eMedicine Specialties > Ophthalmology > Intraocular Pressure
Glaucoma, Angle Closure, Acute
Updated: Jun 18, 2009
Introduction
Background
Angle-closure glaucoma (ACG) is a condition in which the iris is apposed to the trabecular meshwork at the angle of the anterior chamber of the eye. When the iris is pushed or pulled anteriorly to block the trabecular meshwork, the outflow of aqueous from the eye is blocked, which causes a rise in intraocular pressure (IOP). If closure of the angle occurs suddenly, symptoms are severe and dramatic. Immediate treatment is essential to prevent damage to the optic nerve and loss of vision. If closure occurs intermittently or gradually, ACG may be confused with chronic open-angle glaucoma.
Pathophysiology
Angle closure may occur via 2 mechanisms. The iris may be pushed forward into contact with the trabecular meshwork, as in pupillary block or plateau iris, or it may be pulled anteriorly, as occurs with other inflammatory conditions. In either case, the position of the iris causes the normally open chamber angle to close. Aqueous humor that should drain out of the anterior chamber is trapped inside the eye. Pain, blurred vision, and nausea may occur if the ensuing rise in pressure is sudden. Glaucomatous damage to the optic nerve also may occur due to the increased IOP, either in a sudden attack or in intermittent episodes over a long period of time.
Frequency
United States
Fewer than 10% of US glaucoma cases are due to ACG. Hyperopes are at increased risk for acute ACG because their anterior chamber angles are relatively shallow.
International
ACG is more common than open-angle glaucoma in Asia.
Mortality/Morbidity
Accurate early diagnosis and treatment help prevent visual damage.
Race
Races with an anatomically narrower angle, such as Asians and Eskimos, have a higher incidence of ACG than whites. Incidence among American Indians is lower than among whites.
Sex
Among white patients, the incidence of ACG is 3 times higher in women than in men. In black patients, men and women are affected equally.
Age
In older people, incidence of primary ACG increases as the lens enlarges, and the depth and volume of the anterior chamber decrease.
Clinical
History
- In acute primary ACG, the anterior chamber angle is blocked suddenly and IOP rises rapidly, and the patient may present with dramatic symptoms.
- Onset of severe ocular pain, nausea and vomiting, headache, and blurred vision is sudden.
- Patients may complain of seeing haloes around lights. Haloes and blurry vision are the result of corneal edema.
- The attack may have been precipitated by pupillary dilation, possibly during an ophthalmic examination. Patients with acute ACG are extremely uncomfortable and distressed.
- Some patients may experience intermittent episodes of partial angle closure and relatively elevated IOP without ever experiencing a frank attack of ACG.
- Patients may be totally asymptomatic, or they may report incidents of mild pain with slightly blurred vision or seeing haloes around lights. These symptoms resolve spontaneously as the angle reopens.
Physical
- Examination of a patient who presents with suspected ACG should include gonioscopy, tonometry, biomicroscopy, and ophthalmoscopy.
- Diagnosis of ACG is made by gonioscopic visualization of an occluded anterior chamber angle.
- Tonometry demonstrates an elevated IOP, which may be as high as 40-80 mm Hg.
- Biomicroscopy may reveal a fixed or sluggish and middilated pupil, a shallow anterior chamber, corneal epithelial edema and bullae, ciliary injection, and cells and flare. Diffuse lacrimation may be present.
- Ophthalmoscopy may reveal a swollen optic disc in an acute attack or excavation if episodes have been chronic. Unilateral involvement and worsening symptoms are common in acute attacks.
- If an attack persists or if several milder incidents of angle closure have occurred in the past, peripheral anterior synechiae and adhesions may be visible between the cornea and iris. Peripheral anterior synechiae may destroy the trabecular meshwork, while adhesions may cause necrosis and permanent dilation of the iris.
- Glaucoma flecks (also known as flecken glaucoma), or vesicles on the anterior subcapsular lens, also may be seen if acute angle closure has occurred in the past.
