3. What is cataract?
• Origin ?
• Opacification .
• most common cause of reversible blindness (51%
worldwide)
4. Aetiology
Acquired
Congenital
Age- related (90%)
Metabolic disease: DM
Traumatic
Toxin: steroid, chlorpromazine
Secondary to ocular disease: uveitis,
acute angle glaucoma.
Genetic and metabolic disease: down’s
syndrome, galactosemia.
Intrauterine infection: rubella.
Ocular anomalies: aniridia.
Hereditary .
?? Smoking, alcohol, and exposure to UV radiation as factor causing cataract progression,
especially nuclear sclerosing cataract
5. Pathophysiology
• Changes in the lens proteins.
•
Chemical modification of these lens proteins leads to the
change in lens colour.
affect how the lens refracts light and reduce its
clarity, therefore decreasing visual acuity
6. Nuclear sclerotic cataract
• New cortical fibres are produced concentrically and lead to
thickening and hardening of the lens.
• appears yellow.
• can increase the focusing power of the natural lens (myopia,
second sight).
Patient may read without previously needed reading glasses
7. Cortical cataracts
• Defragment of electrolyte and water balance.
• most often seen as whitish spokes peripherally in the lens,
separated by fluid.
8. Posterior sub-capsular cataracts
• due to the migration and enlargement of lens epithelial cells
(Wedl cells) posteriorly.
• DM is a major factor in the formation of this type of cataract.
9. Diabetic cataract
• Osmotic stress due to sorbitol accumulation has been linked
with sudden worsening in patients with uncontrolled
hyperglycaemia.
10. Classification
By age onset
Acquired
Congenital
Lamellar or zonular cataracts are the most commonly seen form of congenital
cataracts.
Usually bi-lateral and symmetrical.
May be due to transient toxic influences during lens development, or may be
inherited in an autosomal-dominant pattern
By etiology
11. Classification
By clinical features
Nuclear sclerotic: generally age-related opacification, primarily involving the nucleus of the lens
Cortical: primarily opacification of the cortex of the lens
Posterior sub-capsular: opacification of the posterior sub-capsular cortex, seen frequently in drugrelated (e.g., with topical corticosteroids) or metabolic cataracts
Anterior sub-capsular: opacification of the anterior sub-capsular cortex, frequently seen in blunt
traumatic injuries
Cerulean: small bluish opacity seen in the lens cortex (often also referred to as blue-dot cataracts)
Snowflake: grey-white sub-capsular opacities that can be seen in cataracts in uncontrolled diabetes
mellitus
Sunflower: yellow or brown pigmentation of the lens capsule in a petal-shaped distribution, seen in
patients with an intra-ocular copper-containing foreign body or Wilson's disease
Christmas tree: polychromatic iridescent crystals, seen in the lens cortex of patients with myotonic
dystrophy
Oil droplet: on retro-illumination, seen in patients with galactosaemia. An accumulation of galactose
and galactitol in lens cells causes an increase in osmotic pressure due to fluid influx.
12. Classification
By stage
Immature
Partially opaque
mature
whole lens is opaque and no clear cortex is visible with a slit
lamp. The mature cataract appears white, No iris shadow is
seen on oblique illumination
Hypermature,
(Morgagnian )
Rare.
the cortex may liquefy and the nucleus becomes free-floating
within the capsule.
If the liquefied cortex leaks through the intact capsule,
wrinkling of the lens capsule may be seen and phacolytic
glaucoma may develop
13. Prevention
Primary prevention
•UV protection (UV filtration in spectacles and sunglasses) or
antioxidants may slow the progression. (??)
•no established way to prevent cataract formation.
Brimmed hats and UVB-blocking sunglasses are reasonable precautions to recommend.
14. Secondary prevention
many implanted intra-ocular lenses have UV chromophores
in them, certain models have fewer than others. This may
mean that UV filters could be placed in postoperative glasses
to help protect the retina from continued exposure
15. Diagnosis
History:
C/O:
blurring or cloudy of vision.
glary vision especially when driving at night.
inadequate glasses prescription. (nuclear sclerosis)
Gradual over years ( problem reading words from TV)
Relatively sudden (DM)
☟ in color richness (blue)
Risk of cataract formation?. Trauma? Ocular disease? Systemic Disease?
Medication? . Intraoperative Floppy Iris Syndrome (alpha 1 blocker)
16. Physical exam
Complete ocular examination:
•VA, pupillary examination, IOP
•A dilated slit-lamp examination using both direct and
retroillumination techniques
•Refraction
Fundus examination
Glare stress test
20. Treatment
• effective and safe.
• Surgical Indication:
Functional imairment
To aid management of other ocular exam
surgical therapy for ocular disease (e.g., lens-related glaucoma or
uveitis)
Congenital or traumatic cataract.
trial of mydriasis (e.g., scopolamine 0.25% q.d.) may be used
successfully in some patients if the patient desires nonsurgical
treatment. The benefits of this therapy are only temporary.
21. Rx
• preoperative treatments—e.g., topical antibiotics for
blepharitis, or atropine for poor dilation.
• Type of surgery:
• ICCE
• ECCE
• Phaco
22. On day of surgery
•
•
•
•
•
•
•
•
Consent.
Ensure mydriasis.
Topical antibiotic.
? Any ophthalmic problem , or infection.
Mark side of operation.
Confirm type of IOL and power.
Positioning for operation.
Scraping and draping.
23. Biometry/IOL selection
•
•
•
•
Usually aiming for emmetropia.
Check power as discussed with the patient.
check the keratometry and axial length
Use appropriate formula
• ?Refractive surgery before.
24. Follow up/ post-op
• 1 day, 1 week, 1 month:
postoperative complication, spectacle change.
What to examine?
prognosis: excellent if not complicated by other ocular disease.
Patient education. When to come back, eye shield.
Will need reading glasses.
26. Complication
• During surgery, the patient starts to cough. What
complications can result from this?
• Shallow chamber, iris prolapse, choroidal effusion / hemorrhage.
