Lens and Cataract

Dr. Sanjay Dhawan
MBBS, MS (Gold Medallist) DO

Cataract

URL http://sdhawan.com/ophthalmology/lens.html
E-mail: sdhawan@sdhawan.com

Topics of Study

1.      I. Cataract

Causes of Cataract

Global / National distribution & population characteristics of Cataract

Diagnosis of cataract. Distinction between immature, mature and hypermature.

Appropriate referral of cataract patient

Outline of surgical management

Visual rehabilitation of Aphakia

Outline of cataract management in young age

2.      II. Congenital Abnormalities of Lens

Ectopia Lentis (Subluxation & Dislocation)

Lenticonus

Crystalline Lens

Embryology

Derived from surface Ectoderm overlying the optic vesicle.

Ectoderm invaginates and break from surface as two layer structure

Basement membrane of epithelium, which is now on the outer side, forms the lens capsule.

Posterior epithelium cells expand to form the embryonic nucleus.

Anterior epithelium continues to regenerate and develop lens fibers throughout life. These fibers continue to get deposited inwards making earliest fibers the deepest.

Anatomy

A globular structure lies behind the iris and in a concavity in the anterior face of vitreous called the Patellar Fossa.

Suspended from the ciliary processes by Zonules

In young patients (< 35 years) lens is adherent to vitreous by Ligament of Weigert.

·        Layers (from without inwards):

  1. Lens capsule (thinnest at posterior pole)
  2. Epithelium (missing from posterior surface)
  3. Cortex
  4. Epinuclear Cortex
  5. Nucleus (from without inwards):

Adult

Adolescent

Infantile

Fetal (contains anterior & posterior Y-sutures)

Embryonic

·        Epithelium divides most actively in the periphery and differentiates in the lens fibers.

Physiology

·        Functions:

  1. Refraction of light (+18 D)
  2. Accommodation: ability to increase refractive power in order to focus near objects.

Metabolism is both aerobic and anaerobic.

Cations and fluid move actively across anterior capsule but passively across posterior capsule (Pump-Leak Mechanism).

Metabolic homeostasis is essential for maintenance of lens transparency.

Glutathione, glutathione reductase and super-oxide dismutase are actively involved in preventing damage from free O2 radical injury.

Optics

+ 18 Dioptre of refraction is contributed by the lens. And in accommodation this power increases.

Typical structure of lens in the form of anterior cortex, nucleus and posterior cortex is optically important as each of these three portions act as a separate lens (lenticules) because the refractive index of nucleus is more than that of cortex. This results in an increase in the total power of the lens, decrease in optical aberration and greater effectiveness of the accommodation.

Accommodation: Contraction of ciliary muscles results in laxity of zonules, which leads to increase convexity of lens due to its inherent elasticity.

Iris not only controls the amount of light that enters the eye by varying the size of pupil (aperture) but also covers the periphery of the lens thereby cutting the optical (spherical) aberrations from it.

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

Etiological

Morphological

Stage of Maturity

Chronological

Etiological Classification

1.      1. Senile

2.      2. Traumatic

Penetrating

Concussion (Rosette Cataract)

Infrared irradiation (Glass Blower’s Cataract)

Electrocution

Ionizing Radiation

3.      3. Metabolic

Diabetes (Snow Storm Cataract)

Hypoglycaemia

Galactosemia (Oil Drop Cataract)

Galactokinase Deficiency

Mannosidosis

Fabry’s Disease

Lowe’s Syndrome

Wilson’s Disease (Sunflower Cataract)

Hypocalcaemia

4.      4. Toxic

Corticosteroids

Chlorpromazine

Miotics

Busulphan

Gold

Amiodarone

5.      5. Complicated

Anterior Uveitis

Hereditary Retinal & Vitreoretinal Disorders

High Myopia

Glaucomflecken

Intraocular Neoplasia

6.      6. Maternal Infections

Rubella

Toxoplasmosis

Cytomegalovirus

7.      7. Maternal Drug Ingestion

Thalidomide

Corticosteroid

8.      8. Presenile Cataract

Myotonic Dystrophy

Atopic Dermatitis (Syndermatotic Cataract)

GPUT & GK Enzyme Deficiencies

9.      9. Syndromes with Cataract

Down’s Syndrome

Werner’s Syndrome

Rothmund’s Syndrome

Lowe’s Syndrome

10. 10. Hereditary

11. 11. Secondary Cataract

·        After-Cataract (after the cataract surgery)

Morphological Classification

1.      1. Capsular

Congenital (Anterior Polar & Posterior Polar)

Acquired

2.      2. Subcapsular

Posterior Subcapsular (Cupuliform)

Anterior Subcapsular

3.      3. Nuclear

Congenital (Discoid, etc.)