- Gray atrophy of the stroma of the iris provides further evidence of a prior attack, if the attack occurred 3 weeks or more prior to examination.
Causes
- Pupillary block is the most common cause of ACG. Normally, aqueous humor is made by the ciliary epithelial cells in the posterior chamber and flows through the pupil to the anterior segment, where it can drain out of the eye through the trabecular meshwork and Schlemm canal. If contact occurs between the lens and the iris, aqueous accumulates behind the pupil, increasing posterior chamber pressure and forcing the peripheral iris to shift forward and block the anterior chamber angle. The anterior surface of the iris may be apposed to the posterior surface of the cornea or to the trabecular meshwork. This blockage causes accumulation of aqueous in the anterior chamber and an acute rise in IOP.
- Plateau iris is a condition in which anterior insertion of the iris to the ciliary body causes the anterior chamber angle to become occluded on dilation of the pupil. The iris may insert on the anterior edge of the ciliary body, close to the trabecular meshwork. It may cause the patient to have genetically narrow angles despite a normal anterior chamber depth. The iris also may appear unusually flat, not bowed as might be expected in ACG. Often, an element of pupillary block exists in cases of plateau iris glaucoma, in which case peripheral iridectomy will lower IOP. If the patient continues to develop angle closure on pupillary dilation after iridectomy has been performed, continue performing miotic therapy to prevent recurrence. A diagnosis of plateau iris can be confirmed with ultrasound biomicroscopy.
- Hyperopia: Patients with hyperopic eyes are more likely to have shallow anterior chambers and narrow angles. These patients are predisposed to develop ACG. Dilation of the eye may precipitate an attack of acute ACG because the peripheral iris relaxes when dilated to midposition. When the iris is relaxed, it may bow anteriorly and maximize iris-lens apposition, possibly causing pupillary block.
- Several medications have been implicated in causing acute ACG. Sulfa-derivative medications, including acetazolamide, sulfamethoxazole, and hydrochlorothiazide, have all been reported to cause acute attacks. Topiramate, a newer antiepileptic medication, has recently been implicated in causing acute narrow-angle glaucoma. Also a sulfa-derivative medication, topiramate blocks glutamate receptors and is labeled for use in treating seizures. The presumed mechanism of angle closure involves swelling of the ciliary body with anterior displacement of the lens-iris diaphragm. Stopping the medication is effective in treating this condition and requires a high index of suspicion by the treating physician.
- Other causes: Several mechanisms can cause the iris-lens diaphragm to be pushed forward. A space-occupying lesion (eg, tumor, swelling associated with ciliary body inflammation) may cause the iris to block the trabecular meshwork. Other conditions associated with this mechanism include central retinal vein occlusion, placement of a scleral buckle, history of panretinal photocoagulation, and nanophthalmos.
Differential Diagnoses
| Cataract, Senile | Headache, Migraine |
| Conjunctivitis, Allergic | Synechia, Peripheral Anterior |
| Conjunctivitis, Bacterial | |
| Conjunctivitis, Viral | |
| Glaucoma, Angle Closure, Chronic |
Other Problems to Be Considered
Acute abdomen
Cluster headache
Gastritis
Workup
Imaging Studies
- Ultrasound biomicroscopy (UBM) - To visualize the angles and surrounding structures
- Anterior segment optical coherence tomography (OCT) - To view the angles and anterior ocular structures
Other Tests
- Gonioscopy
Treatment
Medical Care
Definitive treatment of ACG is laser iridotomy, or, if the iris cannot be accessed by laser, surgical iridectomy. Medical treatment is intended to prepare the patient for laser iridotomy. The cornea should be cleared with osmotic agents, the pupil should be constricted, and IOP should be lowered to prevent acute damage to the optic nerve.
