Diseases of the Lens
Glaucomas
ANATOMY AND PHYSIOLOGY
APPLIED ANATOMY
The lens is a transparent, biconvex, crystalline structure placed between iris tind the vitreous. 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. 1)
Fig. 1. Structure of the crystalline lens.
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 m) and thinnest at the posterior pole (3 m).
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.
(a) Nucleus. It is the central part containing the oldest fibres. It consists of different zones.
Embryonic nucleus is its innermost part (1 to 3 months of gestation). Its fibres meet around the Y-shaped sutures (Fig. 2). Outside the embryonic nucleus, successive nuclear zones are laid down as the development proceeds and, depending on the period of formation, are called as fetal nucleus (corresponding to lens from 3 months gestation till at birth), the infantile nucleus (corresponding to lens from birth to puberty) and the adult nucleus (corresponding to lens in early adult life).
Fig. 2. Y-shaped sutures of the embryonic nuclear fibres
(b) 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 positio: enable the ciliary muscle to act on it.’ are arranged in three groups:
i. The fibres arising from pars plana and ante part of ora serrata pass anteriorly to get insertj anterior to the equator.
ii. The fibres originating from comparative^ anteriorly placed ciliary processes posteriorly to be inserted posterior t« equator.
iii. The third group of fibres passes from] summits of the ciliary processes almost direclB inward to be inserted at the equator.
APPLIED PHYSIOLOGY AND BIOCHEMISTRY
The crystalline lens, being an avascular structure, is dependent for its metabolism on chemical exchanges with the aqueous humour.
The chemical composition of crystalline lens vis-a-vis is aqueous humour and the chemical exch between the two is depicted in Fig. 3.
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Metabolism
Metabolic activity of the lens is largely confined! the cortex and the nucleus is relatively inert. I uses the energy of metabolism for its growth! active transport process. In the lens eighty pert glucose is metabolised anaerobically by the glycolytic pathway, 15 percent by pentose or hexose monophosphate shunt and a small proportion via oxidative Krebs’ citric acid cycle. Sorbitol pathway is relatively inconsequential in the normal lens; however, it is extremely important in the production of cataract in diabetic and galactosemic patients.
CATARACT
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 .
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 sidero-sis) 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.
B. Morphological classification (Fig. 4)
Fig. 4. Morphological shapes of cataract.
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
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. Development cataract may occur from infancy to adolescence. Therefore, such opacities 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 ofteormally formed and remain clear. Congenital and developmental opacities assume most variegated appearance and minute opacities (without visual disturbance) are very common iormal population. These are detected with the beam of slit lamp under full mydriasis.
Etiology
It is not known exactly. 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. These are as follows:
1. Malnutrition during pregnancy has been associated with non-familial zonular cataract.
2. Injections. 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. These include the following:
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 may be classified depending upon the stage of development at which cataract occurred and morphology (shape and pattern) of the opacity. There are numerous varieties of congenital and developmental cataracts. The common ones are described below:
1. 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.
2. Lamellar (zonular) cataract. It is the most common type of congenital cataract, accounting for about 50 percent cases. Here, development of the lens is interfered at a later stage. Typically, this cataract occurs in a zone of foetal nucleus surrounding the embryonic nucleus (Fig. 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.
Fig. 5. Lamellar (zonular) cataract as seen:
A, by oblique illumination;
B, in optical section with the beam of the slit-lamp.
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.
It is usually bilateral and frequently causes severe visual defect.
3. Sutural cataract. It is a comparatively common variety and consists 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:
i. Floriform cataract. Here the opacities are arranged like the petals of a flower.
ii. Coralliform cataract. Here the opacities are arranged in the form of a coral.
iii. Spear-shaped cataract. The lenticular opacities are in the form of scattered heaps of shining crystalline needles.
iv. Anterior axial embryonic cataract occurs as fine dots near the anterior Y-suture.
4. 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.
ii. More commonly, such cataracts are acquired in infantile stage and follow contact of the lens capsule with the back of cornea, usually after perforation due to ophthalmia neonatorum of 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 buried opacity is called ‘imprint’ and the two together constitute reduplicated cataract
5. Posterior polar cataract. It is a very common lens anomaly and consists of a small circular circumscribed opacity involving the posterior pole. This is due to persistence of posterior vascular capsule of the lens.
6. Coronary cataract. 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 iumber 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.
7. Punctate cataract. It is also called blu-dot-cataract or cataracta-punctate-cerulea. 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.
