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Neovascular Glaucoma
Updated: Aug 01, 2016
Author: Hemang K Pandya, MD; Chief Editor: Hampton Roy, Sr, MD

Overview

Background
Neovascular glaucoma (NVG) is classified as a secondary glaucoma. First documented in 1871, historically, it has been
referred to as hemorrhagic glaucoma, thrombotic glaucoma, congestive glaucoma, rubeotic glaucoma, and diabetic
hemorrhagic glaucoma. Numerous secondary ocular and systemic diseases that share one common element, retinal
ischemia/hypoxia and subsequent release of an angiogenesis factor (eg, vascular endothelial growth factor [VEGF]), cause
NVG. These angiogenesis factors causes new blood vessel growth from preexisting vascular structure. Depending on the
progression of NVG, it can cause glaucoma either through secondary open-angle or secondary closed-angle mechanisms.
This is accomplished through the growth of a fibrovascular membrane over the trabecular meshwork in the anterior chamber
angle, resulting in obstruction of the meshwork and/or associated peripheral anterior synechiae.

NVG is a potentially devastating glaucoma, where delayed diagnosis or poor management can result in complete loss of
vision or, quite possibly, loss of the globe itself. Early diagnosis of the disease, followed by immediate and aggressive
treatment, is imperative. In managing NVG, it is essential to treat both the elevated intraocular pressure (IOP) and the
underlying cause of the disease.[1]

It is essential that primary care physicians refer all patients with diabetes, including those with sudden vision loss, to their
local ophthalmologists for a dilated fundus examination. In addition, as neovascular glaucoma may present with severe pain,
emergency medicine physicians should become proficient with slit-lamp examination to evaluation for iris
neovascularization.

Ophthalmologists should remain cautious when managing patients with diabetic and retinal vein occlusion. They should
keep a low threshold for referring patients to their local retina specialists for further management.

Pathophysiology
Retinal ischemia is the most common and important mechanism in most, if not all, cases that result in the anterior segment
changes causing NVG. Various predisposing conditions cause retinal hypoxia and, consequently, production of
angiogenesis factors.

Several angiogenesis factors have been identified as potential agents causing ocular neovascularization. Recent studies
suggest that vascular endothelial growth factor (VEGF) might play a central role in angiogenesis.[2]

Once released, the angiogenic factor(s) diffuses into the aqueous and the anterior segment and interacts with vascular
structures in areas where the greatest aqueous-tissue contact occurs. The resultant growth of new vessels at the pupillary
border and iris surface (neovascularization of the iris [NVI]) and over the iris angle (neovascularization of the angle [NVA])
ultimately leads to formation of fibrovascular membranes. The fibrovascular membranes, which may be invisible on
gonioscopy, accompany NVA and progressively obstruct the trabecular meshwork. This causes secondary open-angle
glaucoma.

As the disease process continues, the fibrovascular membranes along the NVA tend to mature and contract, thereby tenting
the iris toward the trabecular meshwork and resulting in peripheral anterior synechiae and progressive synechial angle
closure. Elevated IOP is a direct result of this secondary angle-closure glaucoma.

Epidemiology
Frequency
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United States

Incidence of NVG is rare.

Mortality/Morbidity

Treatment of NVG is difficult. Maintaining visual acuity in patients with NVG also is difficult.

Age

NVG is more prevalent in elderly patients.

Prognosis
Owing to retinal ischemia and intraocular pressure damage to the optic nerve, visual prognosis is often poor. As with most of
medicine, prevention is the primary goal in patients with vasculopathy.

Presentation

History
A careful and detailed ocular and systemic history is imperative in diagnosing both neovascular glaucoma (NVG) and the
underlying problem causing it.

Physical
A complete ocular examination of both eyes, particularly of the posterior segment, will almost certainly provide the etiology
of neovascularization. Of the 3 most common causes of NVG, ocular ischemic syndrome presents as a diagnostic dilemma
and, thus, deserves special mention.