Surgical Care
- Laser iridotomy: Treatment of choice for pupillary-block ACG is laser iridotomy. Iridotomy with an argon or Nd:YAG laser creates an opening in the iris through which aqueous humor trapped in the posterior chamber can reach the anterior chamber and trabecular meshwork. As aqueous flows into the anterior chamber through the iris defect, pressure behind the iris falls, allowing the iris to recede toward its normal position. This procedure opens the anterior chamber angle and relieves the blockade of trabecular meshwork. If the cornea is extremely cloudy or the patient cannot cooperate, incisional peripheral iridectomy may be performed instead of a laser procedure.
- Laser gonioplasty: Laser may be used to create stromal burns in the peripheral iris. As the iris contracts, the anterior chamber angle deepens. Use laser gonioplasty as treatment of ACG due to plateau iris and nanophthalmos, or use it as a temporary measure to open the angle until laser iridotomy can be performed.
Medication
The medical therapy for acute ACG is directed toward preparing the patient for laser or incisional iridotomy, which will create passage through the iris from the posterior to anterior chamber and will break an acute attack. IOP must be returned to normal, and the cornea must be cleared before a definitive procedure can be undertaken. In acute ACG, several drugs from different classes are used simultaneously to accelerate and maximize their pressure-lowering effects.
Alpha-adrenergic agonists
Topical adrenergic agonists, or sympathomimetics, decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and allergenicity.
Brimonidine (Alphagan)
Selective alpha2-receptor that reduces aqueous humor formation and possibly increases uveoscleral outflow.
Dosing
Adult
1 gtt OU bid
Pediatric
<2 years: Not recommended; severe mental, cardiovascular, and pulmonary depression have been reported in pediatric patients
>2 years: 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; patients receiving MAOIs
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in cardiovascular disease, depression, cerebral or coronary insufficiency, orthostatic hypotension, Raynaud syndrome
Apraclonidine (Iopidine) 0.5%, 1%
Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Reduces IOP whether or not accompanied by glaucoma. Selective alpha-adrenergic agonist without significant local anesthetic activity. Has minimal cardiovascular effect.
Dosing
Adult
1 gtt tid in affected eye(s)
Pediatric
Not established
Interactions
Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAOIs
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in coronary insufficiency, chronic renal failure, recent myocardial infarction, cerebrovascular disease, Raynaud disease, thromboangiitis obliterans, and in patients who are depressed
Beta-blockers
Topical beta-adrenergic receptor antagonists decrease aqueous humor production by the ciliary body. Adverse effects of the beta-blockers are due to systemic absorption of the drug and include decreased cardiac output and bronchial constriction. In susceptible patients, this may cause bronchospasm, bradycardia, heart block, or hypotension. Pulse rate and blood pressure should be monitored in patients receiving topical beta-blocker therapy, and punctal occlusion may be performed after administration of the drops.
Levobunolol (Betagan, AKBeta) 0.25%, 0.5%
Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production
Dosing
Adult
1 gtt bid in affected eye(s)
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 - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
Betaxolol (Betoptic) 0.25%, 0.5%
Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.
Dosing
Adult
1-2 gtt in affected eye(s) bid; consider concomitant therapy if IOP is not at satisfactory level
Pediatric
Not established
Interactions
May have additive systemic effects if patient is already on systemic beta-blockers
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 - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-blockade may potentiate muscle weakness consistent with myasthenic symptoms; product may have sulfites, which may cause hypersensitivity reactions in susceptible persons
Timolol maleate (Timoptic, Timoptic XE) 0.25%, 0.5%
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 - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Product may have sulfites, which may cause allergic-type reactions in susceptible patients
Miotic agents (parasympathomimetics)
Contract ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous. Miosis results from action of these drugs on pupillary sphincter. Adverse effects include brow ache, induced myopia, and decreased vision in low light.
Pilocarpine (Pilocar, Pilagan) 1%, 2%, 4%, 5%, 6%, 8%, 10%, gel 4%
A naturally occurring alkaloid, pilocarpine mimics muscarinic effects of acetylcholine at postganglionic parasympathetic nerves. Directly stimulates cholinergic receptors in the eye, decreasing resistance to aqueous humor outflow.
