Glaucoma is a common complication of ocular surgeries such as cataract extraction, keratoplasty, vitreoretinal surgery, and refractive surgery. The mechanisms of glaucoma include retained viscoelastic, inflammation, pupillary block, and changes to the angle structure. Glaucoma can occur early due to these mechanisms or late due to factors like steroid response or inflammation. Careful case selection, prevention of complications, and close monitoring are important to manage glaucoma risk in postoperative patients.

1. Glaucoma post ocular surgery:
Mechanisms, prevention and management
Haitham Al-Mahrouqi
Ophthalmology Resident, R5

2. Objectives
• Glaucoma and cataract surgery
• Glaucoma and vitreoretinal surgery
• Glaucoma and keratoplasty
• Glaucoma and refractive surgery
Mechanisms, prevention and management

3. Glaucoma and cataract
surgery
Main references
1) AAO BCSC lens and cataract and Glaucoma
2) Becker and Shaffer: Diagnosis and Therapy of Glaucoma

4. Cataract
• The crystalline Lens can cause
glaucoma and lens extraction (does
not need to be cataractous) can be a
mode of managing glaucoma.
• Glaucoma can be a consequence of
cataract surgery.

5. Lens and primary
angle closure
Mechanism:
• Relative pupillary block
• Plateau iris syndrome
• Abnormal lens thickness and
position (non cataractous)

6. Lens induced
glaucoma
(secondary
glaucoma)
• Phacolytic
• Phacoanaphylactic
• Lens particle
Open angle:
• Phacomorphic
• Ectopia lentis
Closed angle:

7. Glaucoma post cataract surgery
• Early (High IOP)
• 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.

8. 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.

9. Early rise in IOP –
Inflammation
• Mild inflammation is normal after cataract surgery.
• Inflammation is higher with prolonged and
complicated surgery.
• Toxic anterior segment syndrome: Severe
inflammation within 24 hrs of surgery due to toxicity
from materials used.
• Although the inflammation can be transient, glaucoma
patients are more likely to have high IOP (due to
compromised drainage).
• Although the transient rise is benign in most patients,
glaucoma patients with already compromised optic
nerves, the transient rise may further destroy more
ganglion cells.

10. 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.

11. 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).

12. 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.

13. 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

14. 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)

15. 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

16. 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

17. Peripheral
anterior
synechiae vs
iris processes

18. 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

19. 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

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

21. Glaucoma post keratoplasty
Reference:
Dada T, Aggarwal A, Minudath K, et al. Post-penetrating keratoplasty glaucoma. Indian J Ophthalmol
2008;56:269–77.

22. Glaucoma post corneal grafting
• Early
• Pupillary block – especially in DSEAK/DMEK due to air/gas bubble.
• Retained viscoelastic material
• Inflammation
• Hyphema
• Malignant glaucoma
• Pre-existing glaucoma
• Late:
• Angle distortion and PAS
• Rejection
• Epithelial downgrowth
• Steroid induced

23. Glaucoma post penetrating keratoplasty
• More common in associated pseudophakia/Aphakia
• More common in second graft
• More common with small grafts
• Occurs in 10-30%
• Mechanism:
• All the previously mentioned mechanisms in cataract surgery can occur, but
more specific;
• Wound distortion, distorts the angle structure leading to possible synechiae.

24. Glaucoma post penetrating
keratoplasty - diagnosis
• Diagnosis is difficult
• Pre-op baseline measurements and investigations are important
(e.g. OCT RNFL, VF).
• Measuring IOP:
• Early when oedema and mires irregular: Tonopen,
pneumotonometer or DCT.
• Later when the surface is regular: Goldman applanation
tonometer
NOTE:
- To account for the astigmatism, measure the IOP with the
mires horizontally and vertically and then take the average.
Otherwise, rotate the prims so the red mark is set at the least
curved meridian of the cornea (along the negative axis)
E.g. -5.00 – 1.00 X 70, the red mark is set at 70 degrees
- Always take into account the pachymetry

