What is a cataract and why does it matter?
A cataract is opacification of the normally clear crystalline lens, so light can no longer pass cleanly to the retina. StatPearls describes it as a progressive disease and a significant cause of blindness worldwide. Patients notice gradual blurring, glare, haloes and photophobia; in a mature cataract a whitish opacity may be visible in the pupil.
Diagnosis is clinical: torch-light examination and slit-lamp evaluation with undilated and then dilated pupils. Spectacles help only in early stages. Once the cataract interferes with routine activities, surgery is the only effective treatment — no drop or tablet reverses a senile cataract.
| Point | What to remember |
|---|---|
| Definition | Opacification of the crystalline lens |
| Commonest type | Age-related (senile) cataract |
| Senile subtypes | Nuclear, cortical, posterior subcapsular (PSC) |
| Most visually disabling for its size | PSC — it sits near the nodal point of the eye |
| Treatment | Surgery with an intraocular lens (IOL) |
| Commonest late complication of surgery | Posterior capsule opacification (PCO) |
What causes congenital and paediatric cataract?
About 60% of bilateral congenital cataracts are idiopathic and about 30% are hereditary; among the hereditary cases autosomal dominant inheritance is the commonest (about 75%). The rest come from intrauterine infection, metabolic disease, chromosomal syndromes, drugs and trauma. Children present with leukocoria, strabismus or nystagmus.
| Cause | Lens clue / exam point |
|---|---|
| Galactosaemia (and galactokinase deficiency) | Oil-droplet cataract; can reverse with early dietary galactose restriction |
| Intrauterine infection (TORCH: toxoplasma, rubella, CMV, HSV, syphilis) | Cataract with microcephaly, sensorineural deafness or chorioretinitis |
| Diabetes mellitus | Vacuolar / snowflake opacities |
| Hypoparathyroidism, hypocalcaemia | Multicoloured flecks |
| Fabry disease | Spoke-like cataract |
| Lowe syndrome | Thin disciform cataract |
| Chromosomal | Trisomies 13, 18, 21; Turner syndrome |
| Drugs | Corticosteroids (especially prednisolone) |
Children are not small adults in surgery. Under about 2 years many surgeons perform lens aspiration with a posterior capsulorhexis and anterior vitrectomy, leaving the child aphakic (corrected with contact lenses or glasses) and implanting an IOL later. Lifelong pressure checks are needed: 30–40% of children develop glaucoma after paediatric cataract surgery, more often when operated before 6 months.
What are the types of age-related (senile) cataract?
| Type | Appearance | Typical symptom |
|---|---|---|
| Nuclear sclerotic | Yellow-brown nucleus from urochrome deposition; rarely black | Myopic shift — some elderly patients read again without glasses (second sight) |
| Cortical | Wedge-shaped (cuneiform) or radial spoke-like opacities, often starting inferonasally | Glare and photophobia |
| Posterior subcapsular (PSC) | Granular, plaque-like opacity in front of the posterior capsule; black and vacuolated on retroillumination | Marked glare and haloes, worse in bright light and for near work |
| Christmas tree | Polychromatic needle-like crystals in deep cortex and nucleus | Uncommon |
Because the PSC opacity lies at the nodal point of the eye, even a small plaque affects vision profoundly. The vacuoles in a PSC are swollen migrating epithelial cells (bladder or Wedl cells) — the same cells that cause posterior capsule opacification after surgery.
| Stage | Description |
|---|---|
| Immature | Lens fibres partially opaque |
| Mature | Lens completely opaque |
| Hypermature | Lens shrunken and wrinkled because fluid leaks out |
| Morgagnian | Variant of hypermature cataract: cortex liquefies and the nucleus sinks inferiorly |
Which diseases and drugs cause secondary cataract?
Chronic anterior uveitis is the commonest cause of secondary (complicated) cataract; the risk rises with the duration and intensity of inflammation and with the steroids used to treat it. Early change is a polychromatic lustre at the posterior pole of the lens.
