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Correlate the structure of the lens with its functions.

Define cataract and describe its epidemiology Classify cataract on the basis of morphology,

aetiology and maturity of cataract. Diagnose a case of cataract; describe the

complications of cataract in children and adults.

Describe the surgical procedures for the treatment of age-related cataract and enlist the complications of cataract surgery.

It is a highly organized transparent spheroid

structure that has evolved to perform refraction of the light entering in the eye. It

does not posses nerve, blood vessels or connective

tissue.

Biconvex LensDiameter varies from 8.8 to 9.2 (9mm) Lens grow in size continuously throughout

life. Its weight is about 60 mgm at the birth and up-to 250 mgm by 80 years of age.

Antero-posterior thickness changes with accommodation. Thickness is 4.75 – 5 mm (4.5mm) (un-accommodated) in adults.

Circumference is known as equator

Lens is suspended in eye by Zonules which are inserted on anterior surface of equatorial lens capsule and attached to ciliary body(Pars Plicata-Ciliary Processes) . Zonular fibres are series of fibrillin rich fibre.

Histologically lens consists of three major components:

1. Capsule – is a thick collagenesebasement membrane which is transparent, elastic acellular envelop, thick at anterior pre-equatorial region (21 micron ), thinnest at the posterior pole (4 micron ). Anterior pole is approximately 14 micron thick.

2. Lens Epithelium – It is a single layer of cells lining the anterior capsule and extends to the equatorial lens bow.

Zone of epithelial cells:a. Central – cells do not actively divide,

they divide under pathological conditions only.

b. Pre-equatorial germinal zone : cells rarely divide.

C. Germinal zone: constitute of the stem cell population. The newly formed cells from germinal zone are forced into transitional zone where they elongate and differentiate to form mass of the lens. The lens capsule regulate the transport of metabolite, nutrients and electrolytes to the lens fibers.

3. Lens substance: It constitute the main mass of the lens. It is divided into-

a. Nucleus

b. Cortex

Nucleus: consists of

(i) Embryonic nucleus (it contains primary lens fibres that are formed in lens vesicle)

(ii) Fetal nucleus: it contains embryonic nucleus and all fibres added to the lens before birth

(iii) Infantile nucleus: it contains embryonic , fetal nucleus together with all the fibres added up-to the age of 4 years.

(iv) Adult nucleus: composed of all fibres added before sexual maturation The nucleus consists of densely compacted lens fibres and higher refractive index than cortex.

25 September 2014 11

LENS Anatomy

Capsule

Cortex

3

4

5

6

3 – Adult Nu

4 - Infantile Nu5 – Foetal Nu

6 – Embryonic Nu.

It is located peripherally and is composed of secondary fibres

formed continuously after sexual maturation. It is further divided

into: Deep cortex

Intermediate cortex

Superficial cortex

Lens fibres contain high concentrations of crystalline.

Crystalline represent the major protein of the lens (constitute 90% of total protein content of lens). Crystalline has the following constituents:

Alpha

Beta and,

Gamma

The lens serves two major functions:

Focusing of visible light rays on the foveaAccomodationPreventing damage from ultra-violet radiation by reaching the retina

Lens function and transparency is dependant on the supply of appropriate nutrient to its various structures. Metabolic needs of a adult lens is met by the aqueous and vitreous.

There is continuous transport of ions into and out of the lens.

The transparency is dependent on highly organized structure of lens, dense packing of crystalline. Avascularity, absence of pigments and optimal hydration.

By act of accommodation it changes focusing power. Accommodation occurs by increasing the curvature of anterior surface thereby changing refractive power of lens.

Light transmission and elasticity of lens decreases with age.

Any opacity in the lens or its capsule, whether developmental or acquired is called cataract.

Developmental opacities are usually partial and stationary, whereas acquired opacities are progressive. They progress until the entire lens is involved, but exceptions are well known in both types.

Classification based on EtiologyClassification based on MorphologyClassification based on MaturityClassification based on the Age of onset

Developmental

Acquired

Hereditary

Intrauterine causeso Rubella

o Toxoplasmosis

o CMV

o Steroids

1. Age related (senile)

2. Secondary cataract (Chronic Uveitis, ACG)

3. Cataract associated with ocular diseases

4. Cataract associated with systemic diseases (pre-senile) (Diabetes, galactosemia etc)

5. Traumatic Cataract

6. Drug induced cataract (Steroids and others)

Capsular (Ant and Post)

Subcapsular (Ant and Post)

Nuclear

Cortical

Immature

Mature

Hypermature

Morgagnian

Congenital

Infantile

Juvenile

Presenile

Senile

Senility

Sunlight (specially UV –A and UV-B component)

Severe Diarrheal dehydration

Vitamin A,C, E deficiency

Diabetes

Smoking

Corticosteroids

Genetic

Caused by degeneration and opacification of existing lens fibres, formation of aberrant fibres or deposition of other material in their place.

Factors causing disturbance of critical intra –and extra-cellular equilibrium of water and electrolyte or deranges the colloid system within the fibres tends to bring about opacification.

