Lens&Cataract
Lens&Cataract
Lens&Cataract
I. Cataract
V Causes of Cataract
V Global / National distribution & population
characteristics of Cataract
V Diagnosis of cataract. Distinction between immature,
mature and hypermature.
V Appropriate referral of cataract patient
V Outline of surgical management
V Visual rehabilitation of Aphakia
V Outline of cataract management in young age
Crystalline Lens
Embryology
V Derived from surface Ectoderm overlying the optic
vesicle.
V Ectoderm invaginates and break from surface as two
layer structure
V Basement membrane of epithelium, which is now on
the outer side, forms the lens capsule.
V Posterior epithelium cells expand to form the
embryonic nucleus.
V Anterior epithelium continues to regenerate and develop lens
fibers throughout life. These fibers continue to get deposited
inwards making earliest fibers the deepest.
Anatomy
V A globular structure lies behind the iris and in a concavity in the
anterior face of vitreous called the Patellar Fossa.
V Suspended from the ciliary processes by Zonules
V In young patients (< 35 years) lens is adherent to vitreous by
Ligament of Weigert.
Epithelium divides most actively in the periphery and differentiates in the lens
fibers.
Physiology
Functions:
Cataract
Definition
Any opacity of the lens or loss of transparency of the lens that causes
diminution or impairment of vision is called Cataract.
Although any lens opacity whether or not it leads to decrease in vision is
technically cataract, yet an opacity in the periphery of the lens, which is
stationary and not hampering vision should be diagnosed just Lens Opacity in
order to avoid causing unnecessary anxiety to the patient.
Classification
V Etiological
V Morphological
V Stage of Maturity
Etiological Classification
1. Senile
2. Traumatic
V Penetrating
V Concussion (Rosette Cataract)
V Infrared irradiation (Glass Blower’s Cataract)
V Electrocution
3. Metabolic
V Diabetes (Snow Storm Cataract)
V Hypoglycaemia
V Galactosemia (Oil Drop Cataract)
V Galactokinase Deficiency
V Mannosidosis
V Fabry’s Disease
V Lowe’s Syndrome
V Wilson’s Disease (Sunflower Cataract)
V Hypocalcaemia
4. Toxic
V Corticosteroids
V Chlorpromazine
V Miotics
V Busulphan
V Gold
V Amiodarone
5. Complicated
V Anterior Uveitis
V Hereditary Retinal & Vitreoretinal Disorders
V High Myopia
V Glaucomflecken
V Intraocular Neoplasia
6. Maternal Infections
V Rubella
V Toxoplasmosis
V Cytomegalovirus
7. Maternal Drug Ingestion
V Thalidomide
V Corticosteroid
8. Presenile Cataract
V Myotonic Dystrophy
V Atopic Dermatitis (Syndermatotic Cataract)
V GPUT & GK Enzyme Deficiencies
9. Syndromes with Cataract
V Down’s Syndrome
V Werner’s Syndrome
V Rothmund’s Syndrome
V Lowe’s Syndrome
10. Hereditary
11. Secondary Cataract
1. Capsular
V Congenital (Anterior Polar & Posterior Polar)
V Acquired
2. Subcapsular
V Posterior Subcapsular (Cupuliform)
V Anterior Subcapsular
3. Nuclear
V Congenital (Discoid, etc.)
V Senile
4. Cortical
V Congenital (Coronary, Coralliform, etc)
V Senile (Cuneiform)
5. Lamellar or Zonular
6. Sutural
7. Others
V Blue-Dot (Cataracta caerulea)
V Membranous
V Cataracta Pulveranta Centralis
V Reduplicated Cataract
Stage of Maturity
Immature
Mature
Intumescent
Hypermature
Morgagnian
Chronological
Congenital (since birth)
Infantile (first year of life)
Juvenile (1 to 13 years of life)
Presenile (13 to 35 years of life)
Senile
Pathogenesis
Two main pathogenetic processes are involved in most (especially senile)
cataract:
V Hydration
V Sclerosis
Hydration
V Increased hydration leads to lamellar separation and collection of
protein-deficient fluid between lens fibers.
V Leads to increased scattering of light and loss of transparency.
