Sunday, October 28, 2007

Senile Cataract by Dr.Kundi

Age Related Cataract (Senile Cataract)Drug Induced CataractTraumatic Cataract
By
Prof. Naimatullah Khan Kundi
Head, 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 & Cataract (Pathology)
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
Nuclear
Cortical
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
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)
Lens & Cataract (Pathology)
Nuclear (cont’d)
Progression slow
BL, (± asymmetric)
Visual impairment greater of distance vision than of near vision
­ 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)
Monocular diplopia:
Abrupt change in the refractive index between the sclerotic nucleus and the cortex
Progressive yellowing of the lens causes poor hue discrimination esp. at the blue end of the visible spectrum
Photopic retinal function may ¯ with advanced nuclear cataract
Lens & Cataract (Pathology)
In very advanced cases the nucleus becomes opaque and brown (brunescent)
Lens & Cataract (Pathology)
Histopathology:
Nucleus homogenous with loss of celluler laminations.

Lens & Cataract (Pathology)
Cortical Cataract
Early changes:
Changes in ionic composition + hydration + cortical opacification
BL, often Asymmetrical
First visible signs of cortical cataract formation (SL bio-microscope) are vacuoles & water clefts in ant. And post. cortex
Cuneiform opacities (cortical spokes): wedge shaped, form near the periphery the lens, with pointed ends oriented toward the center
Lens & Cataract (Pathology)
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)
Their effect on VA varies greatly, depending upon the location of the opacity relative to the visual axis
Common symptom:
Glare from intense focal light sources (e.g. Car head light)
Monocular diplopia may also result
Cortical Cataract (cont’d)
Progression:
vary, some times unchanged for prolonged periods, while others progress rapidly
The wedge shaped opacities may enlarge and coalesce to form large cortical opacities.
Intumscent Cataract:
As lens continues to take up water it may swell
Lens & Cataract (Pathology)
Mature Cataract:
When the entire lens from the capsule to the nucleus becomes white and pacified
Lens & Cataract (Pathology)
Hypermature Cataract:
when degenerated and liquefied cortical material leaks through the lens capsule, leaving capsule wrinkled and shrunken
Lens & Cataract (Pathology)
Morgagnian Cataract:
with further liquefaction of the cortex allows free movements of the nucleus within the capsular bag.

Lens & Cataract (Pathology)
Cortical Cataract (cont’d)
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)
PSCs often seen in patients younger than those presenting with nuclear/cortical cataracts
PSC located in the posterior cortical layer and is axial in location
Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform)
cataract (PSC)
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
Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform) cataract
(PSC)
Near VA tends to be decreased more than distance VA
Some patients experience monocular diplopia
Other causes of PSC:
Age related – main type
Trauma
Corticosteroids
Inflammations
Ionizing radiations
Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform) cataract
(PSC)
Histopathology
Posterior migration of lens epithelial cells in the posterior sub-capsular area, with aberrant enlargement
These swollen epithelial cells are called Wedl (Bladder) cells
DRUG INDUCED CATARACTS
Drug induced cataracts
Corticosteroids
Phenothiazines
Miotics
Amiodarone
Drug induced cataracts
Corticosteroids
Long term use of steroids cause PSCs
Occurrence related to:
Dose
Duration of treatment
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:
Mechanical injury
Physical forces
Radiation
Electrical current
Chemicals
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
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:
­ Aqueous pH
¯ Aqueous Glucose
¯ 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

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