Postoperative inflammation, haemorrhage and PCO

Dropped Nucleus & Suprachoroidal Haemorrhage

The Dropped Nucleus Protocol

• If a hard nuclear fragment drops through a capsular tear into the mid- or posterior vitreous cavity: NEVER chase the fragment into the vitreous with the phaco tip or vitrectomy cutter.
• Blind posterior manipulation with non-vitreoretinal instruments causes giant retinal tears, rhegmatogenous retinal detachment, and catastrophic choroidal bleeding.
• Management: Perform a meticulous bimanual anterior vitrectomy to ensure the anterior chamber and corneal incisions are completely free of vitreous. Implant a sulcus IOL if capsular rim support permits, or leave the eye aphakic. Suture all incisions securely with $10-0$ nylon. Refer the patient urgently to a vitreoretinal surgeon for elective three-port $23\text{G}/25\text{G}$ pars plana vitrectomy with phacofragmatome at timing determined by fragment size, inflammation, pressure, corneal clarity and retinal findings.

Acute Suprachoroidal Haemorrhage

• Etiology: Rupture of a posterior or long ciliary artery into the suprachoroidal potential space between the choroid and sclera, driven by acute intraoperative hypotony in eyes with arteriosclerosis, systemic hypertension, advanced age, glaucoma, or high myopia.
• Clinical Presentation: Sudden, rock-hard globe; abrupt shallowing of the anterior chamber; extrusion of the iris and intraocular contents through the wound; dark brown choroidal elevations visible in the pupil; and immediate loss of the red reflex.
• Emergency Surgical Management:
  1. Immediate Wound Closure: Abandon intraocular maneuvers instantly. Close all clear corneal and paracentesis incisions with pre-placed sutures or digital compression. Re-establishing intraocular pressure tamponades the bleeding artery.
  2. Medical Tamponade: Administer IV mannitol ($1.0-2.0\text{ g/kg}$), systemic antihypertensives, and high-dose intravenous/oral corticosteroids.
  3. Further assessment and drainage: Close and stabilize the eye, then assess the extent with vitreoretinal input and ultrasound. Drainage may be timed to clot liquefaction, but apposition, pain, pressure, retinal involvement and the clinical course determine timing; a fixed 10–14-day delay is not mandatory in every threatened eye.

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Toxic Anterior Segment Syndrome (TASS) vs Acute Postoperative Endophthalmitis

Distinguishing between sterile Toxic Anterior Segment Syndrome (TASS) and acute microbial endophthalmitis is one of the most critical clinical differentials in ophthalmology:

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Acute Postoperative Endophthalmitis: Prevention and Initial Response

Use ocular-surface antisepsis with an appropriate povidone-iodine preparation and validated intracameral antibiotic prophylaxis according to local guidance. Allergy, concentration, contamination and dilution errors matter; prophylaxis must not replace aseptic technique.

Suspected infection requires urgent vitreoretinal assessment, sampling and intravitreal antibiotics. Common empiric coverage is vancomycin 1 mg/0.1 mL plus ceftazidime 2.25 mg/0.1 mL using separately prepared validated syringes. Confirm allergy and local protocol; intravitreal steroid adjuncts have uncertain benefit.

The 1995 Endophthalmitis Vitrectomy Study (EVS) involved acute postoperative infection after cataract or secondary-IOL surgery. Immediate vitrectomy improved outcomes in its light-perception-only subgroup, while tap/inject and vitrectomy had similar outcomes for better initial acuity. Modern surgical systems and different infections require individual decisions: hand-motions acuity does not preclude vitrectomy, and the study cannot be applied unchanged to traumatic, endogenous or fungal disease. Treatment is urgent and cannot await cultures.

TASS and infection overlap in onset, pain and inflammatory signs. A clear vitreous with early diffuse corneal oedema supports TASS, but uncertainty requires assessment and treatment for possible infection rather than an unobserved steroid trial.

Posterior Capsule Opacification (PCO) & Nd:YAG Laser Capsulotomy

Posterior capsule opacification is the most common delayed complication of modern cataract surgery, developing in $20\text{ to }40\%$ of eyes within 2 to 5 years.

Pathogenesis & Morphological Forms

Residual equatorial lens epithelial cells (LECs) survive surgical aspiration, proliferate, migrate across the posterior capsule, and undergo epithelial-mesenchymal transition (EMT):

1. Regeneratory / Pearl-Type PCO: Proliferating epithelial cells swell into large, clusters of globular, nucleated cells: Elschnig pearls (histologically identical to Wedl cells). This is the most common form, causing gradual reduction in visual acuity, contrast sensitivity, and photopic glare.
2. Fibrotic PCO: Myofibroblastic transdifferentiation produces alpha-smooth muscle actin ($\alpha$-SMA), causing capsular wrinkling, contracture, dense fibrosis, and star-shaped folds along the visual axis.

Preventive Surgical Factors

• Square-Edge Optic Geometry: A sharp, $90^\circ$ posterior optic edge acts as a mechanical barrier that arrests migrating lens epithelial cells.
• Complete $360^\circ$ Capsulorhexis Overlap: Ensuring the anterior rhexis leaf completely overlaps the $6.0\text{ mm}$ optic creates an anatomical shrink-wrap seal.
• IOL Material: Hydrophobic acrylic polymers bind fibronectin tightly, establishing superior capsular adhesion and lower PCO rates than hydrophilic acrylic or PMMA.

Nd:YAG Laser Capsulotomy Technique & Complications

• Laser Physics: Neodymium-doped Yttrium Aluminum Garnet (Nd:YAG) pulsed laser ($\lambda = 1064\text{ nm}$, infrared). Operates by optical breakdown and photodisruption: intense localized electrical field ionizes tissue into plasma, producing acoustic shock waves that cut the non-pigmented capsule.
• Technique: Use the device-specific focusing offset and the lowest effective pulse energy. Place an opening appropriate to visual symptoms, pupil size and IOL position while avoiding optic pitting. Energy, offset and aperture diameter are adjustable clinical choices, not fixed settings for every eye.
• Complications:
  • Transient IOP Spike: Peaks at 1 to 4 hours post-laser due to trabecular meshwork clogging by capsular debris and inflammatory cells. Prophylaxis: topical apraclonidine $1\%$ or brimonidine $0.2\%$ before and after the procedure.
  • IOL Pitting / Damage: Optical divots created if the laser is focused directly on the IOL material.
  • Macular oedema: Investigate reduced vision with examination and OCT; risk depends on inflammation and retinal comorbidity.
  • Retinal tears/detachment: Counsel about new flashes, floaters and a curtain, especially with myopia or previous retinal disease. A fixed percentage increase does not apply to every capsulotomy.