V Hydration also leads to denaturation of lens proteins and results in
irreversible opacification.
V Mechanisms of increased hydration are:
Failure of active pump mechanism
Increased leakage across posterior or anterior capsule
Increased Osmotic pressure
Sclerosis
V This process is seen mostly in senile cataract and involves
predominantly the nucleus.
V Increased compaction of lens proteins and fibers due to inter-lamellar
binding of proteins by sulfide bonds.
V Resultant aggregates of very high molecular weight proteins lead to
increased scattering of light and loss of transparency.
V It is part of normal aging phenomenon.
Senile Cataract
Epidemiology
Global
V 38 million people are blind
V 41 % because of cataract
National
V 71 % of blindness in Nepal is because of cataract
V About 72 % of blindness in India is caused by Cataract
Progression
I. Stage of Lamellar Separation
V Hydration leads to separation of cortex from nucleus
V Appreciated on slit lamp biomicroscopy
II. Stage of Incipient Cataract
V Early opacities appear
V Vision unaffected but other symptoms e.g., glare, appear.
III. Immature Cataract
Opacification leading to diminution of vision.
Two morphological forms are seen:
1. Cuneiform Cataract: Wedge shaped opacities appear in the
peripheral cortex and progress towards the nucleus. Vision is worse
in low ambient illumination when the pupil is dilated.
2. Cupuliform Cataract: A disc or saucer shaped area of the cortex
beneath the posterior capsule undergo opacification. The opacity
being central, the vision is worst in bright ambient illumination when
the pupil is constricted.
V Lens appears grayish white in color.
V Iris shadow can be seen on the opacity with oblique
illumination.
IV. Intumescent Cataract
V Sometime during the course maturation the lens imbibes lot of fluid
and becomes swollen.
V Anterior chamber becomes shallow.
V Angle of anterior chamber may close resulting in glaucoma
(Phacomorphic Glaucoma).
V. Mature Cataract
V Entire cortex becomes opaque.
V Vision reduced to just perception of light
V Iris shadow is not seen
V Lens appears pearly white.
Nuclear Cataract
Goes through stage of immaturity and maturity but never becomes
intumescent or hypermature.
Urochrome or melanin pigment deposition may take place giving nucleus a
typical color:
V Yellow
V Black (Cataracta nigra)
V Brown (Cataracta brunescnence)
V Red (Cataracta rubra)
In early stages there is shift of refraction towards myopia. This improves the
near vision of the patient. Consequently the patient who so far required thick
near glasses for reading, can read small print easily without them
(phenomenon of Second Sight).
Clinical Presentation
Symptoms
Glare: When patient looks at a point source of bright light the diffusion of white
and colored light around it drastically reduces vision. Night driving becomes
especially troublesome. Posterior subcapsular cataract (cupuliform) notably
causes disabling glare.
Diplopia / Polyopia: Multiple images of one object may form on the retina due
to irregular refraction from the cataractous lens giving rise to Monocular
Diplopia or Polyopia. This can be differentiated from binocular diplopia by
cover-test and pin-hole test. Binocular diplopia disappears on covering any of
the eye. Monocular diplopia does not disappear if the other eye is covered,
however, it disappears if a pin-hole is placed in front of this eye.
Altered Color Perception: The yellowing of lens nucleus is steadily progressive
leading to change in color saturation of the image seen. The artists with
cataract may render their paintings browner or yellower than real.
Black Spots: Patient may complaint of seeing black spots fixed in his field of
vision. This is unlike black spots seen in vitreo-retinal disorders, which seem to
move around as floaters (muscae volitantes).
Behavioral Changes: Seen especially in children with cataract, who can not
verbalize their complaints. Stumbling over objects, poor performance in
school, loss of interest in surroundings, etc. can be some of the changes that
may draw parents attention towards child’s visual handicap.
Signs
Leukocoria: “White pupil”, infact the pupil appears grayish white in immature,
pearly white in mature and milky white in hypermature stages of cataract.
Cornea & Conjunctiva: These are usually normal. Cornea may become hazy
due to edema if the IOP is increased by lens induced glaucoma. Conjunctiva
may be congested in lens induced glaucoma or uveitis, or if there is
associated infection.