The typical clinical presentation of NVG is the same regardless of the underlying cause. The typical clinical presentation can
be divided into the following 2 stages: the early stage and the advanced stage. These stages generally follow each other in
progression, and the early stage is subdivided further into rubeosis iridis and secondary open-angle glaucoma.

Early stage (rubeosis iridis)

Findings of rubeosis iridis may include the following:

Normal IOP

Presence of tiny, neovascular, dilated capillary tufts at pupillary margin

High magnification on slit lamp (to view earliest finding in NVG)

NVI (irregular, nonradial vessels usually not in the iris stroma)

NVA (can occur with or without NVI)

Careful gonioscopy in all eyes at high risk for NVG even without pupillary and iris involvement

Poorly reactive pupil

Ectropion uvea

Early stage (secondary open-angle glaucoma)

Findings of secondary open-angle glaucoma may include the following:

Elevated IOP

NVI continuous with NVA

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Proliferation of neovascular tissue over the angle

Fibrovascular membranes (develop circumferentially across the angle, blocking the trabecular meshwork)

Advanced stage

In this stage, secondary angle-closure glaucoma is characterized by some or all of the following:

Acute severe pain, headache, nausea, and/or vomiting

Photophobia

Reduced visual acuity (counting fingers to hand motion)

Elevated IOP (≥ 60 mm Hg)

Conjunctival injection

Corneal edema

Plus/minus hyphema

Aqueous flare

Synechial angle closure

Severe rubeosis

Distorted, fixed, mid-dilated pupil and ectropion uveae

Retinal neovascularization and/or hemorrhage

Optic nerve cupping (possibly)

Ocular ischemic syndrome

Ocular ischemic syndrome occurs in the presence of more than 90% of patients with carotid artery stenosis, but it can occur
as a result of aortic arch disease (eg, syphilis, Takayasu arteritis, dissecting aneurysm), in which case the presentation may
be bilateral.

Symptoms include a dull periocular/periorbital pain that can be secondary to the ischemia and/or NVG.

Signs include the following:

Vision can vary from 20/20 to no light perception.

Midperipheral intraretinal hemorrhage (in contrast to diabetic retinopathy and CRVO where the hemorrhage is mostly
situated in the posterior pole)

IOP can be elevated secondary to NVG, decreased secondary to ciliary body hypoperfusion, or normal as a result of
both processes.

Other signs include corneal decompensation, iritis, iris atrophy, cataract, and spontaneous pulsations of the central
retinal artery.

Intravenous fluorescein angiogram will demonstrate prolonged choroidal filling and increased arteriovenous transit
time.

Causes
Relatively frequent causes of NVG include the following:

Central retinal vein occlusion (CRVO)

Proliferative diabetic retinopathy

Carotid artery occlusive disease (CAOD)

Less frequent causes of NVG include the following:

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Branch retinal vein occlusion

Central retinal artery occlusion (CRAO)

Intraocular tumor

Chronic retinal detachment

Secondary to intraocular lens (uveitis-glaucoma-hyphema [UGH] syndrome)

Chronic or severe ocular inflammation

Endophthalmitis

Sickle cell retinopathy

Retinopathy of prematurity

Radiation retinopathy

Eales disease

Coats disease

Carotid-cavernous fistula

Ocular ischemic syndrome/carotid insufficiency

Takayasu disease

Giant cell arteritis

Anterior segment ischemia (ie, previous extraocular muscle surgery)

Trauma

Metastatic intraocular malignant lymphoma[3]

DDx

Differential Diagnoses
Acute Angle-Closure Glaucoma (AACG)

Workup

Workup

Imaging Studies
Image studies may include the following:

Intravenous fluorescein angiogram and electroretinography (ERG) to assess retinal ischemia

B-scan ultrasound

Optical coherence tomography[4] - Images observed per grade of neovascular glaucoma

Grades are as follows:

Grade 1: No modification

Grade 2: A slightly hyper-reflective linear iris secondary to neovascularization

Grade 3: A thickened hyper-reflective iridocorneal angle with possible iridocorneal synechiae

Grade 4: Closed iridocorneal angle associated with iris contraction and uveae ectropion

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Treatment

Medical Care
General principles for treating patients with neovascular glaucoma (NVG) include the following:

Identifying the underlying etiology is fundamental in the management of NVG.

