eMedicine Specialties > Ophthalmology > Intraocular Pressure
Glaucoma, Neovascular
Updated: Jun 26, 2006
Introduction
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, cause NVG. This angiogenesis factor 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.
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 an angiogenesis factor.
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.
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.
Frequency
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.
Clinical
History
A careful and detailed ocular and systemic history is imperative in diagnosing both 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)
- 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)
- Elevated IOP
- NVI continuous with NVA
- 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 (¡Ý60 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:
- 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
Differential Diagnoses
Glaucoma, Angle Closure, Acute
Other Problems to Be Considered
Inflammatory glaucoma
Fuchs heterochromic iridocyclitis
Workup
Imaging Studies
- Intravenous fluorescein angiogram and electroretinography (ERG) to assess retinal ischemia
- B-scan ultrasound
Treatment
Medical Care
- General principles for treating patients with 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. Fifteen percent of patients with nonischemic CRVO 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. 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.
- 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, 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, Betagan, Timoptic), topical brimonidine (eg, Alphagan), topical carbonic anhydrase inhibitor (eg, Trusopt, Azopt), and oral carbonic anhydrase inhibitor (eg, Diamox). Topical pilocarpine is contraindicated because it may increase inflammation. The role of topical latanoprost (eg, 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 also are 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.
- 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.
- Surgical modalities include trabeculectomy with or without an antifibrotic agent and valve implant surgery.
- 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.
- 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. 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.
Medication
The most important medications include a regimen of topical steroids and atropine. Antiglaucoma medications include both topical and oral agents.
Cycloplegic drugs
Paralyze ciliary muscle, preventing ciliary muscle spasm; provide pain relief; and decrease ocular congestion.
Atropine sulfate 1% (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.
Dosing
Adult
1 gtt to affected eye bid/qid
Pediatric
Administer as in adults
Interactions
Coadministration with other anticholinergics have additive effects; pharmacologic effects of atenolol and digoxin may increase with atropine; antipsychotic effects of phenothiazines may decrease with this medication; tricyclic antidepressants with anticholinergic activity may increase effects of atropine
Contraindications
Documented hypersensitivity; asthma; obstructive uropathy; paralytic ileus; toxic megacolon; myasthenia gravis
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in patients with Down syndrome and/or children with brain damage to prevent hyperreactive response; caution in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, hypertension, peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can have dysuria and may require catheterization
Steroidal anti-inflammatory
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.
Dosing
Adult
1 gtt to affected eye qid; taper dosage to clinical severity and response
Pediatric
Administer as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity; ocular fungal infections; ocular viral infections; ocular tuberculosis
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Caution in hypertension; known to cause cataract formation with chronic use; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate); concurrent contact lens wear may increase risk of infection; may delay healing if corneal abrasion is present
Alpha2-adrenergic agonists
Decrease IOP by reducing aqueous humor production.
Brimonidine tartrate 0.5% (Alphagan)
Selective alpha2-receptor that reduces aqueous humor formation.
Dosing
Adult
1 gtt to affected eye bid
Pediatric
Not established
Interactions
Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants, such as barbiturates, opiates, and sedatives, may potentiate effects of brimonidine
Contraindications
Documented hypersensitivity; MAOIs
Precautions
Pregnancy
B - Usually safe but benefits must outweigh the risks.
Precautions
May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack, and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy
Carbonic anhydrase inhibitors
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 hydrochloride 2.0% (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.
Dosing
Adult
1 gtt to affected eye bid/tid
Pediatric
Not established
Interactions
Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral carbonic anhydrase inhibitors
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy)
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.
Dosing
Adult
250 mg PO qid; 500 mg PO bid; one 500 mg PO dose, followed by 250 mg PO qid
Pediatric
8-30 mg/kg/d or 300-900 mg/m2/d PO divided q8h
Alternatively, 20-40 mg/kg/d PO divided q6h; not to exceed 1 g/d
Interactions
Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine; may affect elimination rates of certain drugs cleared by renal elimination; may result in anorexia, tachypnea, lethargy, coma, and death if taken concomitantly with high-dose aspirin
Contraindications
Documented hypersensitivity; hypokalemia; depressed renal or hepatic function; hyperchloremic acidosis; long-term use in chronic noncongestive angle-closure glaucoma
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some patients with diabetes
Prostaglandins
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.
Dosing
Adult
1 gtt of 0.03% solution in affected eye(s) hs; not to exceed 1 dose/d
Pediatric
Not established
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
High incidence of hyperemia; may cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; bacterial keratitis may occur; caution in uveitis or macular edema; do not instill if wearing contact lenses
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.
Dosing
Adult
1 gtt in affected eye(s) hs; not to exceed 1 dose/d
Pediatric
Not established
Interactions
None reported
Contraindications
Documented hypersensitivity; pregnancy
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Commonly causes ocular hyperemia; may cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; bacterial keratitis may occur; caution in uveitis or macular edema; do not instill if wearing contact lenses
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
Dosing
Adult
1 gtt in affected eye(s) bid
Pediatric
Not established
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Well tolerated ocularly; may cause permanent increase in pigment to iris (ie, increases brown pigment) and eyelid; may increase eyelash growth; may cause bacterial keratitis; caution in uveitis or macular edema; do not instill if wearing contact lenses
Beta-adrenergic blockers
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.