Other Signs: Signs of aging may be observed along with cataract and are just
co-incidental e.g., arcus senilis, skin laxity (dermatochalasis), senile entropion
or ectropion, senile ptosis, age related macular degeneration (ARMD), grayish
white granular material on lens surface or iris in pseudoexfoliation, scrolls of
split layers of anterior capsule (exfoliation), tremulous lens (Phacodonesis) if
the zonules are very lax or broken, dry eye syndrome, etc.
Complications of Cataract
Investigation
It involves further evaluation of the eye and general condition of the patient
with regards to the feasibility and prognosis of surgical management of
cataract.
Pupillary Reflexes: Special emphasis is placed on examining the pupillary signs
as they may reveal presence of any visual pathway (afferent) or 3rd nerve
(efferent) disorder. This may affect the final visual outcome e.g., afferent
pupillary defect caused by optic atrophy may prognosticate poor visual result.
Special care should be taken to look for presence of Marcus-Gunn Pupil in which
although both direct and consensual reflexes are present in both the eyes and
pupils appear to be normal, yet on doing swinging flash light test (i.e. rapidly
shifting light from one eye to the other and back) one pupil seems to dilate in
response to light whereas the other constricts. This denotes presence of a
relative afferent pupillary defect (RAPD) in the eye whose pupil seems to dilate.
Note that the defect is partial and unequal in the two eyes.
Intraocular Pressure: Presence of lens induced glaucoma or co-existent primary
glaucoma should always be looked for because increased IOP seriously affect
the course and result of surgery. The IOP has to be well under control before
the surgery for cataract is under-taken because not only high pressure
increases the risk of intra-operative complications (viz. Vitreous loss, expulsive
hemorrhage, etc.) but also there is a high risk of loosing vision (or visual field)
postoperatively as the IOP tends to rise to high level about 2 hours after
cataract operation even in an otherwise normal eye.
Blood Sugar: Diabetes must be ruled out, and if present must be controlled
before surgery. Diabetes can adversely affect any part of the eye especially the
retina (diabetic retinopathy), wound healing is impaired and the risk of infection
is extremely high. Blood sugar should be carefully monitored and kept in strict
control in the peri-operative period.
On the day of operation, however, the anti-diabetics (hypoglycemics) are
omitted to avoid the chance of severe hypoglycemia, and are resumed from the
first postoperative day.
patient’s lens. Then the width of these fringes is reduced and the
narrowest fringes seen by the patient are indicative of his visual
potential.
V Visually Evoked Response (VER): Stimulation of retina by light pattern
leads to suppression of alpha-wave of the EEG recorded from the
occipital cortex. The smallest pattern stimulus which generates this
response denotes the potential vision of the patient. Other
electrophysiological tests can also be used to assess the function of
the macula especially Electroretinogram (ERG) with focal foveal
stimulation.
9. Ultrasonography (USG B-Scan): If the cataract is advanced then the retina
cannot be visualized by ophthalmoscopy, therefore, ultrasound (B-scan) is
used to detect any structural abnormalities.
10. Intraocular Lens Power Calculation: The power of the intraocular lens to be
implanted has to be calculated for each individual.
Three parameters are required as follows:
V Keratometry (K): gives the refractive power of the cornea (in diopters),
using an instrument called Keratometer.
V Biometry or Axial Length of Globe (L): The distance (in mm) from the
apex of cornea to the posterior pole of the eye is measured by a
special ultrasound the A-Scan Biometer.
V A Constant (A): It is supplied by the IOL manufacturer and it’s value
depend on the design of the lens and it’s intended location in the
eye (anterior or posterior chambers).
These values are put in a formula (SRK Formula) to get the power of the lens
to be implanted:
IOL Power = A – 2.5L – 0.9 K
This would make the patient emmetropic. However, in some cases it is
desirable to deliberatively induce a preplanned refractive error postoperatively
e.g. when the other eye has a high refractive error then the planned refractive
error in eye to be operated should be within + 2.5 dioptre of the other eye, in
order to avoid anisometropia (unequal refrctive error) and aniseikonia
(unequal image size).