Instillation frequency and concentration are determined by patient's response. Individuals with heavily pigmented irides may require higher strengths. If other glaucoma medication also is being used, at bedtime, use gtt at least 5 min before gel. May use alone, or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.
Dosing
Adult
1 or 2 gtt tid/qid
Pediatric
Not established
Interactions
May be ineffective when used concomitantly with nonsteroidal anti-inflammatory agents
Contraindications
Documented hypersensitivity; acute inflammatory disease of anterior chamber
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Warn patients that pilocarpine causes pupillary constriction and may cause decreased vision in presence of cataract; also may cause aching pain in eye or artificial myopia because of increased accommodation; caution in acute cardiac failure, peptic ulcer, hyperthyroidism, GI spasm, bronchial asthma, Parkinson disease, recent MI, urinary tract obstruction, and hypertension or hypotension
Prostaglandin analogs
Increase uveoscleral outflow of the aqueous. One mechanism of action may be through induction of metalloproteinases in ciliary body, which breaks down extracellular matrix, thereby reducing resistance to outflow through ciliary body.
Latanoprost (Xalatan) 0.005%
Decreases IOP by increasing outflow of aqueous humor.
Dosing
Adult
1 gtt (1.5 mcg) in affected eye qd in evening; higher frequency administrations may decrease effectiveness
Pediatric
Not established
Interactions
Coadministration with eye drops, containing the preservative thimerosal, may reduce effects (administer at intervals of 5 min between applications)
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Do not administer while wearing contact lenses; may increase brown pigment in iris and change eye color gradually (unknown effect)
Carbonic anhydrase inhibitors
Reduce secretion of aqueous humor by inhibiting carbonic anhydrase in ciliary body. In acute ACG, may be given systemically but are used topically in patients with refractory open-angle glaucoma. Topical formulations are less effective, and their duration of action is shorter than many other classes of drugs. Adverse effects of topical carbonic anhydrase inhibitors are relatively rare, but they include superficial punctate keratitis, acidosis, paresthesias, nausea, depression, and lassitude.
Acetazolamide (Diamox)
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 ACG when delay of surgery desired to lower IOP.
Dosing
Adult
250 mg to 1 g PO/IV q24h
Pediatric
Not established
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, or severe pulmonary obstruction; low blood sodium or potassium, severe kidney and liver dysfunction, adrenal failure, and hyperchloremic acidosis
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor patients for adverse reactions to sulfonamides; may experience paresthesias of extremities, tinnitus, taste alterations, or gastrointestinal distress
Methazolamide (GlaucTabs, Neptazane)
Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.
Dosing
Adult
50-100 mg PO bid/tid
Pediatric
Not established
Interactions
Caution in patients on high-dose aspirin or steroid therapy; may increase toxicity of salicylate, digoxin; coadministration with other diuretics may induce hypokalemia; decreases effects of lithium and alter excretion of other drugs by alkalinizing urine
Contraindications
Documented hypersensitivity; renal impairment
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
Dorzolamide HCl (Trusopt) 2%
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 carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.
Dosing
Adult
1 gtt in affected eye(s) 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 - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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)
Brinzolamide (Azopt) 1%
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 in affected eye(s) tid
Pediatric
Not established
Interactions
May have additive systemic effects if patient is already on oral CA inhibitors
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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)
Dorzolamide HCl/ timolol maleate (Cosopt)
CA inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.
Timolol is a nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion and may slightly increase outflow facility. Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly.
Dosing
Adult
1 gtt into affected eye(s) bid; if more than one topical ophthalmic drug is used, administer at least 10 min apart
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 - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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); product may have sulfites, which may cause allergic-type reactions in susceptible patients
Follow-up
Further Inpatient Care
- Because some patients may experience transient increases in IOP after peripheral iridotomy, check every patient's IOP 1 hour after laser treatment. If medical treatment has not been successful by that time, repeat gonioscopic examination to rule out the presence of peripheral anterior synechiae. If peripheral anterior synechiae are found, the patient may need gonioplasty or incisional surgery.
