eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Unilateral

Ingrid U Scott, MD, MPH, Professor, Department of Ophthalmology and Public Health Sciences, Penn State College of Medicine

Updated: Mar 8, 2007

Introduction

Background

While any type of glaucoma can be unilateral, primary open-angle glaucoma, primary angle-closure glaucoma, primary infantile glaucoma, juvenile-onset glaucoma, and pigmentary glaucoma are generally bilateral diseases, the severity of which may be asymmetric in the two eyes.

This article reviews glaucoma associated with increased episcleral venous pressure (EVP) and glaucoma associated with iridocorneal endothelial (ICE) syndrome.

Several etiologies of unilateral glaucoma are discussed in detail in other articles, including Glaucoma, Pseudoexfoliation; Glaucoma, Uveitic; Glaucoma, Lens-Particle; Glaucoma, Drug-Induced; Glaucoma, Neovascular; Glaucoma, Intraocular Tumors; Glaucoma, Hyphema; Glaucoma, Angle Recession; and Glaucoma, Malignant.

Pathophysiology

Increased EVP

In the early 1900s, Lauber provided histological evidence that the canal of Schlemm was connected to the episcleral venous network. Aqueous humor drains via the anterior surface of the ciliary body or through the trabecular meshwork, Schlemm canal, collector channels, and, subsequently, aqueous veins. These pathways have been termed unconventional and conventional, respectively.

While the unconventional pathway is independent of pressure, outflow via the conventional route is passive and depends largely on the difference between the intraocular pressure (IOP) and EVP; as EVP increases relative to IOP, or as resistance increases, flow decreases.

The 3 general pathophysiological mechanisms of increased EVP are arteriovenous anomalies, venous obstruction, and idiopathic. Arteriovenous anomalies associated with increased EVP include carotid-cavernous sinus fistula, orbital varix, Sturge-Weber syndrome, orbital-meningeal shunts, carotid-jugular venous shunts, and intraocular vascular shunts. Venous obstruction may be caused by a retrobulbar tumor, thyroid ophthalmopathy, superior vena cava syndrome, congestive heart failure, thrombosis of the cavernous sinus or orbital vein, vasculitis involving the episcleral or orbital vein, and jugular vein obstruction.

ICE syndrome

The pathophysiological mechanism underlying ICE syndrome remains unknown. However, the finding of chronic inflammatory cells in the corneal specimens of patients with ICE syndrome suggests a viral etiology. In a study using polymerase chain reaction techniques, 16 of 25 corneas from patients with ICE syndrome and 4 of 6 patients with herpetic keratitis were positive for herpes simplex virus.

Glaucoma associated with ICE syndrome is believed to be due to trabecular meshwork obstruction caused by peripheral anterior synechiae or, less commonly, an abnormal cellular membrane.

Frequency

United States

The frequency of glaucoma associated with increased EVP or with ICE syndrome is unknown.

Glaucoma has been reported to occur in 30% of patients with Sturge-Weber syndrome, 5% of patients with thyroid ophthalmopathy, 11.6% of patients with scleritis, and 4% of patients with episcleritis.

Mortality/Morbidity

• Glaucoma is the third leading cause of blindness in the United States.
• Because glaucoma may progress insidiously without causing symptoms, progressive glaucomatous damage may occur without the patient even being aware of the diagnosis.
• Prompt and continued control of IOP can prevent ocular damage due to glaucoma.

Sex

• Traumatic carotid-cavernous sinus fistulae occur more commonly in males than in females.
• ICE syndrome occurs more commonly in females than in males.

Age

• Spontaneous carotid-cavernous sinus fistulae typically occur in middle-aged to elderly individuals, while traumatic carotid-cavernous sinus fistulae occur most commonly in young persons.
• It has been reported that 60% of patients with glaucoma associated with Sturge-Weber syndrome acquire glaucoma before age 2 years, and the remaining patients develop glaucoma later in childhood or in early adulthood.
• The onset of ICE syndrome generally occurs in early to middle adulthood.

