corona of
club-shaped opacities) encircling the central axis.
Since the opacities are situated peripherally, vision is
usually unaffected. Sometimes the associated large
punctate opacities may marginally reduce the vision.
2. Blue dot cataract. It is also called cataractapunctata-
caerulea. It usually forms in the first two
decades of life. The characteristic punctate opacities
are in the form of rounded bluish dots situated in the
peripheral part of adolescent nucleus and deeper layer
of the cortex. Opacities are usually stationary and do
not affect vision. However, large punctate opacities
associated with coronary cataract may marginally
reduce the vision.
3. Total congenital cataract. It is a common variety
and may be unilateral or bilateral (Fig. 8.7). In many
cases there may be hereditary character. Its other
important cause is maternal rubella, occurring during
the first trimester of pregnancy. Typically, the child is
born with a dense white nuclear cataract. It is a
progressive type of cataract. The lens matter may
remain soft or may even liquefy (congenital
Morgagnian cataract).
Congenital rubella cataract may occur alone or as
part of the classical rubella syndrome which consists
of:
i. Ocular defects (congenital cataract, salt and
pepper retinopathy and microphthalmos).
ii. Ear defects (deafness due to destruction of organ
of Corti).
iii. Heart defects (patent ductus arteriosus, pulmonary
stenosis and ventricular septal defects).
4. Congenital membranous cataract. Sometimes
there may occur total or partial absorption of
congenital cataract, leaving behind thin membranous
cataract. Rarely there is complete disappearance of
all the lens fibres and only a fine transparent lens
capsule remains behind. Such a patient may be

misdiagnosed as having congenital aphakia. This is
associated with Hallermann-Streiff-Francois
Synodrome.
Differential diagnosis
Congenital cataracts presenting with leukocoria
need to be differentiated from various other conditions
presenting with leukocoria such as retinoblastoma,
retinopathy of prematurity, persistent hyperplastic
primary vitreous (PHPV), etc., (also see page 282)
Management of congenital and developmental
cataract
A. Clinico-investigative work up. A detailed clinicoinvestigative
work up is most essential in the
management of paediatric cataract. It should aim at
knowing the prognostic factors and indications and
timing of surgery.
1. Ocular examination should be carried out with
special reference to:
Density and morphology of cataract
Assessment of visual function is difficult in infants
and small children. An idea may be made from the
density and morphology of the cataract by
oblique illumination examination and fundus
examination. Special tests like fixation reflex, forced
choice preferential looking test, visually evoked
potential (VEP), optic-kinetic nystagmus (OKN)
etc. also provide useful information.
Associated ocular defects should be noted (which
include microphthalmos, glaucoma, PHPV, foveal
hypoplasia, optic nerve hypoplasia, and rubella
retinopathy etc.
2. Laboratory investigations should be carried out
to detect following systemic associations in nonhereditary
cataracts:
Intrauterine infections viz. toxoplasmosis, rubella,
cytomegalo virus and herpes virus by TORCH
test.
Galactosemia by urine test, for reducing
substances, red blood cell transferase and
glactokinase levels.
Lowe's syndrome by urine chromatography for
amino acids.
Hyperglycemia by blood sugar.
Hypocalcemia by serum calcium and phosphate
levels and X-ray skull.
B. Prognostic factors which need to be noted are:
Density of cataract,
Unilateral or bilateral cataract,
Time of presentation,
Associated ocular defects, and
Associated systemic defects
C. Indications and timing of paediatric cataract
surgery,
1. Partial cataracts and small central cataracts
which are visually insignificant can safely be
ignored and observed or may need non-surgical
treatment with pupillary dilatation.
2. Bilateral dense cataracts should be removed
early (within 6 weeks of birth) to prevent stimulus
deprivation amblyopia.
3. Unilateral dense cataract should preferably be
removed as early as possible (within days) after
birth. However, it must be born in mind that
visual prognosis in most of the unilateral cases
is very poor even after timely operation because
correction of aphakia and prevention of amblyopia
in infants is an uphill task.
D. Surgical procedures. Childhood cataracts,
(congenital, developmental as well as acquired) can
be dealt with anterior capsulotomy and irrigation
aspiration of the lens matter or lensectomy. Surgical
technique of these procedures is described on page
193.
Note. The needling operation (which was performed
in the past) is now obsolete.
E. Correction of paediatric aphakia. It is still an
unsolved query. Presently common views are as
follows:
Children above the age of 2 years can be
corrected by implantation of posterior chamber
intraocular lens during surgery.
Children below the age of 2 years should
preferably be treated by extended wear contact
lens. Spectacles can be prescribed in bilateral
cases. Later on secondary IOL implantation may
be considered. Present trend is to do primary
implantation at the earliest possible (2-3 months)
specially in unilateral cataract.
Paediatric IOL: size, design and power. The main
concerns regarding the use of IOL in children are the
growth of the eye, IOL power considerations,

increased uveal reaction and long-term safety. Present
recommendation are :
Size of IOL above the age of 2 years may be
standard 12 to 12.75-mm diameter for in the bag
implantation.
Design of IOL recommended is one-piece PMMA
with modified C-shaped haptics (preferably heparin
coated).
Power of IOL. In children between 2-8 years of
age 10% undercorrection from the calculated
biometric power is recommended to counter the
myopic shift. Below 2 years on undercorrection
by 20% is recomended.
F. Correction of amblyopia. It is the central theme
around which management of childhood cataract and
aphakia revolves. In spite of best efforts, it continues
to be the main cause of ultimate low vision in these
children.