Senile

4.      4. Cortical

Congenital (Coronary, Coralliform, etc)

Senile (Cuneiform)

5.      5. Lamellar or Zonular

6.      6. Sutural

7.      7. Others

Blue-Dot (Cataracta caerulea)

Membranous

Cataracta Pulveranta Centralis

Reduplicated Cataract

Stage of Maturity

1.      Immature

2.      Mature

3.      Intumescent

4.      Hypermature

5.      Morgagnian

Chronological

1.      Congenital (since birth)

2.      Infantile (first year of life)

3.      Juvenile (1 to 13 years of life)

4.      Presenile (13 to 35 years of life)

5.      Senile

Pathogenesis

Two main pathogenetic processes are involved in most (especially senile) cataract:

1.      Hydration

2.      Sclerosis

Hydration

Increased hydration leads to lamellar separation and collection of protein-deficient fluid between lens fibers.

Leads to increased scattering of light and loss of transparency.

Hydration also leads to denaturation of lens proteins and results in irreversible opacification.

Mechanisms of increased hydration are:
  1. Failure of active pump mechanism
  2. Increased leakage across posterior or anterior capsule
  3. Increased Osmotic pressure

Sclerosis

This process is seen mostly in senile cataract and involves predominantly the nucleus.

Increased compaction of lens proteins and fibers due to inter-lamellar binding of proteins by sulfide bonds.

Resultant aggregates of very high molecular weight proteins lead to increased scattering of light and loss of transparency.

It is part of normal aging phenomenon.

Senile Cataract

Epidemiology

Global

38 million people are blind

41 % because of cataract

National

71 % of blindness in Nepal is because of cataract

About 72 % of blindness in India is caused by Cataract

Progression

I.                     I.Stage of Lamellar Separation

Hydration leads to separation of cortex from nucleus

Appreciated on slit lamp biomicroscopy

II.                   II. Stage of Incipient Cataract

Early opacities appear

Vision unaffected but other symptoms e.g., glare, appear.

III.                  III. Immature Cataract

·        Opacification leading to diminution of vision.

·        Two morphological forms are seen:

1.      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.      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.

Lens appears grayish white in color.

Iris shadow can be seen on the opacity with oblique illumination.

IV.               IV. Intumescent Cataract

Sometime during the course maturation the lens imbibes lot of fluid and becomes swollen.

Anterior chamber becomes shallow.

Angle of anterior chamber may close resulting in glaucoma (Phacomorphic Glaucoma).

V.                 V. Mature Cataract

Entire cortex becomes opaque.

Vision reduced to just perception of light

Iris shadow is not seen

Lens appears pearly white.

VI.               VI. Hypermature Cataract

·        This may take any of two forms:

1.      1. Liquefactive or Morgagnian Type: The cortex undergoes auto-lytic liquefaction and turns uniformly milky white. The nucleus loses support and settles to the bottom.

2.      2. Sclerotic Cataract: The fluid from the cortex gets absorbed and the lens becomes shrunken. There may be deposition of calcific material on the lens capsule. Anterior chamber deepens and iris becomes tremulous (Iridodonesis). The zonules become weak increasing the risk of subluxation / dislocation of lens.

Liquefied cortex may leak out of the lens resulting in either uveitis or glaucoma (Phacolytic Glaucoma).

Very rarely the entire cortex and nucleus can get completely liquefied and absorbed leaving behind clear anterior and posterior capsules (Pseudo-aphakia). Vision improves to about finger counting at 1 meter.

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:

Yellow

Black (Cataracta nigra)

Brown (Cataracta brunescnence)

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

  1. 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.
  2. Image Blur: Opacification of lens leads to diminution of vision which is characteristically painless and progressive (& does not improve with pin-hole). From a normal of 6/6 the vision continues to deteriorate as the cataract progresses, but as long as the cataract is immature patient will at least be able to count fingers. When cataract matures the vision is reduced to barely perception of light. In hypermature, rarely, the vision may improve a little if the cortex gets absorbed (but not better that finger counting at 1 meter).
    In early stages, however, the near vision may sometimes improve (the phenomenon of Second Sight).
  3. Diurnal Variation of Vision: In central (cupuliform) cataract the vision is worse in bright light of the noon