Acquired Cataract

Age-Related Lens Opacification

Lens � min read
Nuclear Sclerotic Cataract (NSC)
Nuclear Sclerotic Cataract (NSC)
Nuclear Sclerotic Cataract (Advanced)
Nuclear Sclerotic Cataract (Advanced)
Cortical Cataract
Cortical Cataract
Cortical Cataract (Retroillumination)
Cortical Cataract (Retroillumination)
Cortical Cataract Spoke-like Opacities
Cortical Cataract Spoke-like Opacities
Posterior Subcapsular Cataract (PSC)
Posterior Subcapsular Cataract (PSC)
Cataract Grading System
Cataract Grading System

Presentation

  • Progressive, painless blurring of vision.
  • Nuclear sclerotic: gradual myopic shift ("second sight"), possible monocular diplopia, colours appear more yellow/brown.
  • Cortical: glare and reduced contrast sensitivity, may be minimally symptomatic if opacities remain peripheral (spoke-like).
  • Posterior subcapsular (PSC): glare and haloes, disproportionately symptomatic for its size because of its central location; worse in bright light/miosis (night driving, reading in bright sun); tends to occur in younger patients.

Findings

★ Signature Finding

Type-specific slit-lamp appearance: Nuclear sclerosis — central yellow-to-brown opalescence; Cortical — peripheral wedge-shaped ("spoke") opacities on retroillumination; PSC — plaque-like opacity just beneath the posterior capsule, central, best seen on retroillumination.

  • Patients often have overlapping opacities in more than one zone.

Etiology & Mechanism

  • Age-related (senile) cataract — the most common type — is multifactorial: compaction/stiffening of central lens fibres as new cortical layers accumulate, plus oxidative damage and crystallin protein aggregation.
  • Diabetes mellitus — accelerated cortical/PSC change via osmotic lens fibre swelling (sorbitol pathway).
  • Corticosteroid use (topical, systemic, or inhaled) — classic cause of PSC cataract.
  • Blunt or penetrating trauma — can produce rosette/stellate cataract.
  • Chronic uveitis and/or its steroid treatment.
  • Ionizing radiation exposure — classically produces a PSC pattern.
  • High (pathologic) myopia — accelerated nuclear sclerosis.
  • Smoking and UV exposure — recognized environmental risk factors.

Red Flags — Do Not Miss

Critical — Do Not Miss
  • Unilateral, rapidly progressive cataract in a young patient — consider trauma, chronic intraocular inflammation, or an intraocular tumor-related (masquerade) process.
  • Cataract with a red or painful eye, or with iris neovascularisation — consider phacolytic or phacomorphic glaucoma, lens-induced uveitis, or intraocular malignancy.
  • A white/mature (hypermature) cataract — risk of phacomorphic angle closure or phacolytic glaucoma; needs prompt surgical planning rather than routine elective scheduling.

Investigations

  • Comprehensive slit-lamp exam and dilated fundus exam to detect coexisting posterior-segment pathology.
  • B-scan ultrasound if the fundus cannot be visualised, to exclude retinal detachment or intraocular mass before surgery.
  • Ocular biometry (optical or ultrasound) for intraocular lens power calculation.
  • Potential acuity/glare testing to correlate degree of visual complaint with cataract severity.
  • Specular microscopy if coexisting endothelial disease (e.g., Fuchs dystrophy) is suspected preoperatively.

Management

  • Non-surgical measures for early/mild disease: updated refraction, brighter task lighting, anti-glare strategies.
  • Surgical timing is generally guided by the degree of functional visual impairment and the patient's needs rather than a fixed visual-acuity cutoff.

Treatment

  • Definitive treatment is surgical: phacoemulsification with intraocular lens implantation is the standard of care in most settings.
  • Manual small-incision cataract surgery or extracapsular extraction may be used for very dense/mature cataracts or in resource-limited settings.
  • No medical or topical therapy is proven to reverse cataract.

Follow-up

  • Preoperative interval monitoring based on symptoms.
  • Standard postoperative visits (commonly day 1, week 1, and around month 1) to monitor for endophthalmitis, IOP spikes, and cystoid macular oedema.
  • Long-term monitoring for posterior capsular opacification ("secondary cataract"), treatable with Nd:YAG laser capsulotomy when visually significant.

Clinical Pearl

💡 Clinical Pearl

A cataract that develops rapidly and asymmetrically — especially with a shallow anterior chamber or elevated intraocular pressure — should raise suspicion for lens-induced (phacomorphic or phacolytic) glaucoma and prompt urgent rather than routine surgical referral.

Differential Diagnoses

ConditionKey Distinguishing Point
Age-related macular degenerationMetamorphopsia/central scotoma with macular findings on exam; can coexist with and be masked by cataract.
Fuchs endothelial corneal dystrophyCorneal guttae on exam, vision characteristically worse in the morning.
Primary open-angle glaucomaOptic nerve/visual field changes with a clear lens exam.
Diabetic retinopathyFundus findings (microaneurysms, haemorrhages) rather than lens opacity.
Posterior capsular opacificationHistory of prior cataract surgery; resolves with YAG laser capsulotomy.

References