CRVO, diabetic retinopathy, CAOD, and CRAO require systemic workup and appropriate intervention to prevent
further complications.

The management of NVG is approached through the following 4 stages that reflect the progression of the disease:
prophylactic treatment, early-stage treatment, advanced-stage treatment, and end-stage treatment.

Prophylactic treatment

Most patients are either at high risk for developing NVI/NVG or have early NVI with normal IOP. Prevention of NVG is the
single most important aspect in its management.

Reducing the amount of viable retina is known to inhibit and even to reverse new vessel proliferation in the anterior
segment. The mainstay in prevention is retinal ablation achieved via panretinal photocoagulation (PRP) or cryophototherapy
because of media opacities (ie, corneal edema, cataract, vitreous hemorrhage) or other patient factors. Other treatment
options in this stage include goniophotocoagulation.

PRP can be delivered in the following 3 ways: slit lamp delivery system, indirect laser, or endolaser at time of vitrectomy.

The amount of PRP required varies. The Diabetic Retinopathy Study (DRS) guidelines recommend 1200-1500 burns, with a
spot size of 500 µm to be applied to the peripheral retina. Many retina specialists recommend 1500-2000 burns, with a spot
size of 500-800 µm, using a wide-angle fundus contact lens (eg, Rodenstock). The types of laser include argon, krypton
(better with media opacities and retinal hemorrhages), and diode (same utility as krypton laser).

To begin, a 360° peritomy is performed with isolation of the 4 recti muscles. A 2.5-mm retinal cryoprobe is used to create
cryoapplication burns just anterior to the equator. Three spots are placed between each rectus muscle. Two additional rows
of application are performed posterior to the first so that the third row is just outside the major vascular arcades. In total, 32
cryoapplications are performed under direct visualization. The probe tip remains in contact with the sclera until 70° has been
maintained for 5-10 seconds. This procedure causes considerable inflammation, and complications (eg, tractional and
exudative retinal detachment, vitreous hemorrhage) can occur.

Goniophotocoagulation, another laser therapy, is performed directly to NVI before the development of NVG. Its role in
management of NVG is unclear, and it has not proven to be beneficial in preventing synechial closure of angle or advanced
NVG.

All patients should undergo fluorescein angiography to delineate nonischemic CRVO from ischemic CRVO. Virtually no
patients with nonischemic CRVO develop NVG. Overall incidence of NVG is 40% for an ischemic CRVO. NVI and NVG can
appear from 2 weeks to 2 years. More than 80% of patients with NVI/NVG present within the first 6 months. Of patients with
nonischemic CRVO, 15% can convert to ischemic CRVO within 8 months. The strongest predictors of NVI/NVG following
CRVO include extensive retinal capillary nonperfusion of intravenous fluorescein angiography (IVFA), extensive retinal
hemorrhages, short duration of occlusion, and male sex. In the Central Retinal Vein Occlusion Study, PRP was indicated for
IVFA confirmed ischemic CRVO if development of 2 clock hours of NVI occurred or any NVA was present.[5] No benefit
occurred when prophylactic PRP was performed prior to the development of NVI or NVA when frequent follow-up care was
provided.

Prophylactic PRP still is recommended by many retinal specialists before the development of NVI or NVA, especially in case
of the following: clear extensive capillary nonperfusion, extensive systemic vascular disease, patient who is monocular,
and/or noncompliance or poor follow-up results. Preoperative care is fundamental for all types of cataract surgery,
capsulotomy, and vitreous surgery.

For patients with diabetic retinopathy, ensure frequent follow-up care and tight glycemic control. If proliferative diabetic
retinopathy exists, then complete PRP is recommended as treatment.

Early-stage treatment

This stage is characterized by the development of a fibrovascular membrane across some or all of the angle, obstructing the
trabecular meshwork, and an increase in IOP.