| Cause | Cataract | Remember |
|---|---|---|
| Corticosteroids (topical or systemic) | Posterior subcapsular | Also a known drug cause in children |
| Anticholinesterase miotics | Anterior subcapsular | Old glaucoma drops |
| Chlorpromazine | Anterior star-shaped opacity | Antipsychotic drug |
| Diabetes mellitus | Snowflake cortical opacities in young patients | Sorbitol pathway → osmotic overhydration; refraction changes with glucose |
| Wilson disease | Sunflower cataract | Free copper in the lens; KF ring in the cornea — see Wilson disease |
| Myotonic dystrophy | Iridescent Christmas tree opacities (about 90% of patients) | Third decade onwards |
| Atopic dermatitis | Shield-like anterior subcapsular plaque | About 10% of severe cases |
| Acute angle closure | Glaukomflecken — grey-white anterior subcapsular flecks | Pathognomonic of a previous attack |
| Blunt trauma | Rosette (flower-shaped) cataract | Trauma is a common cause of unilateral cataract in the young |
| Electric shock | Milky-white opacity with snowflake-like flecks | Rare |
| Infrared radiation (glassblowers) | True exfoliation of the anterior capsule | Rare |
| Ionising radiation | Posterior subcapsular | Appears months to years later |
How do ICCE, ECCE, SICS and phacoemulsification differ?
| Technique | Incision | Key features |
|---|---|---|
| ICCE (intracapsular) | Single large incision | Whole lens with its capsule removed; dates from the 18th century; now rarely performed |
| ECCE (manual extracapsular) | Large, 9–13 mm; needs sutures | Nucleus expressed, posterior capsule kept, IOL placed; more PCO and corneal oedema than phaco |
| MSICS (manual small-incision) | Scleral tunnel: external 6.5–7 mm, internal 9–11 mm; self-sealing | Outcomes comparable to phaco; much cheaper; short learning curve |
| Phacoemulsification | Clear corneal 2–3 mm (2.8–3.2 mm keratome) | Ultrasonic probe emulsifies and aspirates the nucleus; foldable IOL; self-sealing, astigmatically neutral |
Phacoemulsification was developed by Charles Kelman (1967), inspired by an ultrasonic dental tool. The surgeon makes a clear corneal incision with two side ports, performs a continuous curvilinear capsulorhexis (about 5–6 mm), emulsifies the nucleus, aspirates the cortex and injects a foldable IOL into the capsular bag. MSICS needs a larger 7–8 mm capsulotomy because the whole nucleus is delivered through the tunnel.
What types of intraocular lens are used?
The first IOLs were rigid polymethyl methacrylate (PMMA) lenses placed in the posterior chamber; they suit ECCE and SICS because the incision is large. Small-incision phaco needed foldable lenses, which are made of acrylic or silicone. Toric IOLs correct astigmatism, and multifocal or extended-depth-of-focus lenses aim to reduce dependence on glasses.
- Preferred position: in the capsular bag (posterior chamber IOL), held by haptics — plate, one-piece or three-piece designs.
- Power calculation: keratometry (corneal power), axial length and the lens A-constant are entered into a formula; the estimated lens position is the largest source of error.
- Aphakia without an IOL needs high-power spectacles or contact lenses — still used in infants under about 2 years.
What is posterior capsule opacification and other complications?
Posterior capsule opacification (PCO) — also called after-cataract or secondary cataract — is the most common late complication of cataract surgery. Reported rates range from 0.3% to 28.4%, and it can affect as many as 1 in 5 eyes within three years. It happens because residual lens epithelial cells left on the capsule migrate onto the posterior capsule and opacify it, so vision blurs again months to years after a good result.
| Timing | Complications |
|---|---|
| Intraoperative | Posterior capsule rupture (0.5–5.2%; → retained fragments, corneal oedema, CME; six-fold higher endophthalmitis risk and up to 19-fold retinal detachment risk), iris or ciliary body injury |
| Early postoperative | Transient raised IOP, corneal oedema, toxic anterior segment syndrome, endophthalmitis |
| Late postoperative | PCO (commonest), clinical cystoid macular oedema (Irvine–Gass), retinal detachment (0.1–1.3%) |
Despite these risks, cataract surgery is highly effective: StatPearls notes that up to 95% of patients achieve best-corrected acuity of 20/40 (6/12) after surgery, with gains in quality of life.
How big is cataract blindness in India, and what does NPCBVI do?
Cataract is the leading cause of blindness globally, accounting for over 45% of all blindness, and in India it causes nearly two-thirds of blindness. India was the first country in the world to launch a national blindness-control programme — the National Programme for Control of Blindness (NPCB) in 1976, now the National Programme for Control of Blindness and Visual Impairment (NPCBVI).
- Blindness prevalence fell from 1.1% in 1976 to 0.36% in 2019, mainly through NPCBVI and private partners (National Blindness and Visual Impairment Survey 2015–2019).
- High-volume MSICS with PMMA IOLs in government hospitals and outreach camps is the backbone of cataract services for the poor.
- NPCBVI has built eye wards and deployed mobile ophthalmic units for underserved regions; access barriers (transport, cost, attitudes) still limit effective cataract surgical coverage.