Classified in 3 groups:
I. Optical indications
Whenever the vision of the patient is diminished to an extent that it interferes
with his normal daily life, the cataract can be operated. There is no sharp cut-
off level of visual acuity below which cataract should be operated rather the
decision about timing of surgery is subjective to the patient’s own visual
requirement. A word of caution here is that in mild diminution of vision e.g. 6/
12, patient should be informed about the disadvantage of loss of
accommodation that results from cataract surgery, which may offset the
advantage of gain of 2-3 lines in visual acuity. Glare is another optical
indication especially in individuals involved in night driving.
V Hypermature cataract
V Lens induced glaucoma
V Lens induced uveitis
V Dislocated / subluxated lens
V Intra-lenticular foreign body
V Diabetic Retinopathy to give Laser photocoagulation
V Retinal Detachment or any other posterior segment pathology, the
dignosis or treatment of which is being hindered by opacity of the lens.
Choice of Operation
The operation of choice for cataract is:
Extra-Capsular Cataract Extraction with Posterior Chamber Lens
Implantation
Or simply
ECCE with PCL
Unless contraindicated or better technique (Phacoemulsification &
Foldable IOL) is available.
intact posterior capsule, peripheral part of the anterior capsule and the
zonules. This not only provides support of placement of IOL but also
prevents vitreous from bulging forwards and acts as a barrier between
anterior and posterior segment. All this results in decreasing the incidence
of complications viz. Vitreous loss, corneal edema, endophthalmitis,
cystoid macular edema, aphakic glaucoma, etc. However, capsular
remnants are prone to develop after-cataract.
Phacoemulsification
It is essentially an advancement in the method of doing ECCE. Here the
nucleus is converted into pulp or emulsified using high frequency (40,000
MHz) sound waves, and then is sucked out of the eye through a small (3.2
mm) incision. A special foldable IOL is then inserted into the posterior
chamber through the same incision. The advantages being no or
negligible surgically induced astigmatism and rapid recovery of the
patient.
In contrast to this, in conventional ECCE the incision is large (about 8
mm), therefore, surgical astigmatism poses problems postoperatively and
the wound healing being slow, the visual rehabilitation of the patient is
delayed to about 6-8 weeks.
So, if facilities are available, phacoemulsification is the choice of operation
for cataract.
ECCE ICCE
Lens removal Nucleus removed out of the Lens removed as single piece within its
capsule and cortex sucked out capsule
Posterior capsule & zonules Intact
Incision Smaller (8 mm) Removed
Peripheral iridectomy Not performed Larger (10 mm)
Sophisticated equipment Required Required to avoid pupillary block glaucoma
Time taken More Not required
IOL Implantation Posterior chamber Less
Anterior chamber (with its associated risk of
damage to corneal endothelium leading to
Expertise required Difficult technique Pseudo-phakic Bullous Keratopathy)
Cost More Easier to learn
Complications which are After-Cataract Less
increased Vitreous prolapse & loss Cystoid Macular
Edema Endophthalmitis Aphakic Glaucoma
Fibrous & Endothelial ingrowth Neovascular
Compications which are All the complications mentioned Glaucoma in Proliferative Diabetic Retinopathy
decreased for ICCE After-Cataract
Dislocated Lens Subluxated Lens (>1/3rd
Indications A routine procedure for all zonules broken) Chronic Lens Induced Uveitis
forms of cataract (except where Hypermature Shrunken Cataract with thick
contra-indicated) anterior capsule Intra-lenticular Foreign Body
when integrity of posterior capsule is
Contraindications Dislocated lens Subluxated lens compromised.
(>1/3rd zonules broken) Young Patients (<35 years) who have strong
attachment between lens and vitreous
(Ligament of Weigert)
Preoperative Preparation
Anesthesia
Most cases of cataract are operated under local anesthesia except in young
children. The techniques used are:
Retrobulbar anesthesia.*
Peribulbar anesthesia
Facial nerve block*
* These two are given in combination.
Effects:
Analgesia
Akinesia
Mydriasis
Decrease in IOP
Loss of Oculo-cardiac reflex (reflex stimulation of vagus caused by painful
stimulus of the globe or pulling of muscle, which leads to bradycardia and
can even cause cardiac arrest).