Dosing
Adult
1 gtt to affected eye bid
Pediatric
Not established
Interactions
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Contraindications
Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Beta-blockade may potentiate muscle weakness that is consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons
Timolol maleate 0.5% (Timoptic, Timoptic XE, Blocadren)
May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor.
Dosing
Adult
1 gtt of 0.25% or 0.5% in affected eye(s) bid; if IOP is maintained at satisfactory levels, change dosage to 1 gtt in affected eye(s) qd
If clinical response not adequate, change dosage to 1 gtt of 0.5% solution in affected eye(s) bid; if IOP is still not at satisfactory level, consider concomitant therapy
Pediatric
Administer as in adults
Interactions
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Contraindications
Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock
Precautions
Pregnancy
C - Safety for use during pregnancy has not been established.
Precautions
Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, chronic obstructive pulmonary disease, and mental changes (especially in elderly patients)
Follow-up
Further Outpatient Care
- Ophthalmologists should provide long-term follow-up care for patients with 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 eMedicine's Glaucoma Center and Diabetes Center. Also, see eMedicine's patient education articles Glaucoma Overview, Glaucoma FAQs, Understanding Glaucoma Medications, and Diabetic Eye Disease.
Miscellaneous
Medicolegal Pitfalls
- Early detection of NVG and patient education about its poor prognosis are essential.
References
Albert DM, Jakobiec FA. Neovascular glaucoma. Principles and Practice of Ophthalmology, Clinical Ophthalmology [book on CD-ROM]. Chapter 215.
Browning DJ, Scott AQ, Peterson CB. The risk of missing angle neovascularization by omitting screening gonioscopy in acute central retinal vein occlusion. Ophthalmology. May 1998;105(5):776-84. [Medline].
Epstein DL, Allingham RR, Schuman JS. Chandler and Grant's Glaucoma. 4th ed. 1997;309-18.
Gupta V, Agarwal HC. Contact trans-scleral diode laser cyclophotocoagulation treatment for refractory glaucomas in the Indian population. Indian J Ophthalmol. Dec 2000;48(4):295-300. [Medline].
Lieberman MF, Ewing RH. Drainage implant surgery for refractory glaucoma. Int Ophthalmol Clin. Summer 1990;30(3):198-208. [Medline].
Muller VA, Ruokonen P, Schellenbeck M, et al. Treatment of rubeosis iridis with photodynamic therapy with verteporfin--A new therapeutic and prophylactic option for patients with the risk of neovascular glaucoma?. Ophthalmic Res. Jan-Feb 2003;35(1):60-4. [Medline].
Parodi MB, Iacono P. Photodynamic therapy with verteporfin for anterior segment neovascularizations in neovascular glaucoma. Am J Ophthalmol. Jul 2004;138(1):157-8. [Medline].
Schlote T, Derse M, Rassmann K. Efficacy and safety of contact transscleral diode laser cyclophotocoagulation for advanced glaucoma. J Glaucoma. Aug 2001;10(4):294-301. [Medline].
Shields MB. Textbook of Glaucoma. 4th ed. 1998;269-86.
Sivak-Callcott JA, O''Day DM, Gass JD. Evidence-based recommendations for the diagnosis and treatment of neovascular glaucoma. Ophthalmology. Oct 2001;108(10):1767-76; quiz 1777, 1800. [Medline].
The Central Vein Occlusion Study Group. A randomized clinical trial of early panretinal photocoagulation for ischemic central vein occlusion. The Central Vein Occlusion Study Group N report. Ophthalmology. Oct 1995;102(10):1434-44. [Medline].
Tripathi RC, Li J, Tripathi BJ. Increased level of vascular endothelial growth factor in aqueous humor of patients with neovascular glaucoma. Ophthalmology. Feb 1998;105(2):232-7. [Medline].
Keywords
NVG, open angle, closed angle, vision loss, visual deficit, secondary glaucoma, hemorrhagic glaucoma, thrombotic glaucoma, congestive glaucoma, rubeotic glaucoma, diabetic hemorrhagic glaucoma
Contributor Information and Disclosures
Author
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.
Coauthor(s)
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, and Ontario Medical Association
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, and Ontario Medical Association
Disclosure: Nothing to disclose.
Baseer U Khan, MD, Staff Physician, Department of Ophthalmology, University of Toronto, Canada
Baseer U Khan, MD is a member of the following medical societies: Canadian Ophthalmological Society
Disclosure: Nothing to disclose.
Medical Editor
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 and American Academy of Ophthalmology
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Managing Editor
Martin B Wax, MD, Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Society for Neuroscience
Disclosure: Alcon Labs Salary Employment
CME Editor
Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
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, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.
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