Fibrous metaplasia of fibres (in complicated cataract)

Epithelial cell necrosis (Glaucomflecken)

Deposition of abnormal products of metabolism, drugs or metals.

Biochemical ProcessesoHydration

oDenaturation of Lens Proteins

o Sclerosis

The Changes in the Epithelial Cells and the Capsule

Changes in the Lenticular Fibres

Sclerosis

1. Blurring of vision2. Frequent change of glasses due to rapid

change in refractive index of the lens 3. Painless, progressive gradual diminution of

vision due to reduction in transparency of the lens

4. Second sight or myopic shift in case of nuclear cataract causing index myopia, improving near vision.

5. Loss or marked diminution of vision in bright sunlight or bright light beam in central posterior subcapsular cataract.

6. Monocular diplopia or polyopia in presence of cortical spoke opacities

7. Glare in posterior subcapsular cortical cataract due to increased scattering of light

8. Colored haloes around the light as seen in cortical cataract due to irregular refractive index in different parts of the lens.

9. Color shift , reds are accentuated

10. Visual field loss, generalized reduction in sensitivity due to loss of transparency

Appearance of Black Spots

Reduction of Visual Fields

Uni ocular Polyopia

Lenticular Myopia

Changes in Colour values

Chronic open angle glaucoma

Macular degeneration

Optic atrophy

Corneal dystrophy

Retinopathy associated with systemic disorders (hypertension or diabetes)

Visual Acuity

Direct Distant Ophthalmoscopy (FundalGlow)

Light Reflex

Slit Lamp Examination

Medical

Surgical

Refraction

Dark Glasses

IndicationsVisual Improvement

Medical Indications

Cosmetic Indications

Couching

Intracapsular Cataract Extraction (ICCE)

Extracapsular Cataract Extraction (ECCE)

Phacoemulsification

Surgical Techniques

Complications

Management of complications

Usually unknown

Maternal (and infantile) malnutrition

Maternal Viral (rubella) infection

Placental Haemorrhage causing deficient oxygenation

Hypocalcaemia

Chromosomal abnormality (Down syndrome)

Metabolic disorders (galactosaemia)

25 September 2014Dr Sanjay Shrivastava 41

Informant – usually parents History of white spot in pupillary area Child is usually brought with history of

diminution of vision / does not recognize objects and parents

Unsteady eyes Deviation of eye Associated symptoms of systemic disease, if

present


Diminished vision (at times it is difficult to establish in very young children)

Lenticular opacity Nystagmus Deviation of eye, usually convergent squint There may be other ocular and systemic

abnormalities in cases of rubella nuclear cataract


I. Investigations:

1. Detailed history

2. Detailed clinical examination- visual status, intra-ocular tension, fundusexamination, B scan ultrasonography to exclude posterior segment abnormality like growth/ retinoblastoma, A scan to determine axial length of the eye, retinoscopy and cover test to exclude squint.


3. Laboratory investigations:

A. Blood Test

Blood glucose, calcium and phosphorus

RBC transferase and Galactokinase levels

TORCH test

Hepatitis B virus


B. Urine analysis:

For reducing substance for galactosaemia

For amino acids (to exclude Lowe syndrome in suspected cases)


B. Treatment

1. Timing of surgery

a. Bilateral Dense cataract – by 6 weeks

b. Bilateral partial – if vision is not significantly affected, surgery may be delayed up to the age of 2 years or up to puberty


c. Uniocular dense cataract- urgent surgery within days

d. Partial Uniocular cataract- if vision is not significantly affected, surgery may be delayed up to the age of 2 years or up to puberty


* Uniocular cataract – if vision is affected then early surgery, preferably within first six weeks of birth with immediate fitting of contact lens.

* Fixation develops between 2-4 months of age, therefore any cataract interfering with vision should be dealt before this age, and the earliest possible time is preferred

* Medical/ Paediatric fitness for anaesthesia should be obtained.


3. Operative procedure

a. Aspiration and irrigation (ECCE)

b. Lensectomy (Pars plana or anterior route)

c. Aspiration and irrigation (ECCE) with primary posterior capsulotomy with partial anterior vitrectomy


4. Post-operative visual rehabilitation:

a. Posterior Chamber IOL (PMMA or acrylic polymer foldable lens) in patients who are more than two years in age, Uniocularcataract where contact lens fitting is not possible/ practical.

b. Contact lens – after surgery for uniocular cataract at very young age.


c. Aphakic Spect- In bilateral cataract operated cases below the age of two years. These cases are implanted posterior chamber IOL as secondary procedure at later age.

d. Occlusion therapy for treatment of amblyopia / prevention of amblyopia.


Posterior capsular opacification

Secondary membrane formation

Proliferation of lens epithelium (Sommerringring)

Glaucoma

Retinal detachment


Aquired (Trauma, Large eye ball, High

Myopia)

Hereditary o Marfans Syndrome

o Homocystinuria

o Weil Marchesani Syndrome

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