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31]

Major Review

Neovascular glaucoma
ABSTRACT
Neovascular glaucoma (NVG) is an intractable secondary glaucoma characterized by the growth of new vessels accompanied by a fibrovascular
membrane over the iris and iridocorneal angle. Majority of the cases of NVG are associated with ischemia and hypoxia of retina. The three most
common predisposing conditions are ischemic central retinal vein occlusion, proliferative diabetic retinopathy, and ocular ischemic syndrome.
Early identification of anterior segment neovascularization followed by prompt treatment is very important to prevent significant visual impairment.
A high index of suspicion, with careful anterior segment evaluation and gonioscopy in an undilated pupil, is the key for early detection of
neovascularization of iris and angle. Early stages of the disease can be managed with panretinal photocoagulation along with adjunctive use
of vascular endothelial growth factor inhibitors with or without intraocular pressure lowering agents. Medical management may not be sufficient
in advanced disease and may require surgical intervention.

Keywords: Ischemic central retinal vein occlusion, neovascular glaucoma, panretinal photocoagulation, trabeculectomy,
Vascular endothelial growth factor inhibitors

INTRODUCTION endothelial growth factor inhibitors (anti‑VEGFs),

Neovascular glaucoma (NVG) is a potentially blinding,
intractable secondary glaucoma, characterized by the
development of new vessels on the iris and/or angle,
often resulting in poor visual outcome if not detected
and treated aggressively. In 1906, Coats described the
histological appearance of new vessels on the iris in a
case of central retinal vein occlusion (CRVO).[1] Salus, in
1928, described new vessels over the iris in eyes with
diabetic retinopathy (DR).[2] In 1937, with the introduction
of gonioscopy, new vessels were visualized in the angle
causing progressive angle closure and elevation of
intraocular pressure (IOP). In 1963, Weiss et al. first
proposed the term “NVG,” while describing a case of
glaucoma associated with the presence of new vessels over
the iris and angle.[3] NVG has also been called hemorrhagic
glaucoma, congestive glaucoma, and rubeotic glaucoma.
Majority of NVG patients have severe underlying systemic
and ocular pathology and many patients have advanced
stage of the disease at presentation. This makes NVG
very difficult to treat. However, recent advances in
understanding the pathophysiology, and use of vascular
antifibrotic agents, and glaucoma drainage devices (GDDs)
in the management of NVG have resulted in relatively
better outcomes.
ETIOLOGY
The most common causes of NVG are CRVO, proliferative
DR (PDR), and ocular ischemic syndrome (OIS) [Table 1].
Central retinal vein occlusion
According to central vein occlusion study, the incidence of
NVG following CRVO was 16%.[4] One‑third of CRVO cases
are ischemic at presentation and remaining two‑thirds
nonischemic, with a conversion to ischemic at a rate of
Seshadri J. Saikumar, Anup Manju,
Nair Abhilash
Department of Cataract and Glaucoma, Giridhar Eye Institute,
Kochi, Kerala, India
Address for correspondence: Dr. Seshadri J. Saikumar,
Department of Cataract and Glaucoma, Giridhar Eye Institute,
Kadavanthra, Kochi, Kerala, India.
E‑mail: saikumarsj@yahoo.com

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DOI:
10.4103/kjo.kjo_77_18 How to cite this article: Saikumar SJ, Manju A, Abhilash N. Neovascular
glaucoma. Kerala J Ophthalmol 2018;30:172-7.

172 © 2018 Kerala Journal of Ophthalmology | Published by Wolters Kluwer - Medknow

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Saikumar, et al.: Neovascular glaucoma

Figure 1: Nonischemic central retinal vein occlusion Figure 2: Ischemic central retinal vein occlusion