Clinical

History

• Elicit history of trauma, thyroid disease, congestive heart failure, vasculitis, malignancy, and other systemic diseases.
• Diplopia may be a presenting complaint of patients with a carotid-cavernous sinus fistula, thyroid ophthalmopathy, or retrobulbar tumor.
• Carotid-cavernous sinus fistulae often present after the following:
  • A severe head injury
  • Any penetrating injury to the orbit injuring the medial or inferomedial wall of the orbit and/or the superior orbital fissure
  • Surgery involving the internal carotid artery
  • Rupture of a preexisting aneurysm of the internal carotid artery

Physical

• Ophthalmic examination
  • Increased EVP may cause pulsating exophthalmos, conjunctival chemosis, engorgement of the episcleral vein, restricted ocular motility, ocular bruit, and ocular ischemia.
  • Dilated episcleral vessels are a prominent feature of Sturge-Weber syndrome; choroidal hemangioma is present in 31-50% of patients with Sturge-Weber syndrome.
  • A common clinical sign of an orbital varix is intermittent exophthalmos (exophthalmos occurring when the head is placed in a dependent position, when the patient sneezes, or when the patient performs a Valsalva maneuver).
  • Orbital tumors may cause proptosis and restricted ocular motility.
  • Thyroid ophthalmopathy may cause proptosis, restricted ocular motility, conjunctival chemosis, epiphora, exposure keratitis, and optic nerve compression.
  • Presenting signs of the superior vena cava syndrome include edema of the lid, face, and conjunctiva; vascular engorgement of the fundus, episclera, and conjunctiva; proptosis; optic nerve edema; and glaucoma.
  • IOP may increase while supine and may decrease while sitting.
  • The most common presenting manifestations of ICE syndrome are iris abnormalities (eg, iris atrophy, corectopia, ectropion uveae, peripheral anterior synechiae, iris nevi), decreased vision, and pain. Other features of the syndrome may include fine-hammered silver appearance of the posterior cornea and corneal edema.

Causes

• Glaucoma associated with EVP is due to increased resistance of aqueous outflow from the Schlemm canal and is associated with arteriovenous anomalies, venous obstruction, and idiopathic anomalies.
• Glaucoma associated with ICE syndrome is believed to be due to trabecular meshwork obstruction caused by peripheral anterior synechiae or, less commonly, an abnormal cellular membrane.

Differential Diagnoses

Glaucoma, Low Tension

Other Problems to Be Considered

Increased EVP

Orbital fractures
Other traumatic injuries
Underlying malignancy
Thyroid disease
Congestive heart failure
Other systemic diseases (eg, spontaneous carotid-cavernous fistulae have been reported in association with Ehlers-Danlos syndrome and pseudoexfoliation)

ICE syndrome

Corneal edema

Workup

Laboratory Studies

• Lab studies are indicated based on the suspected etiology (eg, thyroid function test, vasculitis workup) of unilateral glaucoma.

Imaging Studies

• B-scan echography to evaluate for orbital tumor, foreign body, and extraocular muscle enlargement (in thyroid ophthalmopathy and other conditions with EVP); also indicated if fundus cannot be visualized
• CT scan of orbits to evaluate orbital fracture, foreign body, dilation of superior ophthalmic vein, and enlargement of cavernous sinus (present with carotid-cavernous sinus fistulae)
• Angiography to evaluate for arteriovenous anomalies
• Orbital venography to evaluate for orbital varix
• Color Doppler to evaluate for orbital varix

Other Tests

• In patients with increased EVP, gonioscopic examination may reveal reflux of blood in the Schlemm canal.
• Ocular pulse amplitude, as measured by pneumotonometry, is a useful noninvasive tool to evaluate patients with carotid-cavernous fistulae.
• Malignancy workup for patients with superior vena cava syndrome, orbital tumors
• Cardiac workup for patients with congestive heart failure