25. How do you evaluate pressure in
keratoprosthesis
Boston Kpro 1 Boston Kpro 2
osteoodonto-
keratoprosthesis (OOKP)

26. Prevention
• Avoid corneal grafts in uncontrolled glaucoma patients.
• Control any uveitis or HSV disease
Case selection:
• Less tight sutures
• Deep sutures
• Short sutures
• Suture bites equal on either side of wound
• Grafts not too small and not close to limbus
• Donor corneas larger than that of the recipient (0.5-1mm)
Surgical factors with favorable outcome
• Flat AC need to be treated urgently
• Control any associated inflammation and monitor steroid
response.
• Close monitoring of the IOP
Post op factors:

27. Treatment
• Medical treatment:
• Avoid prostaglandin analogues in the early post op period and in those with
HSV keratouveitis.
• Avoid CAI due to impairment of the endothelial function
• Cyclosporin may be used in steroid responsive patients
• Surgical treatment:
• Tubes appear to control the IOP better than Trabs. Trabs may be difficult with
associated altered limbal anatomy.
• Tubes may have a higher incidence of graft failure. Best to implant the tube
posterior to the iris.
Indian J Ophthalmol. 2008 Jul-Aug; 56(4): 269–277.

28. Other lamellar keratoplasties
• Lower incidence of glaucoma in DALK, DSEAK and DMEK due to lower
incidence of distortion to the AC and angle structures.
• For DSEAK and DMEK, Prophylactic inferior PI is needed to to prevent
pupillary block during the bubbling time.
• Keratoprosthesis: Some centres implant a tube shunt device at the
same time as Kpro in those with pre-existing glaucoma and
uncontrolled IOP.
- Ophthalmology. 2016 Jul;123(7):1428-34
- Cornea. 2012 Feb; 31(2): 134–139.

29. Glaucoma post refractive
surgery
Reference:
1) AAO BCSC refractive surgery and Glaucoma
2) Refractive surgery by Dimitri Azar
3) Kozobolis V, Konstantinidis A, Sideroudi H, et al. The Effect of Corneal Refractive Surgery on Glaucoma. J
Ophthalmol 2017;2017. doi:10.1155/2017/8914623

30. Background
• Myopes are more likely to have POAG.
• Pre-op assessment is very important.
• Glaucoma must be very well controlled before
refractive surgery because:
• IOP measurement will not be as accurate
• Refractive procedures which involve
suction (e.g. LASIK, SMILE) can have IOP
rise up to 65mmhg. Few studies have
shown new visual field defects post LASIK.
Nevertheless, most studies did not find
any long-term effect from this transient
rise.

31. Avoid LASIK and SMILE in glaucoma patients
• LASIK and SMILE Require suction cup to stabilize the eye.
• IOP may rise up to 65mmhg leading to ischaemia
• Compromised optic nerves may get affected more.
• Patients with bleb cannot undergo suctioning.
• It is recommended that controlled mild glaucoma or ocular hypertensive patients
to undergo PRK rather than LASIK/SMILE.
J Refract Surg. 2011 Jun;27(6):427-33

32. Glaucoma and PRK
• PRK often require longterm steroids to
prevent/treat haze which can lead to steroid
response glaucoma.

33. Post op measurement of the
IOP
• Myopic correction thins the cornea in the
center whereas hypermetropic correction
thins a ring around the center of the cornea.
• Hypermetropic correction have negligible
change in IOP when measured using
applanation tonometry.
• Myopic correction. IOP is inaccurate due to
thinner cornea and change in the corneal
biomechanics; therefore:

34. Post op measurement of the IOP
1) Measure IOP from the periphery using tonopen/pneumo/icare
2) Air-puff tonometers like ORA or corvis tonometers as they account for the
change in the viscoelastic properties of the cornea.
OR those which are not affected by the corneal thickness or viscoelastic
properties
3) Transpalpebral tonometry
4) DCT
• Avoid measuring IOP in the first 72hrs post LASIK due to flap complications.