Cataract: Definition And Classification

Definition
The crystalline lens is a transparent structure. Its
transparency may be disturbed due to degenerative
process leading to opacification of lens fibres.
Development of an opacity in the lens is known as
cataract.
Classification
A. Etiological classification
I. Congenital and developmental cataract
II. Acquired cataract
1. Senile cataract
2. Traumatic cataract (see page 405)
3. Complicated cataract
4. Metabolic cataract
5. Electric cataract
6. Radiational cataract
7. Toxic cataract e.g.,
i Corticosteroid-induced cataract
ii. Miotics-induced cataract
iii. Copper (in chalcosis) and iron (in siderosis)
induced cataract.
8. Cataract associated with skin diseases
(Dermatogenic cataract).
9. Cataract associated with osseous diseases.
10. Cataract with miscellaneous syndromes e.g.,
i. Dystrophica myotonica
ii. Down's syndrome.
iii. Lowe's syndrome
iv. Treacher - Collin's syndrome
B. Morphological classification (Fig. 8.4)
1. Capsular cataract. It involves the capsule and
may be:
i. Anterior capsular cataract
ii. Posterior capsular cataract
2. Subcapsular cataract. It involves the
superficial part of the cortex (just below the
capsule) and includes:
i. Anterior subcapsular cataract
ii. Posterior subcapsular cataract
3. Cortical cataract. It involves the major part
of the cortex.
4. Supranuclear cataract. It involves only the
deeper parts of cortex (just outside the nucleus).
5. Nuclear cataract. It involves the nucleus of the
crystalline lens.
6. Polar cataract. It involves the capsule and
superficial part of the cortex in the polar region
only and may be:
i. Anterior polar cataract
ii. Posterior polar cataract

Lens: Anatomy, Physiology

The lens is a transparent, biconvex, crystalline
structure placed between iris and the vitreous in
a saucer shaped depression the patellar fossa.
Its diameter is 9-10 mm and thickness varies with
age from 3.5 mm (at birth) to 5 mm (at extreme of
age). Its weight varies from 135 mg (0-9 years) to
255 mg (40-80 years of age).
It has got two surfaces: the anterior surface is
less convex (radius of curvature 10 mm) than the
posterior (radius of curvature 6 mm). These two
surfaces meet at the equator.
Its refractive index is 1.39 and total power is
15-16 D. The accommodative power of lens varies
with age, being 14-16 D (at birth); 7-8 D (at 25
years of age) and 1-2 D (at 50 years of age).
Structure (Fig. 8.1)
1. Lens capsule. It is a thin, transparent, hyaline
membrane surrounding the lens which is thicker over
the anterior than the posterior surface. The lens
capsule is thickest at pre-equator regions (14 μ) and
thinnest at the posterior pole (3 μ).
2. Anterior epithelium. It is a single layer of cuboidal
cells which lies deep to the anterior capsule. In the
equatorial region these cells become columnar, are
actively dividing and elongating to form new lens
fibres throughout the life. There is no posterior
epithelium, as these cells are used up in filling the
central cavity of lens vesicle during development of
the lens.
3. Lens fibres. The epithelial cells elongate to form
lens fibres which have a complicated structural form.
Mature lens fibres are cells which have lost their
nuclei. As the lens fibres are formed throughout the
life, these are arranged compactly as nucleus and
cortex of the lens (Fig. 8.2).
i. Nucleus. It is the central part containing the
oldest fibres. It consists of different zones, which
are laid down successively as the development
proceeds. In the beam of slit-lamp these are seen
as zones of discontinuity. Depending upon the
period of development, the different zones of the
lens nucleus include:

Embryonic nucleus. It is the innermost part of
nucleus which corresponds to the lens upto
the first 3 months of gestation. It consists of
the primary lens fibres which are formed by
elongation of the cells of posterior wall of lens
vesicle.
Fetal nucleus. It lies around the embryonic
nucleus and corresponds to the lens from 3
months of gestation till birth. Its fibres meet
around sutures which are anteriorly Y-shaped
and posteriorly inverted Y-shaped (Fig.8.2).
Infantile nucleus corresponds to the lens from
birth to puberty, and
Adult nucleus corresponds to the lens fibres
formed after puberty to rest of the life.
ii. Cortex. It is the peripheral part which comprises
the youngest lens fibres.
4. Suspensory ligaments of lens (Zonules of Zinn).
Also called as ciliary zonules, these consist
essentially of a series of fibres passing from ciliary
body to the lens. These hold the lens in position and
enable the ciliary muscle to act on it. These fibres are
arranged in three groups:
i. The fibres arising from pars plana and anterior
part of ora serrata pass anteriorly to get inserted
anterior to the equator.
ii. The fibres originating from comparatively
anteriorly placed ciliary processes pass posteriorly
to be inserted posterior to the equator.
iii. The third group of fibres passes from the summits
of the ciliary processes almost directly inward to
be inserted at the equator.
APPLIED PHYSIOLOGY AND BIOCHEMISTRY
The crystalline lens is a transparent structure playing
main role in the focussing mechanism for vision. Its
physiological aspects include :
Lens transparency,
Metabolic activities of the lens, and
Accommodation (see page 39)
Lens transparency
Factors that play significant role in maintaining
outstanding clarity and transparency of lens are:
Avascularity,
Tightly-packed nature of lens cells,
The arrangement of lens proteins,
Semipermeable character of lens capsule,
Pump mechanism of lens fibre membranes that
regulate the electrolyte and water balance in the
lens, maintaining relative dehydration and

Auto-oxidation and high concentration of reduced
glutathione in the lens maintains the lens proteins
in a reduced state and ensures the integrity of
the cell membrane pump.