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With secondary open-angle glaucoma, treatment is identical to prophylactic treatment and includes PRP (filler PRP if
already performed initially), panretinal cryotherapy, and medical therapy.

The most important medical therapy for this stage includes topical atropine 1% to decrease ocular congestion and topical
steroids (eg, prednisolone [Pred Forte, Inflamase Forte]) to decrease inflammation. Standard antiglaucoma medications to
treat secondary open-angle glaucoma are recommended. Other agents include topical beta-blockers (eg, levobunolol
[Betagan], timolol [Timoptic]), topical brimonidine (Alphagan), topical carbonic anhydrase inhibitor (eg, dorzolamide
[Trusopt], brinzolamide [Azopt]), and oral carbonic anhydrase inhibitor (eg, acetazolamide [Diamox]). Topical pilocarpine is
contraindicated because it may increase inflammation. The role of topical latanoprost (Xalatan) is unclear in the treatment of
early NVG.

The successful use of photodynamic therapy with verteporfin directed at the iris and the angle to obliterate
neovascularization and to reduce IOP has been reported.

Advanced-stage treatment

This stage is characterized by synechial closure of the angle and secondary angle-closure glaucoma.

PRP is still the initial and most important treatment, both to prevent further NVI/NVA and angle closure and to prepare the
eye for surgical intervention (see Surgical Care). Surgical intervention is indicated in eyes with potential for useful vision.

Medical therapy is indicated, with topical atropine and steroids being the most important agents. Antiglaucoma medications,
topical beta-blockers, and carbonic anhydrase inhibitors are also recommended. The role of topical brimonidine and
latanoprost in advanced disease is unclear. Topical pilocarpine and echothiophate iodide are contraindicated (may cause
increased inflammation and hyperemia). Oral glycerol and intravenous mannitol are recommended only if IOP is elevated
symptomatically.

Anti-VEGF therapy

Antivascular endothelial growth factor is frequently used for various conditions in which VEGF release is induced in
response to retinal ischemia. It is still under study as an adjunct[6] or alternative treatment for NVG. Anti-VEGFs such as
bevacizumab (Avastin), pegaptanib sodium (Macugen), and ranibizumab (Lucentis) block angiogenic factors that promote
the formation of new vessels, reversing the neovascularization process.[7, 8, 9] The initial use of anti-VEGF agents for the
treatment of retinal neovascularization has been expanded to include other pathology such as neovascular glaucoma.[10]
The quantity of growth factors in the aqueous decrease after intraocular injection of anti-VEGFs, decreasing further
progression of angular damage secondary to IOP increments.[11] However, other investigators have reported a lack of
efficacy of intravitreal bevacizumab in the treatment of neovascularization of the iris and iridocorneal angle but support its
use for diabetic retinopathy and central vein occlusion.[12, 13]

Several studies propose the use of anti-VEGF agents with traditional treatments such as panretinal photocoagulation (PRP),
with or without additional surgery and vary in the timing, combination, and place of injection (intracameral or intravitreal, or
both simultaneously). The most frequent recommendation by various authors for treatment is the adjunct combination of
intravitreal bevacizumab/panretinal photocoagulation for the treatment of neovascular glaucoma (NVG) instead of PRP
alone or as alternative treatment when visibility of the posterior segment is difficult due to opacities of the media (eg,
hemorrhage).[14]

Although intravitreal, and less commonly intracameral, delivery of anti-VEGF agents is preferred for the management of
NVG, several authors describe different protocols of treatment according to the stage of disease and the possible underlying
cause as standardized guidelines of NVG treatment with anti-VEGFs have not yet been established.