Treatment

Medical Care

• Increased EVP
  • Although topical glaucoma medications and oral carbonic anhydrase inhibitors may be used initially to control IOP, the underlying etiology must be resolved to achieve long-term IOP control.
  • Medications that decrease aqueous production are more effective than drugs that increase aqueous outflow.
• ICE syndrome
  • Medications that reduce aqueous production can often control the early stages of glaucoma.
  • Epinephrine may be effective in some cases.
  • The benefit of topical prostaglandins remains to be demonstrated.
  • Miotics are generally ineffective due to mechanical obstruction of the trabecular meshwork.

Surgical Care

• Increased EVP
  • Laser trabeculoplasty is generally ineffective unless there are secondary changes in the outflow channels.
  • Glaucoma filtering surgery may be necessary in cases refractory to medical therapy to completely bypass the resistance due to increased EVP; ciliochoroidal effusions or suprachoroidal hemorrhage may complicate filtering surgery.
  • The optimal treatment of a direct carotid-cavernous sinus fistula is closure of the abnormal arteriovenous communication with preservation of internal carotid artery patency. Techniques to achieve this result include surgical repair of the damaged portion of the intracavernous internal carotid artery, electrothrombosis, embolization, or balloon occlusion of the fistula.
  • Dural carotid-cavernous sinus fistulae may close spontaneously, but, for those lesions causing progressive or unacceptable symptoms and signs, standard embolization or endovascular balloon occlusion is generally performed. If these techniques are unsuccessful, direct surgery on the cavernous sinus may be considered. In cases where anatomy makes a standard intravascular approach impossible, the superior ophthalmic vein can be cannulated and a balloon or coil can be threaded into the area of a direct communication.
• ICE syndrome
  • Laser trabeculoplasty is usually ineffective.
  • Patients with ICE syndrome generally do well with glaucoma filtering surgery, although late failure may develop due to endothelialization of the fistula, which, in some cases, may be reopened with the Nd:YAG laser.

Consultations

• Increased EVP
  • Consultation is indicated depending on the coexisting conditions.
  • Oculoplastic consultation for management of orbital tumors
  • Vitreoretinal consultation for management of choroidal hemangiomas
  • Patients with thyroid ophthalmopathy may benefit from neuro-ophthalmic and/or oculoplastic consultation for management of optic neuropathy.
  • Corneal consultation for management of exposure keratitis
• ICE syndrome - Cornea consultation for management of corneal edema

Medication

Medications used to decrease aqueous production include beta-blockers (topical), carbonic anhydrase inhibitors (topical and/or oral), and alpha 2-agonists.

Beta-adrenergic blockers

Decrease IOP by reducing aqueous production. Reduce elevated and normal IOP, with or without glaucoma.

Timolol 0.25%, 0.5% (Timoptic, Timoptic XE, Blocadren)

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

Dosing

Adult

Timoptic: 1 gtt bid
Timoptic XE: 1 gtt qd

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; cardiac disease; low blood pressure; low pulse rate; pulmonary disease (eg, asthma, COPD); history of depression; history of hyperlipidemia

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May exacerbate or precipitate heart block, asthma, COPD, and mental changes (especially in elderly persons); may alter blood lipid profile

Levobunolol 0.25% or 0.5% (AK Beta, Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increases outflow of aqueous humor.

Dosing

Adult

1 gtt bid

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; severe COPD; 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

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

Metipranolol 0.3% (OptiPranolol)

Beta-adrenergic blocker that has little or no intrinsic sympathomimetic effects and membrane-stabilizing activity. Has little local anesthetic activity. Reduces IOP by reducing production of aqueous humor.