8. Total congenital cataract. It is a common variety and may be unilateral or bilateral. In many cases there may be hereditary characler. 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 Morgagriian 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).
9. 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.
Management of congenital and developmental
cataract
A. What to do and when to do?
1. Small stationary lens opacities, which do not interfere with vision, can safely be ignored.
2. Incomplete central stationary cataracts may be treated by optical iridectomy or use of mydriatics to improve vision considerably.
3.Complete bilateral cataracts should be removed as early as possible (within few weeks of birth) to prevent stimulus deprivation amblyopia.
4. Complete unilateral cataract should also be preferably removed within a few weeks of birth. However, it should be borne in mind that the chances of developing amblyopia with unilateral uncorrected aphakia and unilateral unoperated cataract are equal.
B. Surgical procedures. Childhood cataracts, (congenital, developmental as well as acquired) can be dealt with discission (needling) operation, anterior capsulotomy and aspiration or lensectomy. The needling operation (which was performed in the past) is now almost obsolete.
C. Correction of paediatric aphakia. It is still an unsolved query. The common views are as follows: (i) Children above the age of 5 years can be corrected by implantation of posterior chamber intraocular lens during surgery (ii) Children below the age of 5 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.
D. 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.
ACQUIRED CATARACT
We have studied that congenital and developmental cataracts occur due to disturbance in the formation of the lens fibres, i.e., instead of clear, opaque lens fibres are produced. While, in acquired cataract, opjlgification occurs due to degeneration of the already formed normal fibres. The exact mechanism and reasons for the degeneration of lens fibres are yet not clear. However, in general any factor, physical, chemical or biological, which disturbs the critical intra and extracellular equilibrium of water and electrolytes or deranges the colloid system within the lens fibres, tends to bring about opacification. The factors responsible for disturbing such an equilibrium of the lens fibres vary in different types of acquired cataracts and shall be discussed with the individual type. A few common varieties of acquired cataract are described here.
SENILE CATARACT
Also called as ‘age-related cararact, this is the commonest type of acquired cataract affecting equally persons of either sex usually above the age of 50 years. The condition is usually bilateral, but almost always one eye is affected earlier than the other. Classically, the senile cataract occurs in two forms, the cortical (soft cataract) and the nuclear (hard cataract). The corticalsenile cataract may start as cuneifojm (more commonly) or cupuliform cataract.
It is very common to find nuclear and cortical senile cataracts 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. Anomalous diet as regards 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.
B. Mechanism of loss of transparency. It is basically different iuclear 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 may be as shown below in the flowchart:
Opacification of cortical lens fibres
2. Nuclear senile cataract. In it the usual degenerative changes is intensification of the age-related 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.6). 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.
Fig. 6. Immature senile cataract (cuneiform type): in optical section with the
beam of the slit-lamp.
(b) Cupuliform senile cortical cataract. Here 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 6.) or cupuliform patterns can be recognised till the advanced stage of ISC when opacification becomes more diffuse and irregular. The lens appears greyish white. 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 7).
Fig. 7. Mature senile cataract.
5. Hypermature senile cataract (HMSC). When the mature cataract is left in situ, the stage of hypermaturity sets in. The hypermature cataract occur in any of the two forms:
(a) Morgagnian hypermature cataract: In some patients, after maturity the whole cortex lique-fies and the lens is converted into a bag of milky fluid. The small brownish nucleus settles al bottom, altering its position with change in position of the head. Such a cataract is called Morgagnian cataract (Fig.7). Sometime 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 papillary area. Due to shrinkage of lens, anterior chamber becomes deep and iris becomes tremulous (iridodonesis).
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B. Maturation of nuclear senile cataract
In it the sclerotic process renders the lens inelastic and hard, decreases its ability to accommodate obstructs the light rays. These changes begin centrally and slowly spread peripherally al most 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 brunescenm, Fig.9) or black (cataracta nigra) and rarely red (cataracta rubra) in colour.
Fig.9. Cataracta brunescenm
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 specturm due to presence of water droplets in the lens.
4. Black spots in front of eves. These may be perceived by some patients. These spots are stationary.
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 iature. Patients 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 iear vision is referred to as ‘second sight’. As opacification progresses, vision steadily diminishes, until only perception of light and 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.
2. 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. When-lens is completely transparent completely opaque, no iris shadow is formed. Hence presence of iris shadow is a sign of immature cataract.
3. Oblique illumination examination. It reveals colour of the lens in pupillary area which varies in different types of cataracts.
4. Distant direct ophthalmoscopic examination. 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.
4. Slit-lamp examination should be performed with a fully dilated pupil. The examination reveals complete morphology of opacity (site, size, shape, colour and pattern).