Complications:
Infection
V Peribulbar Anesthesia
This technique virtually eliminates the risk of above complications. With patient
looking straight ahead, a point is chosen 2 mm the junction of medial 2/3rd and
lateral 1/3rd of the inferior orbital margin. A 26 G 1 inch needle is introduced
vertically in completely and 5 mL of the above anesthetic solution is injected. Then
another point is chosen diagonally opposite to it i.e., 2 mm below the junction of
medial 1/3rd and lateral 2/3rd of the superior orbital margin and 3 mL of the
solution is injected. Intermittent pressure is applied as described above.
V Facial Nerve Block
The technique commonly used is called O’Briens Technique. The condylar process
of the mandible is palpated anterior to the tragus by asking the patient to open
and close his mouth. A point is chosen 1 cm below this marking the position of
neck of the mandible. A 23 G needle is introduced at this point till it strikes the
bone (neck of mandible) and then withdrawn a little. 5 mL of the above anesthetic
solution is injected at this point and the needle withdrawn. The effect of the block
is observed by asking to forcibly close his eyes or to show his teeth, an inability to
close the eye or angulation of mouth to the other side indicated blockage of facial
nerve. This prevents squeezing of the eyes by the patient. However, with
peribulbar anesthesia facial block is not required because some anesthetic solution
diffuses directly into the orbicularis oculi muscle and cause its anesthesia.
V Extra-Capsular Cataract Extraction
After anesthesia the eye is cleaned with Povidone-Iodine solution 5% and a sterile
drape is put to isolate the surgical field. Povidone-Iodine 2% is irrigated in the
conjunctival sac and washed with Normal Saline.
V Eye-lids are retracted using a wire speculum.
Superior rectus bridle suture is passed to turn the superior limbus down and
stabilize the globe. Superior rectus forceps are used to hold the insertion of
superior rectus and a 4.0 Silk suture is passed under it.
V Fornix based conjunctival flap is raised by cutting the conjunctiva where it is
attached to the limbus from 10 O’clock to 2 O’clock meridian. Bleeding points and
large vessels are coagulated using a bipolar electro-cautery.
V A groove or partial thickness incision is made at the limbus (mid or blue limbus)
using a piece of razor mounted on blade breaker-holder. This groove extends from
10 O’clock to 2 O’clock meridian and is perpendicular to the limbal surface.
V Anterior chamber is entered by stabbing within this groove at the 11 O’clock
meridian keeping the blade obliquely (parallel to iris plane). Thus the incision gets
a two plane or bi-planar configuration.
V A visco-elastic fluid (Poly-propyl hydroxy methyl cellulose or sodium hyaluronate) is
injected into the anterior chamber. This fluid coats the corneal endothelium
preventing any damage to it, and deepens the anterior chamber giving more
working space.
V An opening is made in the anterior capsule of the lens called the anterior
capsulotomy, using a bent hypodermic 26 or 30 G needle. There are various
techniques of performing anterior capsulotomy e.g., bear-can opener, Christmas
tree, envelope, capsulorrhexis, etc.
V The limbal incision or section is enlarged by cutting in the groove to its entire
extent, using a corneal scissors keeping its blades parallel to the iris plane. So a bi-
planar incision is made extending from 10 O’clock to 2 O’clock meridian.
V The nucleus is expressed by applying alternating pressure at 12 O’clock and 6
O’clock meridian.
V The cortex which remains is removed by suction. This is performed by a special
cannula called the IA Cannula (Irrigation-Aspiration) which has two channels in it;
one for the fluid to go in (irrigation) and second for the fluid and cortex to be
Postoperative Care
24 hours after the operation the bandage is removed and the eye is cleaned.
The eye is examined thoroughly with special emphasis on the visual acuity,
discharge in conjunctival sac, apposition of the wound, corneal clarity, anterior
chamber for depth and hyphaema, etc., pupil, IOL, posterior capsule, retina
and intra-ocular pressure. If any problem is encountered, it has to be dealt
with appropriately.
Topical antibiotic-steroid eye drops are advised to be instilled every 4-6 hourly
and ointment to be instilled at bed time. These drugs are used to control
postoperative inflammation and infection, and are gradually tapered over next
4-6 weeks.
