Age related Cataract

Age Related Cataract (Senile

Cataract)

Drug Induced Cataract

Traumatic Cataract

By

Prof. Naimatullah Khan KundiHead, Department of Ophthalmology

Khyber Teaching Hospital Peshawar

AGE RELATED CATARACT

(SENILE CATARACT)

Lens & Cataract (Pathology) Aging Chances Age related cataract (Senile Cataract)

Very common cause of visual impairment in older adults

50-70% between ages 60-75yrs Pathogenesis:

Multifactorial and not completely understood. As lens ages its wt. Thickness Accommodative power Lens Nucleus compressed and hardened

(Nuclear Sclerosis) as new layers of cortical fibers as formed concentrically

Lens proteins (Crystallines) – chemically modified and aggregate into high molecular wt. proteins

The resulting proteins aggregates cause: Abrupt fluctuations in refractive index Scatter light rays Reduce transparency Chemical modification of nuclear lens proteins also produce

pigmentation (yellow/brownish hue with advancing ages)

concentration of glutathione and K+, conc. of Na+ and Ca++, Hydration

Lens & Cataract (Pathology)

Types

1. Nuclear

2. Cortical

3. Subcapsular (Posterior)


Lens & Cataract (Pathology)Nuclear In adults past middles ages some degree of nuclear

sclerosis and yellowing is considered physiologically normal. This condition interferes minimally with visual function


Nuclear2. Excessive sclerosis and

yellowing (nuclear sclerosis) cause central opacity. Degree of scleroses, yellowing and opacifications evaluated with SL bio-microscope and examination of red reflex (Pupil dilated)

Nuclear (cont’d)

3. Progression slow

4. BL, (± asymmetric)

5. Visual impairment greater of distance vision

than of near vision

6. refractive index and thus myopic shift in

refraction (Lenticular myopia). This myopic

shift transiently enables presbyopic

individulas to read without spectacles

(second sight)


Nuclear (cont’d)

7. Monocular diplopia:

Abrupt change in the refractive index between the

sclerotic nucleus and the cortex

8. Progressive yellowing of the lens causes poor hue

discrimination esp. at the blue end of the visible

spectrum

9. Photopic retinal function may with advanced nuclear

cataract



10. In very advanced cases the nucleus becomes opaque and

brown (brunescent)


11. Histopathology:

Nucleus homogenous with loss of

celluler laminations.

Cortical Cataract1. Early changes:

Changes in ionic composition + hydration + cortical opacification

2. BL, often Asymmetrical3. First visible signs of cortical cataract

formation (SL bio-microscope) are vacuoles & water clefts in ant. And post. cortex

4. Cuneiform opacities (cortical spokes): wedge shaped, form near the periphery the lens, with pointed ends oriented toward the center



5. Cortical Cataract The cortical spokes appear white when viewed

with SL bio-microscope and dark shadows when viewed by retroillumination.

Lens & Cataract (Pathology) Cortical Cataract (cont’d)

6. Their effect on VA varies greatly,

depending upon the location of the opacity

relative to the visual axis

7. Common symptom: Glare from intense focal light sources (e.g. Car

head light)

8. Monocular diplopia may also result


Cortical Cataract (cont’d)

9. Progression: vary, some times unchanged for prolonged

periods, while others progress rapidly

10. The wedge shaped opacities may enlarge and coalesce to form large cortical opacities.

11. Intumscent Cataract: As lens continues to take up water it may swell


12. Mature Cataract: When the entire lens from the capsule to

the nucleus becomes white and pacified


13. Hypermature

Cataract: when degenerated

and liquefied cortical

material leaks

through the lens

capsule, leaving

capsule wrinkled and

shrunken

14. Morgagnian

Cataract: with further

liquefaction of the

cortex allows free

movements of the

nucleus within the

capsular bag.


Morgagnian cataract


Cortical Cataract (cont’d)

15. Histopathology: Hydropic swelling of the lens fibers

Globules (morgagnian) of eosinophilic

material observed in slit-like spaces

between lens fibers


Posterior Subcapsular (cupuliform) cataract (PSC)

1. PSCs often seen in patients younger

than those presenting with

nuclear/cortical cataracts

2. PSC located in the posterior cortical

layer and is axial in location



3. First indication: subtle iridescent sheen in

the posterior cortical layers (SLB exam)

Later stages:

Granular opacities and

A plaque like opacities of posterior

subcapsular cortex appear


Posterior Subcapsular (cupuliform)cataract (PSC)