35. Corvis tonometer

36. Ocular response analyzer

37. Dynamic contour tonometer: Pascal law
• The cornea is tension free
when the pressure is equal on
both sides. (Pascal’s Law)

38. Transpalpebral tonometer
• Can be useful for self-
use.
• Within 1-3mmhg of GAT
accuracy.
- Chakraborty AK, Majumder M, Sen S. Comparison of transpalpebral tonometer with Goldmann
applanation tonometer. Taiwan Journal of Ophthalmology 2014;4:110–5. doi:10.1016/j.tjo.2014.03.002

39. Practical
conclusion: IOP
measurement
in post
refractive
surgery patients
Refractive surgery clinics: DCT
is the preferred method
In the hospital:
pneumotonometer, tonopen
or icare may be measured
from the periphery in myopes.

40. Implantable collamer lens
and glaucoma
• Made up from collamer material
• Soft, foldable and biocompatible
• Can correct high myopia and hyperopia
(3.00 to 23.0D) + astigmatism.
• General guidelines:
• ACD > 3.0mm
• ACA > 30 degrees
• ICL length should be 1.00mm larger than
WTW.
• Avoid in angle closure patients or
uncontrolled glaucoma.

41. Complications
• Anterior subcapsular cataract: 5% in 5-years
• Endothelial cell loss rate: 1 – 2 % / year (aging is
0.5% / year)
• Glaucoma is often transient. The pupillary block
is eliminated with central aquapore or PI. ICL
may need to be removed if uncontrolled
glaucoma.
With the new aquapore pupillary block is reduced.
Also, the cataract is reduced due to natural
circulation of the aqueous.

42. Glaucoma post vitreoretinal
surgery
Reference:
1) AAO BCSC Vitreoretinal and Glaucoma
2) Retina by Rayn
3) Kornmann HL, Gedde SJ. Glaucoma management after vitreoretinal surgeries. Curr Opin Ophthalmol 2016;27:125–
31. doi:10.1097/ICU.0000000000000238

43. Background
• Glaucoma is a known complication of retinal
surgery
• Some patients may be predisposed:
• E.g. Myopes are more likely to get POAG
and retinal detachments.
• Adjuncts used in retinal surgery, for example,
SO, Scleral buckle, gases, PFCL can lead to to
glaucoma.

44. Vitrectomy and glaucoma
• Incidence ranges between 10-20%
• Higher incidence with concurrent cataract surgery, scleral buckle, gasses or
SO.
• Vitrectomy without the above still predispose to late onset secondary open
angle glaucoma.
• Mechanism: Postulated that the oxygen from the retina (high oxygen
concentration) diffuses to the AC which induces oxidative stress to the
angle structure.
• Treatment:
• Aqueous suppressants
• Trab vs Tube depending on the conjunctiva status

45. Scleral buckle and glaucoma
• Scleral buckle is associated with angle closure in 1-4%
• Scleral buckle is thought to impair venous blood flow.
The ciliary body gets swollen and rotates anteriorly
pushing the iris forward.
• Usually self resolves as the ciliary body congestion
improved with time.
• Medical management:
• Cycloplegia to move the iris-lens diaphragm posteriorly
• Anti-glaucoma medications
• Surgical management:
• PI is not useful as there is often no pupillary block
mechanism.
• Due to conjunctival scarring from the retina surgery, tube
surgery is preferred. Still may be challenging due to
crowding of the buckle if it was encircling.

46. Intravitreal gas and glaucoma
• Expansile more likely to cause glaucoma than non-expansile concentrations.
• Gases are usually short lived and get absorbed with time.
• Mechanism: Posterior pushing mechanism leading to secondary angle closure. In
addition, pupillary block may also play a role.
• Treatment:
• Face down position
• PI may help
• Aqueous suppressants

47. Silicone oil and glaucoma
• Incidence varies widely depending on type of SO (emulsification of SO
5000 is lower), surgery involved, overfill.
• Mechanism:
• Angle closure: Can be pushing mechanism from the overfill, pupillary block,
or anterior pulling mechanism from the inflammation in the angle and NVI.
• Open angle: Emulsified SO block the trabecular meshwork or chronic
inflammation.
• Treatment:
• Prophylactic inferior PI
• Anti-glaucoma medications
• Removal of the SO (if emulsified or overfill) Vs glaucoma filtration surgery

48. Thank you