Several reports about the favorable response to intravitreal anti-VEGF agents in NVG have been published. In a review of
26 original papers between 2006 and August 2008, efficacy and safety of the procedure in 127 eyes was analyzed in a
series of cases: None had been performed in a clinical randomized controlled assay. The efficacy calculated in the sample
was 68.7%, and the recurrence rate was 18.6% at 4.2 months of follow-up. Ophthalmic complications were under 0.78%,
and no systemic complications were found.[15]

Intravitreal bevacizumab is the most frequent anti-VEGF adjunct treatment used for NVG due to the lower cost. Systematic
review of the efficacy and safety of intravitreal bevacizumab (IVB) in the treatment of neovascular glaucoma (NVG)
establishes bevacizumab is well tolerated, effectively stabilizes INV activity, and controls IOP in patients with INV when used
alone and at an early-stage of NVG.[16]

Randomized clinical trials are now being reported. Intraocular doses described for treatment with bevacizumab are 1
mg/0.05 mL, 1.25 mg/0.05 mL, or 2.5 mg/0.05 mL, according to the stage and recurrence of NVG.

In a case of ocular ischemic syndrome, a single injection of intravitreal bevacizumab (1.25 mg/0.05 mL injection) detained all
signs of neovascularization just one day after injection but failed to control IOP.[17]

Postintravitreal injection of a single dose of bevacizumab (1.25 mg) promotes quick response of pain relief 1 week
postinjection;[18] this safely facilitates further surgical intervention to lower IOP when treating refractory NVG.

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End-stage treatment

This stage is characterized by complete angle closure by peripheral anterior synechiae with no remaining useful vision.

The primary goal of treatment in this stage is pain control. Medical therapy includes topical atropine 1% and steroids. If
corneal decompensation occurs, use a bandage contact lens. Cyclodestructive procedures are performed if medical therapy
fails to provide symptomatic relief. With cyclocryotherapy, the IOP-lowering effect is achieved by destroying secretory ciliary
epithelium and/or reducing blood flow to the ciliary body. It is indicated as a last resort only if relief of pain is the main goal.
In a large series, 34% of eyes achieved IOP of less than 25 mm Hg; however, 34% of eyes became phthisical and 57% of
eyes lost all light perception. Other complications include sympathetic ophthalmia and anterior segment ischemia.

With Nd:YAG laser transscleral cyclophotocoagulation, 2 approaches, contact and noncontact, are used. In the contact
approach, one study reported a 40% decrease in IOP to less than 19 mm Hg in eyes with NVG. In the noncontact approach,
out of 27 eyes with NVG, only 15% achieved satisfactory IOP control.

The results of diode laser transscleral cyclophotocoagulation are similar to Nd:YAG cyclophotocoagulation.

Direct laser cyclophotocoagulation is performed under direct observation using the argon laser. Two approaches, transpupil
or with endoscopy, are used. Its role in NVG management is secondary. Success in controlling IOP is limited (may have less
inflammation and pain versus cyclocryotherapy).

Retrobulbar alcohol injection is indicated after all medical and surgical options have been explored and the patient does not
want an enucleation. Complications include external ophthalmoplegia and blepharoptosis. Enucleation is indicated only if
intractable pain is not relieved by any other treatment modality.

Surgical Care
Surgical care is indicated in patients with remaining useful vision. Preoperative care is fundamental to the postoperative
success of any surgical intervention.

With surgical care, ensure that adequate PRP is completed to reduce vasoproliferative stimulus. Atropine and steroids are
indicated to decrease inflammation, and antiglaucoma medication is indicated to decrease IOP. Wait approximately 3-4
weeks to allow the eye to quiet down.

Trabeculectomy with or without antifibrotic therapy and valve implant surgery

Surgical modalities include trabeculectomy with or without an antifibrotic agent and valve implant surgery.[8]

Trabeculectomy with the antifibrotic agents mitomycin-C and 5-fluorouracil (5-FU) is one modality. Trabeculectomy in NVG
has a significant failure rate. Using standard trabeculectomy (without antifibrosis), an IOP of less than 25 mm Hg on one
medication or less has been reported to occur in 67-100% of patients in 3 studies. Using injections of 5-FU subconjunctivally
in the postoperative period, the surgical success has been reported to be 68% over 3 years. Inject 0.1 mL of 5 mg/mL 5-FU
subconjunctivally either superiorly above the bleb or inferiorly (just above the lower fornix). Mitomycin-C used
intraoperatively has been shown to be more effective than 5-FU in routine trabeculectomies. No significant follow-up studies
exist on the use of mitomycin-C with trabeculectomy in NVG.

