Age related Cataract

This presentation is original uploaded to http://kpkmedicalcolleges.tk by Dr.Suleman

1. Age Related Cataract (Senile Cataract)
Drug Induced Cataract
Traumatic Cataract
By
Prof. Naimatullah Khan Kundi
Head, Department of Ophthalmology
Khyber Teaching Hospital
Peshawar

2. AGE RELATED
CATARACT
(SENILE CATARACT)

3. 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

4. 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)

5. Types
1.Nuclear
2.Cortical
3.Subcapsular (Posterior)
Lens & Cataract (Pathology)

6. 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

7. Lens & Cataract (Pathology)
Nuclear
2.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)

8. 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)
Lens & Cataract (Pathology)

9. Nuclear (cont’d)
7.Monocular diplopia:

Abrupt change in the refractive index between the sclerotic
nucleus and the cortex
7.Progressive yellowing of the lens causes poor hue
discrimination esp. at the blue end of the visible spectrum
8.Photopic retinal function may ¯ with advanced nuclear
cataract
Lens & Cataract (Pathology)

10. Lens & Cataract (Pathology)
10.In very advanced cases the nucleus becomes opaque and brown
(brunescent)

11. Lens & Cataract (Pathology)
11.Histopathology:

Nucleus homogenous with loss of celluler
laminations.

12. Cortical Cataract
1.Early changes:
Changes in ionic composition + hydration + cortical
opacification
2.BL, often Asymmetrical
3.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
Lens & Cataract (Pathology)

13. Lens & Cataract (Pathology)
5.Cortical Cataract

The cortical spokes appear white when viewed with SL
bio-microscope and dark shadows when viewed by
retroillumination.

14. 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

15. Lens & Cataract (Pathology)
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

16. Lens & Cataract (Pathology)
12.Mature Cataract:
When the entire lens from the capsule to the
nucleus becomes white and pacified

17. Lens & Cataract (Pathology)
13.Hypermature Cataract:
when degenerated and
liquefied cortical
material leaks through
the lens capsule,
leaving capsule
wrinkled and shrunken

18. 14.Morgagnian Cataract:
with further liquefaction
of the cortex allows free
movements of the
nucleus within the
capsular bag.
Lens & Cataract (Pathology)

19. Morgagnian cataract

20. Lens & Cataract (Pathology)
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

21. Lens & Cataract (Pathology)
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

22. Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform)
cataract (PSC)
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

23. Lens & Cataract (Pathology)
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

24. Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform) cataract
(PSC)
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 type
2.Trauma
3.Corticosteroids
4.Inflammations
5.Ionizing radiations

25. Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform) cataract
(PSC)
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

26. DRUG INDUCED
CATARACTS

27. Drug induced cataracts
1.Corticosteroids
2.Phenothiazines
3.Miotics
4.Amiodarone

28. Drug induced cataracts
Corticosteroids

Long term use of steroids cause PSCs

Occurrence related to:
1.Dose
2.Duration of treatment
3.Susceptibility to steroids (vary)

29. Drug induced cataracts
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

30. 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

31. 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)

32. Drug induced cataracts
Miotics
Visually significant cataracts common in
elderly patients (Topical
anticholinesterase)
Progressive cataract not reported in
children (Echothiophate for
accommodative esotropia)

33. Drug induced cataracts
Amiodarone
Antiarrythmia medication has been
reported to cause stellate anterior axial
pigment deposition (Visually insignificant)

34. TRAUMATIC CATARACT

35. Traumatic Cataract
Traumatic lens damage may be caused by:
1.Mechanical injury
2.Physical forces
Radiation
Electrical current
Chemicals
3.Osmotic influences (diabetes mellitus)

36. 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

37. Vossius ring due to blunt trauma

38. 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)

39. 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

40. 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

41. 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

42. Radiation-induced cataracts
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

43. 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

44. Radiation-induced cataracts
Ultra-voilet radiations (UV)
Prolong exposure to UV radiations in the
UVB range (Sun exposure) is associated
with ­ risk of:

Cortical

PSCs

(Epidemiologic Evidence)

45. 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

46. 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