Neovascular glaucoma is a form of secondary open-angle glaucoma caused by the growth of new blood vessels in the eye in response to retinal ischemia. The blood vessels are accompanied by a membrane that can obstruct aqueous outflow and pull the iris forward, restricting access to the angle and leading to synechial angle closure. Treatment involves controlling intraocular pressure with medications, performing panretinal photocoagulation, and using anti-VEGF drugs or surgeries like trabeculectomy to dry up the neovascularization when possible. Long-term follow up is important due to risks of uncontrolled pressure, hyphema, and vision loss.

1. NEOVASCULAR
GLAUCOMA
D R TA L H A FA R O O Q PA S H A
P G R O P H T H A L M O L O G Y

2. INTRODUCTION
•A form of secondary open angle with
subsequent progression to secondary synechial
angle closure.
•Caused by new blood vessels forming in
response to retinal ischemia
•Vessels are associated with a membrane
•The membrane can obstruct aqueous outflow
•The contraction of membrane can lead to PAS
formation

3. PATHOPHYSIOLOGY
•Ischemic retina produces vasogenic substances
that stimulate the growth of new vessels
(VEGF)
•Vessels are accompanied by a membrane that
restricts aqueous access to the angle (even
areas that aren’t closed by synechiae)
•The membrane pulls the iris forward

4. PATHOPHYSIOLOGY
•Intraocular surgery – like cataract surgery – can
breakdown the natural barriers and increase the
risk for anterior segment neovascularization

5. CAUSES
•Ischemic central retinal vein occlusion (90 day
glaucoma)
•Diabetes mellitus
•Arterial retinal vascular disease
- Such as CRAO and ocular ischemic syndrome
• Miscellaneous causes ie. retinal detachment, chronic
intraocular inflammation

6. SYMPTOMS
• Pain
• Redness
• Photophobia
• Decreased vision

7. SIGNS
• Mild anterior chamber cells or flare
• Conjunctival injection
• Corneal edema with acute IOP rise
• Cataract
• Ectropion Uveae
• Optic disc cupping
• Visual field loss

8. SIGNS – IRIS
• Fine vessels around pupillary margin

9. SIGNS- IRIS
• Later diffuse
vessels on the iris
surface

10. SIGNS- IRIS

11. SIGNS - IRIS

12. SIGNS - ANGLE
• Early neovascularization without synechiae

13. SIGNS - ANGLE
• Sometimes a red blush to the trabecular meshwork
• The membrane that accompanies the vessels impairs
outflow
• Note that angle vessels can be present without iris
vessels

14. SIGNS- ANGLE
• Later the membrane pulls the iris over the angle and
causes synechial angle closure
• Elevated IOP > 60mmHg

15. SIGNS - ANGLE
• Because the corneal endothelium is normal the
synechiae don’t extend pass Schwalbe line
- Unlike ICE (irido corneal endothelium syndrome)

16. SIGNS - ANGLE

18. MANAGEMENT
• History (Determine the underlying etiology)
• Complete Ocular Examination
IOP
Gonioscopy
Dilated fundus exam

19. INVESTIGATIONS
Systemic Investigations
• Blood pressure
• Fasting blood sugar
• CBC
• Fasting lipid profile
• Carotid doppler
• Renal profile

20. INVESTIGATIONS
Ocular investigations
• B - Scan
• Fluorescein angiography (confirming etiology and
delineating ischemia)
• Anterior segment OCT (angle assessment)

21. DIFFERENTIAL DIAGNOSIS
• Primary angle closure glaucoma : no NVI’s and NVA’s
• Uveitic glaucoma : KP’s , NVA’s present, NVI’s are
rare
• Fuchs Heterochromia Iriditis : Stellate KP’s, NVA’s
present, NVI & NVG rare
• ICE syndrome : Corneal decompensation, correctopia,
iris atrophy
• Old trauma : Angle recession, iris pigment clumps, No
NVIs

22. TREATMENT
• Where possible treat the underlying pathology
• Frequent review (specially first few months after
CRVO)
Medical treatment
• Aqueous suppressants
• Miotics are contraindicated, prostaglandin derivatives
used with caution
• Topical steroids and cycloplegics

23. TREATMENT
Panretinal photocoagulation for proliferative diabetic
retinopathy
For other conditions such as CRVO, PRP without
delay
If retinal view poor one can
use indirect ophthalmoscopy or
in operating room with iris hooks
Trans-scleral cryotherapy

24. TREATMENT
• Intraocular VEGF inhibitors like bevacizumab (Avastin
®) or Ranibizumab (Patizra ®) have proven to be
effective in drying up anterior segment
neovascularization
• Intracameral injection is an alternative to intravitreal
route
- CRAO in ocular ischemic syndrome

25. TREATMENT
Other treatment options
•Ciliary body ablative procedures ie. Cyclodiode or
cyclocryotherapy ; if visual prognosis is poor
• Filtration Surgery if visual acuity is hand movement
(HM) or better
Trabeculectomy with active NVG has a poor
prognosis
Tube shunts
• Pars plana vitrectomy and retinal detachment repair

26. FOLLOW UP
• Long term follow up is needed
Complications :
• Uncontrolled IOP
• Hyphema
• Loss of vision

27. KEY POINTS
• A common secondary open angle glaucoma with
progression to synechial angle closure
• Should not be confused with pupillary block
• Can have NVA without NVI
Need to do regular gonioscopy
• Treat the underlying cause

28. THANKYOU 