A retrospective cohort study from January 1994 to March 2007 of 101 eyes found that the prognostic factors for failure of
trabeculectomy with MMC for NVG were younger age and previous vitrectomy in patients with NVG, having a fellow eye
with NVG in patients with disease caused by diabetic retinopathy, and persistent proliferative membrane and/or retinal
detachment after vitrectomy.[19]

Valve implant surgery is another modality and is indicated when trabeculectomy fails or extensive conjunctival scarring
exists, thereby preventing a standard filtering procedure. Molteno, Krupin, and Ahmed valve implants commonly are used.
[20] One large series using the Krupin valve reported 79% of eyes with NVG had a 67% success rate in controlling IOP (<
24 mm Hg) with mean follow-up of 23 months. Long-term results are mixed. Using the Molteno implant, 60 eyes with NVG
achieved a satisfactory IOP (< 21 mm Hg) and maintenance of visual acuity over 5 years of only 10.3%. If combined with
the need for vitrectomy, consideration of pars plana tube-shunt insertion may reduce anterior segment complications.

Complications include postoperative hypotony with associated complications, blockage of internal fistula, blockage of
external filtration site (fibrosis of the filtering bleb), and corneal endothelial loss.

Adjunct anti-VEGF therapy

In a short case series, the use of intracameral bevacizumab prior to trabeculectomy with MMC improved NVG.[21]

The postoperative inhibition of angiogenesis after glaucoma surgery has also been described. Possible routes of
bevacizumab administration are subconjunctival application during trabeculectomy, postoperative needling, or intravitreal
injection during a filtrating procedure.[22]

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Bevacizumab has also been injected into the silicone oil in eyes with neovascular glaucoma after vitrectomy for advanced
diabetic retinopathy with favorable outcomes.[23]

Intravitreal bevacizumab is useful to safely and effectively implant an aqueous shunting tube in eyes with severe NVG and
intractable IOP, in addition to postoperative panretinal photocoagulation that reduces the recurrence of neovascular activity
improving the success rate of aqueous shunting surgery.[24]

Medication

Medication Summary
The most important medications include a regimen of topical steroids and atropine. Antiglaucoma medications include both
topical and oral agents.

Cycloplegic drugs

Class Summary
Paralyze ciliary muscle, preventing ciliary muscle spasm; provide pain relief; and decrease ocular congestion.

Atropine ophthalmic (Isopto, Atropair, Atropisol)

Acts at parasympathetic sites in smooth muscle to block response of sphincter muscle of iris and muscle of ciliary body to
acetylcholine, causing mydriasis and cycloplegia.

Steroidal anti-inflammatory

Class Summary
Decreases ocular inflammation.

Prednisolone acetate 1% (Pred Forte)

Treats acute inflammations following eye surgery or other types of insults to eye. Decreases inflammation and corneal
neovascularization. Suppresses migration of polymorphonuclear leukocytes and reverses increased capillary permeability.
In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if signs and symptoms do not improve
after 2 days, reevaluate patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.

Alpha2-adrenergic agonists

Class Summary
Decrease IOP by reducing aqueous humor production.

Brimonidine (Alphagan)
Selective alpha2-receptor that reduces aqueous humor formation.

Carbonic anhydrase inhibitors

Class Summary
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By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit carbonic
anhydrase in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.

Dorzolamide (Trusopt)
Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being
used, administer drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at
renal tubule and increasing renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous
humor.

Acetazolamide (Diamox, Diamox Sequels)

Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for
adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-
closure glaucoma when delay of surgery desired to lower IOP.

Prostaglandins

Class Summary
Used to reduce IOP in patients who are intolerant or resistant to other IOP-lowering medications. They are contraindicated
in glaucomas in which inflammation is a prominent ocular finding.

Bimatoprost (Lumigan)
Prostaglandin analog that selectively mimics effects of naturally occurring substances, prostamides. Exact mechanism of
action unknown but believed to reduce IOP by increasing outflow of aqueous humor through trabecular meshwork and
uveoscleral routes.

