age related cataract
DESCRIPTION
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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)
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
Lens & Cataract (Pathology)
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)
Lens & Cataract (Pathology)
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
Lens & Cataract (Pathology)
Lens & Cataract (Pathology)
10. In very advanced cases the nucleus becomes opaque and
brown (brunescent)
Lens & Cataract (Pathology)
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
Lens & Cataract (Pathology)
Lens & Cataract (Pathology)
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
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
Lens & Cataract (Pathology)
12. Mature Cataract: When the entire lens from the capsule to
the nucleus becomes white and pacified
Lens & Cataract (Pathology)
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.
Lens & Cataract (Pathology)
Morgagnian cataract
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
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
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
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
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 type2. Trauma3. Corticosteroids4. Inflammations5. Ionizing radiations
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
DRUG INDUCED CATARACTS
Drug induced cataracts
1. Corticosteroids
2. Phenothiazines
3. Miotics
4. Amiodarone
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)
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
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)
Drug induced cataracts
Miotics Visually significant cataracts common
in elderly patients (Topical
anticholinesterase)
Progressive cataract not reported in
children (Echothiophate for
accommodative esotropia)
Drug induced cataracts
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
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
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
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)
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