Complications.
1.Phacoanaphylactic uveitis. A hypermature cataract may leak lens proteins into anterior chamber. These proteins may act as antigens and induce antigen-antibody 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. Subluxatian or dislocation of Lens. It may occur due to degeneration of zonules in hypermature stage.
MANAGEMENT OF CATARACT IN ADULTS
Treatment of cataract essentially consists of its surgical removal. However, certaion-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: (i) Adequate control of diabetes mellitus, when discovered. (ii) Removal of cataractogenic drugs such as corticosteroids, phenothiazenes and strong miotics, may delay or prevent cataractogenesis. (iii) Removal of irradiation (infrared or X-rays) may also delay or prevent cataract formation. (iv) Early and adequate treatment of ocular disease like uveitis may prevent 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:
i. Refraction, which often changes with considerable rapidity, should be corrected at frequent intervals.
ii. 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.
iii. Use of dark goggles in patients with central opacities is of great value and comfort when worn outdoors.
iv. 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 focusing. 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. In general, patients with a visual acuity of less than 6/36 (Snellen’s) may be advised surgical management.
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 indicathion. Sometimes patient 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 but before contemplating surgery. This should include:
1. A general overhaul 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, 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:
(a) Retinal function tests. The retinal function must 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 to 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 iature, 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. 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) lntraocular pressure (IOP) measurement. Preoperative evaluation is incomplete without the measurement of IOP. The presence of raised IOP needs a priority management.
Preoperative medication and preparation
1.Topical antibiotics such as tobramycin or gentamicin QID for 3 days just before surgery is advisable as prophylaxis against endophthalmitis.
2. Systemic antibiotics such as gentamicin 80 mg intramuscular at night and in the morning before surgery are preferred by a few surgeons.
3. 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.
4. An informed and detailed consent should be obtained.
5. 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.
6. 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.
7. 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 408).
Types 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 chymotrypsin (which will dissolve the; 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 15 years) it has been almost entirely replaced by planned extracapsular technique. Indications of ICCE are as follows:
1. In developing countries, like
2. If facilities for microsurgery are not available then ICCE is performed in patients beyond the age of 40 years.
3. If surgeon is not trained in microsurgery then ICCE can be performed.
4. Absolute indications are markedly subluxated and dislocated lens.
II. Extracapsular cataract extraction (ECCE)
In this technique, major portion of anterior capsule with epithelium, nucleus and cortex are removet leaving behind intact posterior capsule.
Indications
1. Presently (in general) ECCE is being considered as the procedure of choice over ICCE.
2. The absolute indications of ECCE are:
• When posterior chamber intraocular lens implantation is to be performed.
• In patients having high myopia with degenerated fluid vitreous.
• Patients below the age of 40 years where ICCE is contraindicated due to strong zonules.
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.
METHODS OF EXTRACAPSULAR CATARACT EXTRACTION
1. Discission (Needling)
It is an obsolete operation and so not performed now-a-days. It is mentioned here only for historical interest. It used to be performed in congenital or acquired cataract during childhood. In this technique a cruciate incision was made in the anterior capsule with a Ziegler’s knife, the lens matter was stirred up and left as such for self-absorption. There used to be a high incidence of postoperative complications namely thick after cataract, uveitis and glaucoma.
2. Linear extraction (Curette evacuation)
It is also an obsolete procedure and thus abandoned and again mentioned only for historical interest. Before the modern ECCE, this procedure was performed in patients between the ages of 15 and 35 years of age after full mydriasis. In this technique after opening the anterior chamber a large piece of anterior capsule is removed with a large toothed capsule forceps. Lens matter including nucleus and cortex is expressed out using lens curette or lens spatula and lens expressor. Remaining cortical matter is aspirated with a cannula.
3. Conventional extracapsular cataract extraction
The ECCE is performed under an operating microscope, with full mydriasis. It is the surgery of choice for almost all types of childhood and adult cataracts unless contraindicated.
Absolute indications
1. All patients with cataract below the age of 40 years.
2. Cataract associated with high myopia and degenerated vitreous.
3. When posterior chamber intraocular lens is to be implanted.
4. Patients with history of vitreous prolapse and/or aphakic retinal detachment in previously operated eye.
Absolute contraindications. Markedly subluxated and dislocated lens.
Surgical steps
(a) Initial steps up to making a partial thickness groove at limbus are similar to ICCE except that the size of the limbal groove is slightly smaller (10 to 2 O’clock).
