Download as PDF, PPTX
More Related Content
Similar to Glaucoma post cataract surgery
Glaucoma post cataract surgery
- 1. Glaucoma post cataractsurgery: Mechanisms, prevention and management Dr Haitham Al-Mahrouqi Cornea and Anterior Segment Al-Nahdha Hospital
- 2. Cataract and glaucoma • Thecrystalline Lens can cause glaucoma and lens extraction (does not need to be cataractous) can be a mode of managing glaucoma. • Glaucoma accelerates cataract and controlled IOP can prevent cataract development. • Glaucoma can be a consequence of cataract surgery.
- 3. Glaucoma post cataractsurgery • Early • Retained viscoelastic (peak IOP rise at 4-6 hours) • Inflammation (uveitis or trabeculitis) • Hyphema • Pseudophakic/Aphakic Pupillary block • Malignant glaucoma • Suprachoroidal hemorrhage • Late • Steroid induced • Trabecular meshwork anatomical changes e.g. Aphkia • Peripheral anterior synechiae • Epithelial ingrowth • Retained lens matter • Uvieits – glaucoma – hyphema (UGH) syndrome.
- 4. Early rise inIOP – Retained viscoelastic device • Viscoelastic is very important in cataract surgery. • It is imperative not to leave a lot of residual viscoelastic material especially in glaucoma patients. • Should not inflate the bag with dispersive viscoelastic. • Takes about 3-5 days to be absorbed • Manage medically or surgically by removal of viscelastic if uncontrolled IOP.
- 5. Early rise inIOP – Inflammation • Mild inflammation is normal after cataract surgery. • Inflammation is higher with prolonged and complicated surgery. • Although the inflammation can be transient, glaucoma patients are more likely to have high IOP (due to compromised drainage) and more likely to be affected due to compromised optic nerve. • Toxic anterior segment syndrome: Severe inflammation within 24 hrs of surgery due to toxicity from materials used. DDx Endophthalmitis • Re-activation of HSV keratitis/uveitis: Prophylaxis pre- op is important.
- 6. Early rise inIOP – hyphema • Uncommon • Can occur in patients with NVI, FHI • Bleeding during surgery normally stops on its own. • To prevent further bleeding, must maintain a pressurized chamber especially when removing instruments. • Manage as hyphema.
- 7. Early rise inIOP – Psuedophakic/aphakic pupillary block • Occurs more if there is complicated surgery • Vitreous loss can precipitate pupillary block by iridovitreal contact. • Reverse implantation of angulated sulcus IOL • A lot of inflammation can lead to posterior synechiae and subsequent iris bombe • Aphakia is associated with a change in the configuration of the angle and compromised aqueous drainage (more likely to be late onset).
- 8. Early rise inIOP – Malignant glaucoma • More common in short hypermetropic eyes. • Anterior rotation of ciliary body with aqueous being trapped in the vitreous cavity and pushing the iris lens diaphragm forward. • Must exclude pupillary block (need to have a PATENT PI) and choroidal haemorrhage prior to the diagnosis. • Management: • Ensure patent PI • Aqueous suppressants, Diamox, mannitol, cycloplegia • Surgery (disruption of the anterior hyaloid face): • Chandler procedure • Yag iridozonulohyeloidectomy • PPV
- 9. Early rise inIOP – Suprachoroidal hemorrhage • Higher risk in ECCE, ICCE where there is prolonged hypotony. • Drainage is indicated if: • Kissing choroids • Flat AC with iridocorneal contact • Concurrent rhegmatogenous RD
- 10. Late glaucoma –Steroid induced • Steroid response rarely occurs before 2 weeks (can happen at any point after) • Risk of significant steroid response: • 5% of population • 25% of family history of glaucoma • 90% POAG • Mechanism: Deposition of GAG on the TM • Depends on the route (periocular > intraocular > topical), potency and frequency. • Discontinuation of the steroid normalizes IOP after 4-6 weeks (if not used for more than 1 year)
- 11. Late glaucoma – Aphakicglaucoma • Commonly seen in children • A reason why not to operate congenital cataract before 4 weeks in children. • Higher with small corneal diameter and shorter AL. • Speculated mechanism: • Abnormal maturation of the angle (thought that the lens plays a role in maturation) • Lens proteins left behind which are toxic • Chronic inflammation • Treatment: • Medical: Avoid brimo • Surgical: Tube surgery
- 12. Late glaucoma – Prolongedinflammation • Inadequate control of the inflammation induced by e.g. retained lens material, viscoelastic, pre-existing uveitis, HSV uveitis. • Can lead to posterior synechiae and peripheral anterior synechiae. PAS Retained lens material
- 13.
- 14. Late glaucoma: Uveitis-Glaucoma- Hyphema (UGH)syndrome • Classically described with anterior chamber IOLs with poor fixation. • Continuous staffing of the IOL with iris produces pigment release, inflammation, NVI, recurrent hyphema, corneal oedema and CME. • Can occur with single piece IOLs implanted in the sulcus. • Treatment: • Control the inflammation • IOL may need to be explanted Single piece 3-piece Kelman AC IOL3- piece
- 15. Late glaucoma – Epithelialdowngrowth • Rare in modern time • DDx ICE syndrome, PPCD • Can occur after any intraocular surgery (less common with small wound surgery like phaco) or trauma. • Epithelium divides intraocularly leading to corneal oedema, PAS and intractable glaucoma. • Diagnosis can be made with ocular fluid analysis or argon laser spot on iris (if it blanches, it is epithelial downgrowth). • Treatment (difficult and often fails): • Intracameral 5-FU, b-radiation, cryo • Excision of involved tissue Case Rep Ophthalmol Med. 2015;2015:325485
- 16. Glaucoma post cataract surgery - conclusion Thereare many causes Can be early or late Management includes full assessment and managing the underlying cause.
- 17.