Table 1: Causes of neovascular glaucoma with nonischemic CRVO do not develop NVG unless there
Most common causes Proliferative diabetic retinopathy is associated DR or OIS.
CRVO
Ocular ischemic syndrome
Other causes Ocular tumors
A study by Hayreh S S et al. suggested that, in the early acute
Ocular irradiation stage, ischemic CRVO can be reliably differentiated from
Chronic uveitis nonischemic CRVO using information provided by selected
Retinal vasculitis
Coat’s disease
diagnostic clinical tests:[6]
Eales’ disease
Frosted branch angiitis 1. Functional tests: These consist of visual acuity, visual
Giant cell astrocytoma of the retina
Peripheral retinal detachment field plotted with a Goldmann perimeter, relative afferent
X‑linked retinoschisis pupillary defect, and electroretinography
Frost disease 2. Morphological tests: These consist of ophthalmoscopy
Cryoglobulinemia
Churg‑Strauss syndrome and fundus fluorescein angiography (FFA) [Table 2].
Sickle cell retinopathy
Retinopathy of prematurity Proliferative diabetic retinopathy
CRVO – Central retinal vein occlusion
NVG is more commonly associated with PDR [Figure 3], although
it may occur without retinal or optic disc neovascularization.
Table 2: Clinical tests to differentiate ischemic central retinal
The incidence of neovascularization of iris (NVI) is 65% in PDR[7]
vein occlusion from nonischemic central retinal vein occlusion
due to increased vasoproliferative mediators in the anterior
Functional tests Sensitivity (%) Specificity (%)
segment. Pars plana vitrectomy (PPV) for PDR increases the
Visual acuity
≤20/400 91 88
incidence of NVI and of NVG, especially if the eye is left aphakic.
Peripheral visual fields* Presence of rubeosis before vitrectomy or unrepaired retinal
No I‑2e 97 73 detachment after vitrectomy is also risk factors. Intraocular
Defective I‑4e 92 87 silicone oil, on the other hand, decreases the incidence of NVI.[8]
Defective V‑4e 100 100 Cataract surgery can lead to the progression of DR and hence
Relative afferent pupillary defect increases the risk of NVG. However, an intact posterior capsule
≥0.9 log units 80 97 has a protective effect.[9]
Electroretinography 80 80
b‑wave amplifiers ≤60%
Ocular ischemic syndrome
*Peripheral visual fields plotted with Goldmann perimeter
OIS is caused by reduced blood flow to the eye which leads
to anterior and/or posterior segment ischemia. Anterior
10% [Figures 1 and 2]. NVG develops in 45% of ischemic segment ischemia causes iris or angle neovascularization
CRVO, with the maximum risk during 1st 7–8 months.[5] and NVG. OIS is most commonly associated with carotid
NVG is a complication only of ischemic CRVO. Therefore, if artery occlusive disease. Other less common causes include
a patient is identified with ischemic CRVO, one should have vascular occlusive disease of the aortic arch, ophthalmic,
a high index of suspicion for development of NVG. Eyes central retinal, or ciliary arteries.

Kerala Journal of Ophthalmology / Volume 30 / Issue 3 / September-December 2018 173