(b) Anterior capsulotomy. It can be performed by any of the following methods: 1. 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 360° (Fig. 10.A).
2. Linear capsulotomy (Envelop 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.
3. 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.
(c) Removal of anterior capsule. It is removed with the help of, a Kelman-McPherson forceps (Fig. 10.B).
(d) Corneoscleral section. It is completed from 2-10 O’ clock position as described in ICCE (Fig. 10.C).
(e) 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.
(f) Removal of nucleus. After hydrodissection the nucleus can be removed by any of the following techniques:
1. Pressure and counter-pressure method. In it the posterior pressure is applied at position with corneal forceps or lens spatula and the nucleus is expressed out by counter-pressure exerted at position with a lens hook (Fig. 10.D).
2. 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.
(g) Aspiration of the cortex. The remaining cortex is aspirated out using a two-way irrigating and aspiration cannula (Fig. 10Е).(h) Rest of the steps from closing the incision till the application of pad and bandage are the same as described in ICCE technique.
Fig. 10. rgical steps of extracapsular cataract extraction with posterior chamber intraocular lens implantation: A, anterior capsulotomy can-opener’s technique; B, removal of anterior capsule; C, completion of corneo-scleral section; D, removal ol nucleus (pressure and counter-pressure method); E, aspiration of cortex; F, insertion of inferior haptic of posterior chamber IOL; G, insertion of superior haptic of PC-IOL; H, dialing of the IOL; I, corneo-scleral suturing.
4. Phacoemulsification
It is presently the most popular method of extracapsular cataract extraction. It differs from the conventional ECCE as follows:
1. Corneoscleral incision required is very small (3 mm). Therefore, sutureless surgery is possible with self-sealing scleral tunnel or clear comeal incision.
2. Continuous curvilinear capsulorrhexis (CCC) of 4-6 mm is preferred over other methods of anterior capsulotomy (Fig. 10.A).
3. Hydrodissection i.e., separation of capsule from the cortex by injecting fluid exactly between tie two (Fig. 10.B) and hydrodelineation i.e., separating nucleus from epinucleus by injecting fluid between the two (Fig. 10.C) are must for phacoemulsification. These procedures facilitate nucleus rotation and manipulation during phacoemulsification.
4. Nucleus is emulsified and aspirated by phacoemulsifier. Phacoemulsifier basically acts through a hollow 1 mm titanium needle which vibrates 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 commoames are ‘chip and flip technique’, ‘divide and conquer technique’ (Fig. 10. D&E) and ‘phaco chop technique’.
5. Remaining cortical lens matter is aspirated with the help of an irrigation-aspiration technique (Fig.10.F).
Laser phacoemulsification. This technique is under trial and perhaps soon may replace the conventional phacoemulsification. In it the lens nucleus is emulsified utilizing laser energy. The advantage of this technique is that the laser energy used to emulsify cataractous lens is not exposed to other intraocular structures (c.f. ultrasonic energy).
Advantages and disadvantages of phacoemulsi-lication vis-a-vis conventional ECCE, The potential advantages of phacoemulsification, compared with conventional ECCE, include more rapid wound healing, short convalescence and early stabilization of refractive error with less astigmatism. The main disadvantages are an expensive machine and a higher incidence of complications by beginners because the technique is relatively difficult to master.
Fig. 10. Surgical steps of pnacoemulsification : A, Continuous curvilinear capsulorrhexis; B, Hydrodissection; C, Hydrodelineation; D&E; Nucleus emulsification by divide and conquer technique (four quadrant cracking);
F, Aspiration of cortex.
CONGENITAL ANOMALIES OF THE LENS
1. Coloboma of the lens. It is seen as a notch in the lower quadrant the of the equator (Fig.11). It is usually unilateral and often hereditary.
2. Congenital ectopia lends.
3. Lenticonus. It is the cone-shaped elevation of the anterior pole (lenticonus anterior, Fig. 12) or posterior pole (lenticonus posterior). Lenticonus anterior may occur in Alport’s syndrome. On distant direct ophthalmoscopy, both present as an oil globule lying in the centre of the red reflex. Slit-lamp examination confirms the diagnosis.
4. Congenital cataract.
5. Microspherophakia. In this condition the lens is spherical in shape (instead of normal biconvex) and small in size. Microspherophakia may occur as an isolated familial condition or as a feature of other syndromesv e.g. Weil-Marchesani or Marfans syndrome.
Fig. 11. Coloboma of the lens.
Fig. 12. Lenticonus anterior.
