Malignant Glaucoma

1. Malignant Glaucoma
Dr.Dipak Gulhane
Dr.Rita Dhamankar

3. NORMAL ANTERIOR SEGMENT OCT

4. UBM IMAGES

5. Malignant Glaucoma / Aqueous
Misdirection Syndrome
Definition
Von Graefe 1869
A shallow or flat anterior chamber with an
inappropriately high intraocular pressure despite a patent
iridectomy
European Glaucoma Society; II edition
Secondary angle closure glaucoma with ‘’posterior’’ pushing
mechanism, without pupillary block, caused by the ciliary body
and iris rotating forward

6. Malignant Glaucoma – Aetiology
 Surgery for angle-closure glaucoma
 Spontaneously
 Cessation of topical cycloplegic therapy
 Initiation of topical miotic therapy
 Laser iridotomy
 Laser capsulotomy
 Laser cyclophotocoagulation

7. Malignant Glaucoma – Aetiology
 Cataract extraction
 Seton implantation
 Central retinal vein occlusion
 Argon laser suture lysis
 Hyperopia
 Short axial lengths, or nanophthalmos.[4]

8. Pathogenesis
Posterior misdirection of aqueous flow
Hyaloid membrane into or behind the vitreous
body
Increase in vitreous volume
Shallower anterior chamber
Increase in intraocular pressure

10. Malignant glaucoma: cilio-lenticular
block

11. Malignant glaucoma: cilio-vitrean
block

12. Clinical Presentation
 High index of suspicion - necessary
 A red, painful eye is surgery for acute angle-closure
glaucoma
 Immediately after surgery , may occur during surgery or
months to years later
 Cessation of cycloplegic therapy or the institution of
miotic drops

13. Clinical Presentation
 Slit-lamp
 Shallow or flat anterior chamber both centrally and
peripherally
 No iris bombé to make the appropriate diagnosis
 IOP is elevated and the anterior chamber is axially shallow
 Attempt to reform the anterior chamber postoperatively
through the paracentesis site with viscoelastic substance,
 Great posterior resistance may be noted
 Anterior chamber may not deepen
 IOP may rise substantially.

14. Trigger factors
 Small, crowded anterior segment
 Angle closure
 Swelling and inflammation of the ciliary processes
 Anterior rotation of the ciliary body
 Forward movement of the lens-iris diaphragm

15. DIFFERENTIAL DIAGNOSIS
Criterion Aqueous
Misdirection
Pupillary Block Suprachoroidal
Hemorrhage
Serous Choroidal
Effusions
Intraocular
pressure
Normal or
elevated
Elevated Normal or
elevated
Low
Anterior chamber
depth
Shallow; flat
centrally and
peripherally
Shallow; flat
peripherally, but
deeper centrally
Shallow; flat
centrally and
peripherally
Shallow; flat
centrally and
peripherally
Relief by
iridectomy
No Yes No No
Ophthalmoscopy Choroid and retina
flat
Choroid and retina
flat
Bullous light
brown choroidal
elevations
Bullous dark
brown or dark red
choroidal
elevations
Ultrasound
biomicroscopy
Anterior rotation
of ciliary body and
lens
Iris bombé with
lens in normal
position
- -

16. DIFFERENTIAL DIAGNOSIS
Criterion Aqueous Misdirection Pupillary
Block
Suprachoroidal
Hemorrhage
Serous Choroidal
Effusions
B-scan
ultrasound
- - Smooth, thick, dome-
shaped movement
with little after-
movement
Smooth, thick, dome-
shaped membrane
with little after-
membrane
Heterogeneous
echogenic space
Echolucent
suprachoroidal space
Onset Intraoperative or early
postoperative period.
Early
postoperative
period
Intraoperative or
early postoperative
period
Intraoperative or
early postoperative
period
Occasionally months to
years later

17. Pupilary block v/s Malignant Glaucoma

19. Investigationes
 Ultrasound A scan: axial length
 Ultrasound B scan: exclude other pathologies
 Ultrasound biomicroscoscopy

20. Ultrasound biomicroscopy
 Confirm the diagnosis by the visualitation of the
anterior segment structures:
 Irido-corneal touch
 Appositional angle closure
 Anterior rotation of the ciliary body
 Apposition to the iris

21. MANAGEMENT
 Medical therapy
 Laser therapy
 Pars plana vitrectomy

22. Medical treatment
First step (good results in 50% of cases)
Cycloplegia with atropin 1%x 4-6/d
Mydriasis with phenilephrin 2,5%x 4-6/d
Mechanism of action
posterior push of the irido-cristalinian diaphragm
cilliary muscles relaxation
Long time treatment with atropin required
recurences (sometime for several years)
β blockers, AIC , α agonists
Hyperosmotics agents: Glycerol (po), Manitol (2g/kg iv)
Miotics Are Contraindicated

23. Laser Therapy
 The second line of treatment
 Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser -
aphakic and pseudophakic
 Large peripheral iridectomy
 Anterior hyaloid rupture to release the trapped aqueous
from the vitreous
 Several openings are made peripherally
 Placement of the iridectomies should be peripheral
 Peripheral placement will enable anterior migration of
the aqueous

24. Laser Therapy
 Corneal-lenticular contact
 Risk of corneal decompensation
 Chamber should be reformed following Nd:YAG laser
hyaloidotomy
 Slit lamp
 Viscoelastic substance via a 30-gauge cannula
 Through the original paracentesis

25. Pars plana vitrectomy
MECHANISM
 To debulk the vitreous
 To disrupt the anterior hyaloid face.
NEEDED
 Medical or or laser therapy fails
 Phakic eyes for which laser treatment is not a good option,

26. Pars plana vitrectomy
Pseudophakic
vitrectomy + anterior hialoidotomy
Phakic
Pars plana vitrectomy ± lensectomy
Lensectomy: - corneal oedema
- dens cataract
- no anterior chamber formation
during vitrectomy

28. Fellow eye
 Narrow angle is present
 The laser peripheral iridectomy is performed before
 Risk of aqueous misdirection may be reduced after
iridectomy if the angle remains open and the IOP is
normal
 Failure to provide prompt therapy to the fellow -
bilateral blindness.[2]

29. Conclusion
 The prognosis depends of the severity and the anterior
situation
 Malignant glaucoma remains a most difficult clinical problem
in terms of diagnosis and management
 The precise mechanism remains unclear and that why the
management is controversial

30. THANK YOU