Patient is instructed to avoid head-bath for 1 week, lifting heavy weights for
about 3 months and abstain from contact-sports for about 1 year.
Complications of Cataract Surgery
These can be grouped as:
Intra-operative
Post-operative
V Early
V Late
Intra-operative Complications
Post-operative Complications
Early
V Corneal edema
V Wound leak
V Iris prolapse
V Shallow or flat anterior chamber
V Hyphaema
V Hypotony
V Glaucoma
V De-centered or displaced IOL
V Endophthalmitis
Late
V After-cataract
V Cystoid macular edema (CME)
V Vitreous touch syndrome
V Vitreous wick syndrome
V Irvine Gass syndrome (vitreous touch or wick & CME)
V UGH syndrome (uveitis, glaucoma and hyphaema)
V Bullous Keratopathy
V Glaucoma
V Visual Rehabilitation after Cataract Surgery (Aphakia)
The Problem
Removal of the lens from the eye or aphakia leads to:
V Absolute high hypermetropia (caused by loss of about 18 dioptre of
convergence power).
V Astigmatism
V Loss of accommodation
V Altered Color Perception
V More of UV rays (in A-band) reach the retina
V The hypermetropia is high (about 10 dioptre) because of loss of
convergence provided by the lens and it is absolute because no part of it
can be compensated by exertion of accommodation as theaccommodation
is lost.
Rehabilitation
Three methods are mainly used to tackle the problems of aphakia:
Intra-Ocular Lens (IOL)
Spectacles
V Contact-Lenses
V IOL Implantation
This the best method to manage the optical and visual problems of
aphakia. Currently available IOLs are safe, inexpensive and of good
optical quality. Implantation of IOL is easy if done at the time of
removing cataract. As a secondary procedure it may be difficult and
risky. The advantages of IOL become obvious when one looks at the
disadvantages of aphakic spectacles as follows. However, the
problem of loss of accommodation is still not solved with IOLs and
the patient may need to wear near correction for reading (although
multi-focal IOL are available but they are not very successful).
V Aphakic Spectacles
To correct the refractive error in aphakia about 10 dioptre of convex
lenses are required for distance vision and about 13 dioptre for near
vision. Such high power lenses are associated with numerous
physical and optical problems. And these problems become even
more troublesome if the aphakia is unilateral (the other eye being
normal). The most important of these problems are:
V Physical Problems: These glasses are heavy and wearing them
constantly can be associated with great physical discomfort. IOL
does not cause any discomfort.
V Magnification: Each dioptre of convex power leads to about 3 %
magnification of image and a difference of image size between
the two eyes of about 7 % is tolerable. Thus 10 dioptre aphakic
spectacles lead to about 30 % magnification of the image
which give rise to diplopia i.e., two images of one object are
seen one small (from normal eye) and other larger (from
aphakic eye). Moreover, when the objects appear larger they
appear falsely closer than reality, and this leads to physical in-
coordination. In IOL magnification is only about 1-2 %.
V Roving Ring Scotoma: The edge of a convex lens acts as a prism
and the higher the power of the convex lens the greater is the
prism angle (alpha). The light falling on the prism bends
towards its base by an angle alpha/2 , therefore, greater the
angle alpha the more will be the bending. In aphakic
spectacles, the angle alpha being large, the light falling at the
edge of the lens bends towards the center of the lens (base of
prism) and does not reach the pupil and is, therefore, not seen.
This results in an area of the visual field which is not visible to
the patient, or scotoma. And because the edge of the lens is
present all around the lens like a ring, so it gives rise to a ring
shaped scotoma. The position of this scotoma is not fixed in the
visual field because the eye keeps moving (or roving) in relation
to the aphakic spectacle. Hence, the result is a roving ring
scotoma. This is not seen with IOL.
V Jack-in-the-box Phenomenon: The presence of the above
scotoma leads to another interesting phenomenon. If an
interesting object appears in the periphery of the patients
visual field, it appears blurred (because the light is passing from
the side of the spectacle frame). The person tends to move his
head towards the object in order to see it clearly. But as he
turns the head the object comes to lie in the area of scotoma
and thus disappears. As he turns his head further the object
comes to lie in from of the spectacle in the visible area and so
reappears again clear and sharp. This sudden disappearance
and sharp reappearance of the objects is called jack-in-the-box
phenomenon. Not seen with IOL.
