This document discusses neovascular glaucoma, also known as rubeotic glaucoma. It begins by defining the terminology and describing the clinical features. The main causes of neovascular glaucoma are diabetic retinopathy, central retinal vein occlusion, and carotid artery occlusive disease, all of which result in ocular tissue hypoxia. This hypoxia leads to the release of angiogenic factors like vascular endothelial growth factor that induce new blood vessel growth on the iris and in the anterior chamber angle, causing glaucoma. Later sections discuss theories of neovasculogenesis, angiogenic and vasoinhibitory factors, clinical course, differential diagnosis, medical management, and surgical options.

1. NEOVASCULA
R GLAUCOMA

2. TERMINOLOGY
• In 1906, Coats described new vessel
formation on the iris in eyes with central
retinal vein occlusion
• This neovascularization of the iris is
commonly known as Rubeosis iridis

3. • Rubeosis iridis is frequently associated with a
severe form of glaucoma, which has been given
different names on the basis of various clinical
features:
• Hemorrhagic glaucoma, referring to the
hyphema that is present in some cases
• Congestive glaucoma, describing the frequently
acute nature of the condition and
• Thrombotic glaucoma, implying an underlying
vascular thrombotic cause.

4. • However the term rubeotic glaucoma or
neovascular glaucoma, was proposed by
Weiss and colleagues is the term found most
often in the current literature
• Neovascular glaucoma is an important entity
because it often causes great morbidity and
visual loss.

5. FACTORS PREDISPOSING TO
RUBEOSIS IRIDIS
• Diabetic retinopathy and
central retinal vein occlusion (CRVO)
are the primary pathologic processes
involved in the development of ocular
neovascularization .
• 36% of all cases of NVG arise from CRVO, 32%
from proliferative diabetic retinopathy, and
13% from carotid artery occlusive disease

6. The common denominator in all of these diseases
is OCULAR TISSUE HYPOXIA.

7. Diabetic Retinopathy
• Approximately one third of patients with
rubeosis iridis have diabetic retinopathy
• Neovascular glaucoma is usually seen in eyes
with proliferative diabetic retinopathy, but
it can be seen in eyes with nonproliferative
retinopathy if there are large areas of
capillary nonperfusion
• Lens and vitreous may act as mechanical
barriers to the forward movement of
angiogenic factors elaborated by the retina.
The vitreous may also serve as an
endogenous inhibitor of angiogenic stimuli.

8. . After pars plana vitrectomy for diabetic
retinopathy, the reported incidence of NVI
ranges from 25% to 42%, whereas that for
NVG ranges from 10% to 23% , with most of
these cases developing during the first 6
months after surgery
In these cases, NVI and NVG occur more
often in aphakic eyes
Postoperative neovascular glaucoma is also
more common when rubeosis iridis is present
before vitrectomy

9. • An unrepaired retinal detachment after
vitrectomy for diabetic retinopathy is also a
risk factor for postoperative rubeosis iridis.
The acute onset or exacerbation of rubeosis
iridis after diabetic vitrectomy can indicate
the presence of a peripheral traction retinal
detachment .
• A completely attached retina and
aggressive anterior or peripheral
photocoagulation therapy are the most
important factors in controlling or preventing
neovascular glaucoma after vitrectomy for
proliferative diabetic retinopathy

10. • Intraocular silicone oil also reduces the
incidence of anterior segment
neovascularization, possibly by acting as a
diffusion or convection barrier to the
posterior movement of oxygen from the
anterior chamber or the anterior movement
of an angiogenesis factor

11. Intracapsular cataract surgery alone in eyes
with diabetic retinopathy has been
associated with an increased incidence of
postoperative NVI and NVG
• The incidence is similar with extracapsular
extraction and a primary capsulotomy.
• Leaving the posterior capsule intact
appears to reduce the likelihood of this
complication, although a subsequent laser
capsulotomy in patients with diabetes may
lead to NVG

12. Retinal Vascular Occlusive
Disorders
• Central retinal vein occlusion accounted for 1/3 of
all cases of NVI in one series
• Approximately 50% of eyes develop NVG
following ischaemic central retinal vein occlusion.
• Extensive peripheral retinal capillary non-
perfusion on fluorescein angiography is the most
valuable predictor of the risk of subsequent NVG
• Glaucoma typically occurs 3 months after the
occlusion (‘100-day glaucoma’) but intervals from
4 weeks to 2 years have been documented

13. • Older patients with central retinal vein
occlusions often have associated
glaucoma or elevated IOP.
• The presence of pre-existing POAG increases
the risk of NVG after central retinal vein
occlusion
• Adequate treatment of the pre-existing
glaucoma does not prevent the onset of
neovascularization.
• Furthermore, pre-existing open-angle
glaucoma may make any subsequent
neovascular glaucoma more refractory to
treatment.