Dosing

Adult

1 gtt bid

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; sinus tachycardia; cardiac failure; cardiogenic shock; second- and third-degree AV block

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May exacerbate or precipitate heart block, asthma, COPD, and mental changes (especially in elderly persons); may alter blood lipid profile

Carteolol 1.0% (Ocupress)

Blocks beta 1- and beta 2-receptors and has mild intrinsic sympathomimetic effects.

Dosing

Adult

1 gtt bid

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; congestive heart failure; asthma; cardiac conduction defects; breastfeeding

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Product may have sulfites, which may cause allergic-type reactions in certain susceptible persons

Betaxolol 0.25% or 0.5% (Betoptic)

Selectively blocks beta 1-adrenergic receptors with little or no effect on beta 2-receptors. Reduces IOP by reducing production of aqueous humor.

Dosing

Adult

1 gtt bid

Pediatric

Administer as in adults

Interactions

May have additive systemic effects if patient is already on systemic beta-blockers

Contraindications

Documented hypersensitivity; bronchial asthma; severe COPD; 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 consistent with myasthenic symptoms; product may have sulfites, which may cause hypersensitivity reactions in susceptible persons

Alpha 2-adrenergic agonists

Act to decrease aqueous humor formation.

Brimonidine 0.2% (Alphagan)

Selective alpha 2-receptor that reduces aqueous humor formation and increases uveoscleral outflow.

Dosing

Adult

1 gtt tid

Pediatric

Administer as in adults

Interactions

Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants (eg, barbiturates, opiates, sedatives) may potentiate effects of brimonidine

Contraindications

Documented hypersensitivity; patients receiving 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

Apraclonidine 0.5% or 1% (Iopidine)

Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. A relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

Dosing

Adult

1 gtt tid prelaser and postlaser or surgery, short term

Pediatric

Not established

Interactions

Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAOIs

Contraindications

Documented hypersensitivity; patients on MAOIs or have taken them in the past 14 d

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

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

Enzyme found in many tissues of the body, including the eye. Catalyzes a reversible reaction where carbon dioxide becomes hydrated and carbonic acid dehydrated. By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit CA in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.

Acetazolamide (Diamox, Diamox Sequels)

Inhibits enzyme CA, reducing the 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

125 mg or 250 mg PO bid/qid or 5-10 mg/kg q6-8h or 500 mg SR cap bid

Pediatric

5 mg/kg PO q6h

Interactions

Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Contraindications

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May exacerbate or precipitate lethargy, depression, weight loss, acidosis, renal stones, and bone marrow suppression; patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients

Dorzolamide 2% (Trusopt)

Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits CA, 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 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 CA 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)

Methazolamide (Neptazane)

Reduces aqueous humor formation by inhibiting enzyme CA, which results in decreased IOP.

Dosing

Adult

25-50 mg PO bid/tid

Pediatric

Not established

Interactions

May increase toxicity of salicylate, digoxin; coadministration with other diuretics may induce hypokalemia; decreases effects of lithium and alters excretion of other drugs by alkalinizing urine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in respiratory acidosis and diabetes mellitus; impairs mental alertness and/or physical coordination; hematuria, glycosuria, polyuria, hepatic insufficiency, bone marrow suppression, thrombocytopenia/purpura, agranulocytosis, urticaria, pruritus, and rash may occur

Brinzolamide 1% (Azopt)

Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than one topical ophthalmic drug is being used, administer drugs at least 10 min apart.

Dosing

Adult

1 gtt tid

Pediatric

Not established

Interactions

May have additive systemic effects if patient is already on oral CA inhibitors

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration (discontinue therapy and evaluate patient before restarting therapy)

Prostaglandin derivatives

These agents may decrease intraocular pressure by increasing the outflow of aqueous humor.

They are administered once per day (except for unoprostone, which is administered twice daily). Potential adverse effects of these medications are similar to latanoprost (eg, eyelash growth, increased iris pigmentation). These agents are considered by some glaucoma specialists as first-line agents for glaucoma, mainly because of the lack of systemic adverse effects.

