Glaucoma post 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

13. Peripheral
anterior
synechiae vs
iris processes

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 IOL
3- 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

16. Glaucoma
post cataract
surgery -
conclusion
There are many causes
Can be early or late
Management includes full
assessment and managing the
underlying cause.

17. Thank you