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Saikumar, et al.: Neovascular glaucoma
Figure 3: Proliferative diabetic retinopathy
PATHOGENESIS
Majority of the cases of iris and angle neovascularization are
associated with hypoxia and ischemia of retina. As a response to
tissue hypoxia, vascular endothelial cells secrete pro‑angiogenic
factors such as VEGF, tumor necrosis factor, insulin growth factor,
and platelet‑derived growth factor. This, in turn, stimulates a
chain reaction characterized by the activation, proliferation, and
migration of the endothelial cells and the formation of new blood
vessels. Iris and angle neovascularization is associated with the
development of a fibrovascular membrane over the anterior
surface of the iris and iridocorneal angle. This membrane is
difficult to visualize, blocks aqueous humor outflow through
trabecular meshwork, and increases the IOP. Subsequently,
the contraction of this membrane leads to the development of
progressive anterior synechiae and angle closure.
Stages of neovascular glaucoma
NVG can be divided into three stages:
1. Rubeosis iridis
2. Secondary open‑angle glaucoma
3. Secondary angle‑closure glaucoma.
Rubeosis iridis
NVI starts from the pupillary margin as tiny tufts or red
spots that can be easily missed unless examined carefully
at the slit lamp with an undilated pupil under high
magnification [Figure 4]. Rubeosis iridis is usually present
before neovascularization of the angle. However, in some
cases, neovascularization can start at the angle. Therefore,
gonioscopy with an undilated pupil is essential in all high‑risk
cases to diagnose early angle neovascularization even when
pupillary margin and iris are not involved.
Weiss and Gold classification of iris and anterior chamber
angle neovascularization.[10]
174 Kerala Journal of Ophthalmology / Volume 30 / Issue 3 / September-December 2018
• Iris Grade 1: Fine surface neovascularization of the
pupillary zone of the iris involving <2 quadrants
• Anterior chamber angle Grade 1: Fine neovascular twigs
cross scleral spur and ramify on trabecular meshwork
involving <2 quadrants
• Iris Grade 2: Surface neovascularization of the pupillary
zone of the iris involving more than 2 quadrants
• Anterior chamber angle Grade 2: Neovascular twigs cross
scleral spur and ramify on trabecular meshwork involving
more than 2 quadrants
• Iris Grade 3: In addition to neovascularization of the
pupillary zone, neovascularization of the ciliary zone of
the iris and/or ectropion uveae involving 1–3 quadrants
• Anterior chamber angle Grade 3: In addition to
neovascularization of trabecular meshwork, peripheral
anterior synechiae (PAS) involving 1–3 quadrants
• Iris Grade 4: Neovascularization of the ciliary zone of
the iris and/or ectropion uveae involving 3+ quadrants
• Anterior chamber angle Grade 4: PAS involving
3+ quadrants.
Secondary open‑angle glaucoma
The new vessels from the pupillary margin grow radially
on the surface of the iris toward the angle, cross the
ciliary body band and scleral spur on to the trabecular
meshwork [Figure 5]. A fibrovascular membrane, invisible
on gonioscopy, accompanies the new vessels, blocks the
trabecular meshwork, and raises the IOP.
Secondary angle‑closure glaucoma
In the late stage, myofibroblasts in the fibrovascular
membrane proliferate and contract to form PAS and cause
angle‑closure glaucoma.
The clinical features of advanced stage of NVG are as
follows [Figure 6]:
• Severe decrease in visual acuity
• Eye pain
• Conjunctival and episcleral congestion
• Corneal edema
• Aqueous flare
• Very high IOP
• Florid NVI and angle
• Ectropion Uveae
• Synechial angle closure on gonioscopy.
Diagnosis of neovascular glaucoma
A high index of suspicion is required to diagnose early NVG,
where IOP is not elevated and only subtle signs are present.
Examination of the iris and gonioscopy in an undilated
pupil is essential. Fluorescein angiography of the iris can
be useful in differentiating iris neovascularization from
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Saikumar, et al.: Neovascular glaucoma
Figure 4: Rubeosis iridis
Figure 5: Neovascularization of angle
Figure 6: Anterior segment photograph of advanced glaucoma with florid
iris neovascularization and ectropion uveae
normal iris vessels as the latter do not leak fluorescein.
FFA is important to illustrate the extent and area of retinal
ischemia. Electroretinogram also can help in diagnosing
retinal ischemia. Recently, anterior segment optical
Kerala Journal of Ophthalmology / Volume 30 / Issue 3 / September-December 2018
coherence tomography and ultrasound biomicroscopy are
being used more frequently for the diagnosis and staging
of the disease as they illustrate anterior chamber structures
in greater detail.
MANAGEMENT
Management of NVG can be divided into two types:
1. Treatment of underlying disease process responsible for
rubeosis
2. Treatment of elevated IOP.
TREATMENT OF UNDERLYING DISEASE PROCESS
Panretinal photocoagulation
Panretinal photocoagulation (PRP) remains the mainstay in
controlling the neovascular drive and should be considered
in all cases of NVG when retinal ischemia is present.[11]
Furthermore, the success rate of glaucoma filtering surgeries
increases with adequate preoperative PRP. The exact
mechanism by which PRP works is not clear. It destroys the
photoreceptor‑retinal pigment epithelium complex, which
accounts for the majority of retinal oxygen consumption,
allowing oxygen from choroidal circulation to diffuse into
the inner retina. This, in turn, decreases the inner retinal
hypoxia and reduces the stimulus for release of angiogenic
factors. PRP is commonly performed over 1–3 sessions.
Additional laser treatment needs to be done until complete
regression of new vessels. Sometimes PRP is very difficult
or not possible if the view of the fundus is very hazy. In
these situations, if the patient needs an intraocular surgery,
endocyclophotocoagulation can be performed along with PPV
instead of preoperative PRP. The outcome of treatment with
PRP is variable, depending on the underlying cause of NVG
and also the stage in which the disease was diagnosed. Lang
documented complete regression of retinal neovascularization
in 67%–77% and normalization of IOP in 42% of diabetic patients
treated with PRP.[12] In CRVO, PRP is indicated in the ischemic
form and also in anterior segment neovascularization.[4] This
is still a matter of controversy. According to Hayreh et  al.,
in their study, approximately one‑third of the eyes with
iris neovascularization treated with PRP would never have
developed NVG.[5] They also reported that eyes with ischemic
CRVO always have a large permanent central scotoma,
resulting in poor central visual acuity. Following PRP, the large
central scotoma combined with severe loss of peripheral visual
fields may virtually blind the eye. In OIS, uveal ischemia alone
can be responsible for neovascularization and PRP should be
performed only if FFA shows retinal ischemia due to retinal
capillary obliteration.[13] Furthermore, PRP may paradoxically
increase IOP. Surgical carotid endarterectomy would be the
best treatment in these cases.[14]
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Saikumar, et al.: Neovascular glaucoma
Vascular endothelial growth factor inhibitors
The role of anti‑VEGFs in the management of NVG has been
studied extensively. Anti‑VEGF injection leads to regression
of anterior and posterior segment neovascularization and
reduction of IOP. Anti‑VEGF agents that are currently used
include bevacizumab, ranibizumab, and aflibercept. However,
there is no evidence available to suggest that either of the
agents is superior to others in managing NVG. Intravitreal
injection of bevacizumab causes regression of iris and angle
neovascularization within 24–48 h compared to PRP, which
takes 2–3 weeks. Bevacizumab is also effective in reducing
intraocular inflammation and pain, and in a few reports, IOP
lowering has been noted in the open‑angle stage.[15] However,
anti‑VEGFs are used only as an adjunct to PRP, medical
therapy, and surgery. The most frequent recommendation
is the combination of intravitreal anti‑VEGF and PRP.
Bevacizumab‑induced regression of neovascularization is
often temporary and recurrence is possible,[16] while PRP
provides a more permanent reduction of the ischemic
angiogenic stimulus. PRP with adjunctive use of intravitreal
anti‑VEGF agent along with antiglaucoma medications may
be sufficient to control IOP in the open‑angle stage of NVG.
Surgical intervention for IOP lowering is often required in
advanced stage with synechial angle closure. In cases, where
PRP is not possible due to media opacities, intravitreal
bevacizumab can be given followed by trabeculectomy with
mitomycin C (MMC).[17]
A recent study [18] reports that intravitreal aflibercept
may be effective for NVI and open‑angle stages of NVG.
However, repeated intravitreal anti‑VEGF injections may
cause both transient as well as sustained elevation of
IOP.[19] Further research is needed to evaluate the long‑term
effect of anti‑VEGFs, on visual acuity, IOP, and ocular
neovascularization, in the management of NVG.
TREATMENT OF ELEVATED INTRAOCULAR PRESSURE
Medical management
Topical antiglaucoma medications which suppress aqueous
humor production (Beta blockers, topical carbonic anhydrase
inhibitors, and alpha‑2 adrenergic agonists) are the first
step to reduce IOP. Prostaglandin analogs which work by
increasing the uveoscleral outflow are not useful if the angles
are closed. Furthermore, prostaglandin analogs cause further
breakdown of the blood aqueous barrier with worsening of
