Glaucoma can develop after cataract surgery due to various mechanisms. Early causes within the first few days include retained viscoelastic material, inflammation, hyphema, pupillary block, and malignant glaucoma. Late causes after 2 weeks can be steroid-induced glaucoma, changes to the trabecular meshwork from aphakia, peripheral anterior synechiae, epithelial ingrowth, retained lens matter, or uveitis-glaucoma-hyphema syndrome from intraocular lens complications. Managing the underlying cause through medical or surgical treatment is important to control post-operative glaucoma.
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Managing Glaucoma Risk After Cataract Surgery
1. Glaucoma post cataract surgery:
Mechanisms, prevention and
management
Dr Haitham Al-Mahrouqi
Cornea and Anterior Segment
Al-Nahdha Hospital
2. Cataract and
glaucoma
• The crystalline 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 cataract surgery
• 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 in IOP –
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 in IOP –
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 in IOP –
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 in IOP –
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 in IOP –
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 in IOP –
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 –
Aphakic glaucoma
• 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 –
Prolonged inflammation
• 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
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 –
Epithelial downgrowth
• 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