11.2 Cataract, Glaucoma & Red Eye Emergencies

Cataract: Classification, Clinical Features & Surgical Techniques

A cataract is defined as any opacification of the crystalline lens or its capsule, leading to painless, progressive impairment of vision. It is the most common cause of avoidable blindness globally (accounting for ~50-60% of blindness in India under NPCBVI).

Etiological & Morphological Classification

1. Senile (Age-related) Cataract: Most common type (>90%), occurring in individuals >50 years due to oxidative stress, protein aggregation, and loss of lens fiber transparency.
   • Cortical Cataract: Opacification begins in the lens cortex forming wedge-shaped spokes (cuneiform cataract). Patients complain of glare, monocular diplopia, and reduced contrast sensitivity.
   • Nuclear Cataract: Opacification of the lens nucleus with sclerosis and yellowing/browning (cataracta nigra). Causes progressive index myopia ("second sight" where near vision temporarily improves without reading glasses).
   • Posterior Subcapsular Cataract (PSC): Opacification in the posterior cortical layer adjacent to the capsule. Causes marked reduction in distance and near vision, especially in bright sunlight (due to miosis).
2. Congenital & Developmental Cataract: Present at birth or early childhood (e.g., Rubella syndrome, Galactosemia, Zonular/Lamellar cataract).
3. Complicated Cataract: Secondary to intraocular disease (e.g., chronic anterior uveitis, high myopia, retinitis pigmentosa). Classic appearance: Polychromatic lustre ("bread-crumb" or "fish-scale" appearance) starting at posterior pole.
4. Toxic / Drug-induced: Systemic or topical corticosteroids (causing PSC), chlorpromazine, miotics.

Clinical Stages of Senile Cortical Cataract

• Stage of Incipient Cataract: Early cortical spokes or nuclear dots; vision minimally affected; red reflex present.
• Stage of Immature Cataract (IMSC): Lens is partially opaque; clear cortex remains between capsule and opacity; iris shadow test is positive.
• Stage of Mature Cataract (MSC): Lens is completely opaque and pearly white; iris shadow is absent; red reflex lost; vision reduced to Hand Movements (HM) or Perception of Light (PL).
• Stage of Hypermature Cataract (HMSC):
  • Morgagnian Cataract: Cortex liquefies into a milky fluid and the dense brown nucleus sinks to the bottom of the capsular bag.
  • Sclerotic Cataract: Lens disintegrates, shrinks due to water loss, and capsular bag wrinkles. May cause phacolytic glaucoma (lens protein leakage triggering macrophage inflammation and trabecular meshwork clogging) or phacomorphic glaucoma (intumescent swollen lens causing angle closure).

Surgical Techniques for Cataract Extraction

Indication for surgery is primarily visual impairment interfering with daily activities or secondary complications (phacolytic/phacomorphic glaucoma).

Post-Operative Complications

• Posterior Capsular Opacification (PCO): Most common late complication (20-30% cases), caused by proliferation of residual lens epithelial cells (Elschnig pearls or Soemmerring ring). Treated non-invasively with Nd:YAG Laser Capsulotomy.
• Acute Endophthalmitis: Devastating intraocular infection occurring 2-7 days post-op (most commonly Staphylococcus epidermidis or Pseudomonas). Presents with pain, lid edema, hypopyon, vitreous haze, and loss of red reflex. Managed with emergency intravitreal injection of Vancomycin (1 mg/0.1 mL) + Ceftazidime (2.25 mg/0.1 mL).

Glaucoma & Ocular Emergencies (Red Eye Differential Diagnosis)

Glaucoma is a group of progressive optic neuropathies characterized by structural optic nerve head cupping, retinal ganglion cell loss, and characteristic visual field defects, usually associated with elevated Intraocular Pressure (IOP > 21 mmHg; normal IOP = 10-21 mmHg).

Primary Open-Angle Glaucoma (POAG)

POAG is a chronic, bilateral, insidious disease characterized by open anterior chamber angle and increased resistance to aqueous humor outflow through the trabecular meshwork.

• Clinical Presentation: Asymptomatic in early stages ("silent thief of sight"). Discovered incidentally on screening. Late symptoms include peripheral vision loss and tunnel vision.
• Diagnostic Triad:
  1. Elevated IOP: >21 mmHg measured by Goldmann Applanation Tonometry (GAT).
  2. Optic Disc Changes: Vertical cup-to-disc (C:D) ratio >0.5 or asymmetry >0.2 between eyes, neuroretinal rim thinning (following ISNT rule: Inferior > Superior > Nasal > Temporal rim thickness), bayoneting of vessels, disc hemorrhages (Drance hemorrhage).
  3. Visual Field Defects: Automated Perimetry (Humphrey) shows early paracentral scotoma, Seidel scotoma, Arcuate / Bjerrum scotoma, Roenne central step, and ultimate tunnel vision with temporal island preservation.
• Medical Management: First-line: Topical Prostaglandin analogues (Latanoprost 0.005%, Bimatoprost) once daily (increases uveoscleral outflow). Second-line: Topical Beta-blockers (Timolol 0.5% - decreases aqueous production; contraindicated in asthma/heart block), Alpha-2 agonists (Brimonidine), Carbonic anhydrase inhibitors (Dorzolamide).
• Surgical: Selective Laser Trabeculoplasty (SLT) or Trabeculectomy (guarded filtration surgery forming a subconjunctival bleb).

Acute Angle-Closure Glaucoma (AACG)

AACG is an ophthalmic emergency occurring in anatomically predisposed hypermetropic eyes with shallow anterior chamber. Mydriasis causes pupillary block, forward bowing of peripheral iris (iris bombé), closure of anterior chamber angle, and rapid spike in IOP (often 50-70 mmHg).

• Clinical Features: Sudden excruciating ocular/periorbital pain, radiating along trigeminal nerve, vomiting, severe headache, rainbow-colored haloes around light bulbs (due to corneal edema), rapid decrease in visual acuity.
• Physical Examination: Ciliary congestion, steamy/hazy cornea, shallow anterior chamber, mid-dilated non-reactive pupil, and stony-hard eyeball on digital palpation.
• Emergency Pressure-Lowering Management:
  1. IV Mannitol (20% solution, 1-2 g/kg body weight) infused over 30 mins (hyperosmotic agent drawing fluid from vitreous).
  2. Oral Acetazolamide 500 mg stat followed by 250 mg QID (carbonic anhydrase inhibitor).
  3. Topical Pilocarpine 2% drops every 15 mins for 1 hour once IOP drops below 40 mmHg (causes miosis, pulling peripheral iris away from trabecular meshwork).
  4. Topical Timolol 0.5% and Brimonidine drops.
  5. Definitive Treatment: Bilateral Nd:YAG Laser Peripheral Iridotomy (LPI) once cornea clears (creates bypass channel between posterior and anterior chambers to eliminate pupillary block in affected and fellow prophylactic eye).

Differential Diagnosis of Acute Red Eye