Travoprost ophthalmic solution (Travatan)

Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but
believed to reduce IOP by increasing uveoscleral outflow.

Unoprostone ophthalmic solution (Rescula)

Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but
believed to reduce IOP by increasing uveoscleral outflow and facilitating conventional outflow through the trabecular
meshwork

Beta-adrenergic blockers

Class Summary
The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous
humor production.

Levobunolol (AKBeta, Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production.

Timolol maleate 0.5% (Timoptic, Timoptic XE, Blocadren)

May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor.

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Follow-up

Further Outpatient Care

Ophthalmologists should provide long-term follow-up care for patients with neovascular glaucoma (NVG), closely monitoring
for any worsening in the patient's condition.

Intensity of follow-up care is related to the conditions predisposing the patient to the development of NVG (ie, CRVO,
diabetic retinopathy).

Complications
Complications include uncontrolled glaucoma, hyphema, and loss of vision.

Prognosis
Generally, NVG carries a very guarded prognosis. Prognosis is highly dependent on the following 2 factors: prevention and
treatment of NVG early in its course and the underlying disease process.

Patient Education
Patients with NVG must be educated about the disease process and its poor prognosis.

For excellent patient education resources visit eMedicineHealth's Eye and Vision Center and Diabetes Center. Also, see
eMedicineHealth's patient education articles Glaucoma Overview, Glaucoma FAQs, Glaucoma Medications, and Diabetic
Eye Disease.

Contributor Information and Disclosures

Author

Hemang K Pandya, MD Fellow in Vitreoretinal Disease and Surgery, Dean McGee Eye Institute, University of Oklahoma
College of Medicine

Hemang K Pandya, MD is a member of the following medical societies: American Academy of Ophthalmology, American
Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Michigan State Medical Society,
Michigan Society of Eye Physicians & Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Asheesh Tewari, MD Michigan Retina Center, PC

Asheesh Tewari, MD is a member of the following medical societies: American Academy of Ophthalmology, American
Society of Retina Specialists, Michigan Society of Eye Physicians & Surgeons, Michigan State Medical Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Bausch and Lomb; Dutch
Ophthalmic<br/>Serve(d) as a speaker or a member of a speakers bureau for: Allergan.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of
Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Martin B Wax, MD Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice
President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon

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Laboratories, Inc

Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American
Glaucoma Society, Society for Neuroscience

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical
Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American
College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Bradford Shingleton, MD Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff,
Department of Ophthalmology, Massachusetts Eye and Ear Infirmary

Bradford Shingleton, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Ophthalmology

Disclosure: Nothing to disclose.

Iqbal Ike K Ahmed, MD, FRCSC Clinical Assistant Professor, Department of Ophthalmology, University of Utah

Iqbal Ike K Ahmed, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology,
American Society of Cataract and Refractive Surgery, Canadian Ophthalmological Society, Ontario Medical Association

Disclosure: Nothing to disclose.

Baseer U Khan, MD

Baseer U Khan, MD is a member of the following medical societies: Canadian Ophthalmological Society

Disclosure: Nothing to disclose.

Khalid Hasanee, MD Glaucoma and Anterior Segment Fellow, Department of Ophthalmology, University of Toronto

Khalid Hasanee, MD is a member of the following medical societies: Canadian Medical Association, Canadian
Ophthalmological Society, Ontario Medical Association

Disclosure: Nothing to disclose.

Jacqueline Freudenthal, MD Co-Investigator, Ophthalmic Consultants Centre, Toronto

Jacqueline Freudenthal, MD is a member of the following medical societies: American Academy of Ophthalmology,
Association for Research in Vision and Ophthalmology, Canadian Ophthalmological Society

Disclosure: Nothing to disclose.

Acknowledgements

Yasser A Khan, MD Consulting Staff, Credit Valley Eye Care

Yasser A Khan, MD is a member of the following medical societies: Canadian Medical Association, Canadian
Ophthalmological Society, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

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