V Pin Cushion Effect: The magnification of image is more at the
periphery of the lens due to prism effect. Therefore, all the
objects appear stretched out at the corners like a pin-cushion.
Not seen with IOL.
Contact Lenses
Contact lenses, also, solve most of the problems related to the aphakic
spectacles and reduce the magnification to about 3-4 %. But for the old
patients handling the contact lenses is difficult due poor vision and lack of
physical dexterity. In the young they are a very good alternative to aphakic
spectacles and sometimes the only choice e.g., in unilateral aphakia (in
absence of adequate support for IOL).
Pediatric Cataract
Postoperative Inflammation and Fibrosis: The immune system of the child being
very active responds violently to surgery and thereby, leads to severe
postoperative uveitis and fibrosis. This severely mar the results of operation. To
deal with this problem some surgeons advocate Pars Plana Lensectomy as the
technique of choice for removal of cataract in children. But this technique make
implantation of IOL difficult.
After-cataract: The epithelial cells of the anterior capsule being very actively
dividing a child is very prone to develop dense and thick after-cataract. This can
be very difficult to treat because the children do not cooperate for YAG Laser
treatment and being thick the laser sometimes fail to penetrate it. Therefore,
some surgeons make an opening in the posterior capsule at the end of operation
for cataract (Primary Posterior Capsulotomy).
IOL Power Calculation: As the eyeball of the child is still growing it poses a
problem in calculating the power of the IOL to be implanted as the later is based
on the axial length of the globe. If a IOL of emmetropic power is implanted this
leads to myopia as the child grows up. Therefore, it is recommended that the
child be made hypermetropic by about 3 dioptre, so that as the child grow the
eye becomes nearly emmetropic.
Dislocation of Lens
Causes
Congenital
Familial
Ectopia lentis
Ectopia lentis et pupillae
Marfan’s Syndrome
Weil-Marchesani Syndrome
Homocystinuria
Hyperlysinemia
Sulphite-di-oxide Deficiency
Aniridia
Acquired
Hypermature cataract
Trauma
Chronic uveitis
Intra-ocular tumor
High myopia
Buphthalmos
Treatment
V Spectacles: If the clear lens is subluxated in such a way that most of the
pupil is still occupied by the lens then spectacle correction of the
refractive error is all that requires to be done.
V Extra-capsular Cataract Extraction: If the subluxated lens is cataractous
but only 1/3rd zonules are broken then ECCE with IOL can be done.
V Intra-capsular Cataract Extraction (Wire vectis technique): If more than 1/
3rd zonules are broken or the lens is dilocated into the anterior chamber
then it can be removed by ICCE using the wire vectis technique. An
instrument shaped like a loop of wire is inserted behind the lens to
remove it.
V Pars Plana Surgery: If the lens is dislocated into the vitreous then pars
plana route is used to remove it. The lens is nibbled out if it is soft using a
VISC probe. If lens is hard then it is first brought to anterior chamber from
where it is removed using a wire vectis.
Miscellaneous Conditions of Lens
Lenticonus
Anterior surface of the lens (rarely posterior surface) is projected into a
conical projection giving rise to high myopia. This condition is commonly
associated with renal anomalies in Alport’s Syndrome.
Lens Coloboma
A notch shaped defect is found as a rare congenital anomaly in the
equator of the lens. It can even be acquired if an intra-ocular tumor
presses on the lens.
After-Cataract
Opacification of posterior capsule after ECCE or Pahcoemulsification
caused by proliferation of lens epithelial cells from the anterior capsule, is
called after-cataract. If it leads to significant diminution of vision (> 2 lines
on Snellen’s Chart) then an opening can be created in the posterior
capsule with the help of Nd-YAG Laser (Neodymium - Yttrium Aluminium
Garnet Laset with a wavelength of 1064 nm) by photodisruption. This
opacification may take two characteristic forms: Elschnig’s pearls & Ring of
Sommering.