Further Outpatient Care
- Once a peripheral iridotomy has been performed, the patient should continue using the medications that were chosen to treat the acute glaucoma for 1 day after leaving the hospital or clinic. Arrange a 1-day posttreatment visit. At this visit, check the IOP again, and examine the eye. After 1 day, the patient may discontinue the antiglaucoma medications that were used in the acute attack, but the patient should be maintained on corticosteroids for 1 week.
- Examine the patient's other eye gonioscopically and biomicroscopically to assess for narrow or occluded angles, as well as for evidence of prior attacks of ACG. If evidence of prior attacks or predisposition for future angle closure is seen, prophylactic peripheral iridotomy may be considered.
Inpatient & Outpatient Medications
- See Further Outpatient Care.
Complications
- Loss of vision can occur without prompt treatment.
Prognosis
- The prognosis is favorable with early detection and treatment.
Patient Education
- Inform the patient to promptly seek professional treatment if pain and/or decreased vision occur.
Miscellaneous
Medicolegal Pitfalls
- Failure to diagnose ACG is the most important medicolegal area. Because patients present with remarkable systemic symptoms (eg, nausea, vomiting), the eyes may be overlooked as the source of the violent reactions. Ophthalmologists must have a high index of suspicion for acute ACG.
References
Cantor L, et al. Glaucoma. In: Basic and Clinical Science Course. Section 10. 1996-7.
Epstein DL, Allingham RR, Schuman JS. Chandler and Grant's Glaucoma. 4th ed. 1997.
Hitchings RA. Glaucoma: current thinking. Br J Hosp Med. Mar 20-Apr 2 1996;55(6):312-4. [Medline].
Lai JS, Tham CC, Chan JC. The clinical outcomes of cataract extraction by phacoemulsification in eyes with primary angle-closure glaucoma (PACG) and co-existing cataract: a prospective case series. J Glaucoma. Feb 2006;15(1):47-52. [Medline].
Liesegang TJ. Glaucoma: changing concepts and future directions. Mayo Clinic Proceedings. 1996;71:689-694.
Nolan W. Anterior segment imaging: ultrasound biomicroscopy and anterior segment optical coherence tomography. Curr Opin Ophthalmol. Mar 2008;19(2):115-21. [Medline].
Shields MB. Textbook of Glaucoma. 4th ed. 1998.
Sihota R, Dada T, Gupta R, et al. Ultrasound biomicroscopy in the subtypes of primary angle closure glaucoma. J Glaucoma. Oct 2005;14(5):387-91. [Medline].
Xu L, Cao WF, Wang YX, Chen CX, Jonas JB. Anterior chamber depth and chamber angle and their associations with ocular and general parameters: the Beijing Eye Study. Am J Ophthalmol. May 2008;145(5):929-36. [Medline].
Keywords
acute angle glaucoma, acute angle-closure glaucoma, acute angle closure glaucoma, angle closure glaucoma, angle-closure glaucoma, ACG, narrow-angle glaucoma, narrow angle glaucoma, narrow angles, vision loss, visual deficit
Contributor Information and Disclosures
Author
Robert J Noecker, MD, MBA, Associate Professor, Department of Ophthalmology, University of Pittsburgh School of Medicine; Director, Glaucoma Service, Vice Chair, Department of Ophthalmology, University of Pittsburgh Medical Center Eye Center
Robert J Noecker, MD, MBA is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, American Medical Association, American Society of Cataract and Refractive Surgery, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.
Coauthor(s)
Malik Y Kahook, MD, Clinical Instructor of Ophthalmology, Fellow in Glaucoma, Department of Ophthalmology, University of Pittsburgh Medical Center
Malik Y Kahook, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Association for Research in Vision and Ophthalmology, and Colorado Medical Society
Disclosure: Alcon Consulting fee Consulting
Medical Editor
Kilbourn Gordon III, MD, FACEP, Urgent Care Physician
Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society
Disclosure: Nothing to disclose.
Pharmacy Editor
Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
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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