Patient complains of glare and

vision

PSC obscures more of the pupillary area

when miosis is induced by: Bright light

Accommodation

Miotics

In bright light



5. Near VA tends to be decreased more than distance VA

6. Some patients experience monocular diplopia

7. Other causes of PSC:1. Age related – main type2. Trauma3. Corticosteroids4. Inflammations5. Ionizing radiations



8. Histopathology

1. Posterior migration of lens epithelial

cells in the posterior sub-capsular

area, with aberrant enlargement

2. These swollen epithelial cells are called Wedl (Bladder) cells

DRUG INDUCED CATARACTS

Drug induced cataracts

1. Corticosteroids

2. Phenothiazines

3. Miotics

4. Amiodarone


Corticosteroids

Long term use of steroids cause PSCs

Occurrence related to:

1. Dose

2. Duration of treatment

3. Susceptibility to steroids (vary)


Corticosteroids (cont’d) Cataract Formation:

Systemic / Topical / Sub-conjunctival Nasal spray Eye lid dermatitis (steroids treatment)

Histopathology: Similar to senescent PSC changes

Some steroid-induced PSCs in children may be reversible with cessation of the drug

Drug induced cataracts Phenothiazines

Chloropromazine, Thioridazine Phenotiazines, a major group of Psycho-tropic medications, can cause

pigmented deposits in the anterior lens epithelium in an axial configuration

Deposits appear to be affected by dose and duration Visual changes associated with phenothiazine are usually insignificant

Drug induced cataracts Miotics

Anticholinesterases (Ecothiophate, demacrium) pilocarpine, phospholine lodide

These can cause cataracts Cataract dose and duration related Cataract may progress to posterior cortical

and nuclear First appears as small vacuoles within and

posterior to the anterior lens capsule and epithelium (Best appreciated by retroillumiunation)


Miotics Visually significant cataracts common

in elderly patients (Topical

anticholinesterase)

Progressive cataract not reported in

children (Echothiophate for

accommodative esotropia)


Amiodarone

Antiarrythmia medication has been

reported to cause stellate anterior

axial pigment deposition (Visually

insignificant)

TRAUMATIC CATARACT

Traumatic Cataract

Traumatic lens damage may be caused

by:

1. Mechanical injury

2. Physical forces Radiation

Electrical current

Chemicals

3. Osmotic influences (diabetes mellitus)

Traumatic Cataract

Contusion (Blunt injury)

Vossius ring Blunt trauma to eye can sometimes cause

pigment from pupillary ruff to be imprinted

on anterior lens surface in a ring shape

It is visually insignificant

It indicates previous trauma

Vossius ring due to blunt trauma

Traumatic Cataract

Contusion (Blunt injury) Blunt, non perforating

injury may cause lens opacification (acute event / late sequela)

Cataract may involve a portion or entire lens

Often the initial manifestation is a stellate / rosette-shaped opacification, axial in location (PSC)

Traumatic Cataract

Contusion (Blunt injury) Rosette cataract may progress to

opacification of entire lens

In some cases lens capsule may be

ruptured by the force of blunt

trauma, with subsequent hydration

and rapid opacification of the lens

Traumatic Cataract

Contusion (Blunt injury) Perforating and penetrating injuries

Penetrating injury of lens often results in

opacification of cortex at site of rupture,

progressing rapidly to complete

opacification

A small perforating injury of the lens capsule

may heal, resulting in a small focal cortical

cataract

Radiation-induced cataracts

Ionizing radiations Lens is extremely sensitive to

ionizing radiations Cataract clinically apparent after

period of up to 20 yrs Latency related to:

Dose and Age of patient A young patient with more actively

growing lens cells is more susceptible


Ionizing radiations (cont’d)

Clinically: Punctate opacities within posterior

capsule and feathery anterior sub-capsular opacities that radiate towards the equator of the lens

These may progress to complete opacification

Radiation-induced cataracts Infra-red radiations (Glasses

blower’s cataract)

Intense heat and infra-red radiations

cause outer layer of the anterior

capsule to peel off as a single layer

(true exfoliation) May be associated with cortical

cataract Rarely seen today


Ultra-voilet radiations (UV)

Prolong exposure to UV radiations in

the UVB range (Sun exposure) is

associated with risk of:

Cortical

PSCs

(Epidemiologic Evidence)

Radiation-induced cataracts Micro-wave Radiations

Non-ionizing radiations with wavelength between IR and short waves on the electromagnetic spectrum

No evidence of cataract by microwaves Biological effect – thermal Microwaves could theoretically cause

cataract: Dose levels would be so high as to induce

hyperthermic brain damage

Chemical injuries Alkalis and Acids Alkalis injuries to ocular surface result in cataract Alkalis compounds penetrate eye readly causing:

1. Aqueous pH

2. Aqueous Glucose

3. Aqueous Ascorbate

Cortical cataract: Acutely or delayed effect Associated injuries: Damage to cornea,

conjunctiva, iris etc. Acids: Tends penetrate eye less easily than alkali Acid injuries are less likely to result in cataract

formation

Health & Medicine

Age related Cataract