intraocular inflammation. Pilocarpine is contraindicated as
it increases inflammation, causes miosis, worsen synechial
angle closure, and decreases uveoscleral outflow. Topical
corticosteroids are used concurrently to treat any associated
inflammation. Atropine may be used for cycloplegia, to
increase uveoscleral outflow and to reduce the incidence of
176 Kerala Journal of Ophthalmology / Volume 30 / Issue 3 / September-December 2018
hyphema. Systemic medications such as osmotic agents and
oral carbonic anhydrase inhibitors can be given along with
topical medications to further reduce IOP. They help to clear
the cornea which helps us to make a proper diagnosis and
provide appropriate treatment. However, medical therapy is
less useful in patients with extensive synechial angle closure.
Surgical management
Glaucoma surgery is helpful in the open‑angle stage of
NVG, to control IOP until PRP takes effect, and in synechial
angle‑closure stage, for long‑term IOP control. Surgical
interventions for NVG include trabeculectomy with
antimetabolites, GDDs, and cyclodestructive procedures.
TRABECULECTOMY
The success of trabeculectomy alone is limited by severe
inflammation associated with NVG. However, the adjunct
use of antimetabolites has improved the success rate of
trabeculectomy. Intraoperative use of MMC reduces the
risk of bleb failure due to subconjunctival scarring. High
dose (0.04%) and/or longer duration of contact (2–3 min) of
MMC can be used. Subconjunctival use of 5‑Fluorouracil (5 FU)
or MMC can be considered postoperatively in patients who
show early signs of bleb failure or aggressive vascularization.
Sisto et  al.[20] achieved 54% success rate with the use of
intraoperative MMC with a mean follow‑up of 18 months
and 55% success rate with the use of postoperative 5 FU
with a mean follow‑up of 35 months. Regression of NVI
and reduced intraocular inflammation before surgery
increases the success rate of trabeculectomy. With the use
of preoperative bevacizumab, success rate may improve
up to 95%.[21] Therefore, it is recommended that sufficient
PRP and/or anti‑VEGF agents should be given before
trabeculectomy with MMC. Surgical intervention should be
planned within a week of injection of anti‑VEGF. Combined
cataract and glaucoma surgery can be planned if media is
hazy due to cataract, followed by PRP whenever possible. If
media is hazy due to vitreous hemorrhage and clarity does
not improve after a short period of observation, PPV with
endolaser photocoagulation may be considered.
Glaucoma drainage devices
GDDs are considered in the management of NVG when
trabeculectomy fails or when there is high risk of failure
because of excessive conjunctival scarring. Use of anti‑VEGFs
is recommended at least 24 h before surgery. The problems
with GDD implantation in NVG are early postoperative
hypotony, blockage of tube in the anterior chamber and
postoperative fibrous encapsulation. Various drainage devices
such as Molteno implant, Baerveldt implant, and Ahmed
glaucoma valve have been used in the management of NVG
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Saikumar, et al.: Neovascular glaucoma
and show no statistically significant difference in either
IOP lowering effect or overall success.[22] However, some
studies have reported that success rate with valve surgeries
significantly decreases over time in eyes with NVG.[23‑27]
Furthermore, Shen reported a comparable surgical outcome
with augmented trabeculectomy and Ahmed glaucoma valve
implantation in eyes with NVG.[28]
Cyclodestructive procedures
Cyclodestruction remains an effective treatment option
in eyes with refractory NVG having poor visual prognosis.
These procedures destroy the ciliary body to reduce
aqueous humor production. They may be highly effective in
achieving IOP control. However, it is difficult to titrate the
effect on ciliary body and excessive treatment may lead to
hypotony and phthisis. Transscleral cyclophotocoagulation or
endocyclophotocoagulation may have a lower complication
rate compared with cyclocryotherapy.
In painful blind eyes, it is reasonable to try retrobulbar alcohol
injection. Some intractable cases may require enucleation or
evisceration.
CONCLUSION
NVG is a potentially devastating secondary glaucoma and
remains a therapeutic challenge. Early diagnosis and proper
management are crucial to prevent or reduce the extent of
visual loss. Early stage of the disease with open angles can
be managed with antiglaucoma medications and PRP along
with adjunctive use of anti‑VEGF agents. Advanced disease
with synechial angle closure resulting in very high IOP may
be refractory to antiglaucoma medications and often requires
surgical interventions.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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