14. • Eyes with ischemic central retinal vein
occlusions should receive panretinal
photocoagulation (or cryoablation if no laser
is available) to reduce the incidence of
neovascular glaucoma.
• Careful follow-up is mandated even in those
with the non-ischemic type because of the
observation that one-third of eyes with
central retinal vein occlusion and good
perfusion at the onset show signs of ischemia
by 3 years

15. Extraocular Vascular Disorders
• Carotid artery obstructive disease is probably
the third most common cause of neovascular
glaucoma, accounting for 13% of all cases
• Carotid artery obstruction does not cause
neovascular glaucoma in all cases because
there is usually sufficient collateral flow to
prevent widespread retinal ischemia.

16. • Neovascular glaucoma associated with carotid
artery disease often has a confusing presentation
and a variable course.
• If anterior segment ischemia is severe, the
vessels on the iris may be less visible, and the IOP
may be normal or even low despite extensive
neovascular closure of the angle.
• These eyes often suffer wide swings in IOP,
depending on the perfusion to the ciliary body.
• Patients who undergo surgery to relieve or bypass
carotid artery obstruction may experience a
dramatic rise in IOP when the ciliary body blood
supply improves and aqueous humor formation
increases.

17. • Panretinal photocoagulation may be less
successful in eliminating iris
neovascularization in patients with carotid
artery obstruction because the anterior
segment of these eyes is also ischemic and is
not affected by retinal ablation techniques

18. THEORIES OF
NEOVASCULOGENESIS
• RETINAL HYPOXIA
• The pathogenesis of neovascular glaucoma is
that retinal ischemia liberates angiogenic
factors that diffuse forward and induce new
vessel formation on the iris and in the angle
• Inflammation and hypoxia often coexist in the
microenvironment leading to new vessel
formation.
• Inflammatory mediators are now known to play
a role in new vessel formation and remodeling,
along with their role in inflammation

19. ANGIOGENESIS FACTORS
• Human retinas and other vascular ocular tissues
have angiogenic activity related to a key
angiogenic peptide, vascular endothelial growth
factor (VEGF)
• Several cell types in the retina synthesize VEGF,
but under conditions of retinal ischemia, Müller
cells appear to be the primary source.
• Four VEGF isoforms (VEGF121, VEGF165, VEGF189,
and VEGF206) have been identified, which are
generated by alternative mRNA splicing from the
same gene
• VEGF165 is the most abundant form in the
majority of tissues.

20. • VEGF is a potent angiogenic stimulator,
promoting several steps of angiogenesis,
including proliferation, migration, proteolytic
activity, and capillary tube formation, thus
playing a crucial role in both normal and
pathologic angiogenesis.
• It is also known as a vascular permeability factor
on the basis of its ability to induce vascular
hyperpermeability and endothelial cell
proliferation as well as migration

21. • Vasoproliferative factors have been detected
in increased amounts in the eyes of both
animal models and patients with neovascular
glaucoma.
• It is found in concentrations 40–100 times
normal in the aqueous humor of patients
with neovascular glaucoma
• And most recently is the impressive
regression of new vessels induced by
molecular-specific antiangiogenic factors,
such as bevacizumab.

22. VASOINHIBITORY FACTORS
• It has been postulated that ocular tissues
may produce substances that inhibit
neovascularization.
• The vitreous and lens are possible sources of
these vasoinhibitory factors which could
explain why vitrectomy or lensectomy
increases the risk for rubeosis iridis in eyes
with diabetic retinopathy.
• Retinal pigment epithelial cells release an
inhibitor of neovascularization

24. CLINICOPATHOLOGIC COURSE

29. DIFFERENTIAL DIAGNOSIS

31. MANAGEMENT

39. SURGICAL MANAGEMENT