Bimatoprost ophthalmic solution (Lumigan)

A prostamide analogue with ocular hypotensive activity. Mimics the IOP-lowering activity of prostamides via the prostamide pathway. Used to reduce IOP in open-angle glaucoma or ocular hypertension.

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

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

Travoprost ophthalmic solution (Travatan)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

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; may cause bacterial keratitis; caution in uveitis or macular edema; do not instill if wearing contact lenses

Unoprostone ophthalmic solution (Rescula)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

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

Commonly causes ocular hyperemia; 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

Follow-up

Further Outpatient Care

• Close monitoring of IOP and vigilance for evidence of glaucomatous injury (as manifested by examination of the patient's optic discs and by visual field testing) are warranted.

Complications

• If the patient does not comply with the use of medications, further deterioration of the visual field may occur.

Prognosis

• The prognosis for glaucoma is favorable if IOP can be maintained over the lifetime of the patient.

Patient Education

• For excellent patient education resources, visit eMedicine's Glaucoma Center. Also, see eMedicine's patient education articles Glaucoma FAQs and Understanding Glaucoma Medications.

Miscellaneous

Medicolegal Pitfalls

• Prompt diagnosis and complete treatment of glaucoma are important to arrest further deterioration of the visual field.

References

1. Albert DM, Jakobiec FA, Azar DT. Glaucoma associated with increased episcleral venous pressure. In: Principles and Practice of Ophthalmology. 2nd ed. WB Saunders Co;2000: 2781-2792.

2. Alvarado JA, Underwood JL, Green WR, et al. Detection of herpes simplex viral DNA in the iridocorneal endothelial syndrome. Arch Ophthalmol. Dec 1994;112(12):1601-9. [Medline].

3. Cibis GW, Tripathi RC, Tripathi BJ. Glaucoma in Sturge-Weber syndrome. Ophthalmology. Sep 1984;91(9):1061-71. [Medline].

4. Font RL, Ferry AP. The phakomatoses. Int Ophthalmol Clin. 1972;12(1):1-50. [Medline].

5. Gandolfi SA, Cimino L, Sangermani C, et al. Improvement of spatial contrast sensitivity threshold after surgical reduction of intraocular pressure in unilateral high-tension glaucoma. Invest Ophthalmol Vis Sci. Jan 2005;46(1):197-201. [Medline].

6. Jain SS, Rao P, Kothari K, et al. Posterior scleritis presenting as unilateral secondary angle-closure glaucoma. Indian J Ophthalmol. Sep 2004;52(3):241-4. [Medline].

7. Kirsch M, Henkes H, Liebig T, et al. Endovascular management of dural carotid-cavernous sinus fistulas in 141 patients. Neuroradiology. Jul 2006;48(7):486-90. [Medline].

8. Manor RS, Kurz O, Lewitus Z. Intraocular pressure in endocrinological patients with exophthalmos. Ophthalmologica. 1974;168(4):241-52. [Medline].

9. Uram M, Zubillaga C. The cutaneous manifestations of Sturge-Weber syndrome. J Clin Neuroophthalmol. Dec 1982;2(4):245-8. [Medline].

10. Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol. Mar 1976;60(3):163-91. [Medline].

11. Weiss DI. Dual origin of glaucoma in encephalotrigeminal haemangiomatosis. Trans Ophthalmol Soc U K. 1973;93(0):477-93. [Medline].

Keywords

open angle, closed angle, vision loss, visual deficit, open-angle glaucoma, episcleral venous pressure, EVP, glaucoma associated with iridocorneal endothelial syndrome, ICE syndrome

Contributor Information and Disclosures

Author

Ingrid U Scott, MD, MPH, Professor, Department of Ophthalmology and Public Health Sciences, Penn State College of Medicine
Ingrid U Scott, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Macula Society, Phi Beta Kappa, and Retina 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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