eMedicine Specialties > Emergency Medicine > Ophthalmology
Glaucoma, Acute Angle-Closure: Treatment & Medication
Updated: Aug 12, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Prehospital Care
The patient should be brought to the hospital in an expeditious manner to have intraocular pressure (IOP) reduced. The patient should remain in the supine position as long as possible. The urge to wear eye patches, covers, or blindfolds should be resisted. By maintaining the conditions that cause pupillary dilation, these articles help perpetuate the attack. Their potential negative effects outweigh any cosmetic benefit.
Emergency Department Care
The treatment of acute angle-closure glaucoma (AACG) consists of IOP reduction, suppression of inflammation, and the reversal of angle closure. Once diagnosed, the initial intervention includes acetazolamide, a topical beta-blocker, and a topical steroid.
Acetazolamide should be given as a stat dose of 500 mg IV followed by 500 mg PO. A dose of a topical beta-blocker (ie, carteolol, timolol) will also aid in lowering IOP. Studies have not conclusively demonstrated the superior neuronal or visual field protectiveness of one beta-blocker over another. Both beta-blockers and acetazolamide are thought to decrease aqueous humor production and to enhance opening of the angle. An alpha-agonist can be added for a further decrease in IOP.
Inflammation is an important part of the pathophysiology and presenting symptomology. Topical steroids decrease the inflammatory reaction and reduce optic nerve damage. The current recommendation is for 1-2 doses of topical steroids.
Addressing the extraocular manifestations of the disease is critical. This includes analgesics for pain and antiemetics for nausea and vomiting, which can drastically increase IOP beyond its already elevated level. Placing the patient in the supine position may aid in comfort and reduce IOP. It is also believed that, while supine, the lens falls away from the iris decreasing pupillary block.
After the initial intervention, the patient should be reassessed. Reassessment includes evaluating IOP, evaluating adjunct drops, and considering the need for further intervention, such as osmotic agents and immediate iridotomy.
Approximately 1 hour after beginning treatment, pilocarpine, a miotic that leads to opening of the angle, should be administered every 15 minutes for 2 doses. In the initial attack, the elevated pressure in the anterior chamber causes a pressure-induced ischemic paralysis of the iris. At this time, pilocarpine would be ineffective. During the second evaluation, the initial agents have decreased the elevated IOP and hopefully have reduced the ischemic paralysis so pilocarpine becomes beneficial in relieving pupillary block.
Pilocarpine must be used with caution. Theoretical concerns exist about its mechanism of action. By constricting the ciliary muscle, it has been shown to increase the axial thickness of the lens and to induce anterior lens movement. This could result in reducing the depth of the anterior chamber and worsening the clinical situation in a paradoxical reaction. Despite this, pilocarpine is recommended to be used as an additional agent.
No standard rate of reduction for IOP exists; however, Choong et el identified a satisfactory reduction as IOP less than 35 mm Hg or a reduction greater than 25% of presenting IOP.7 If the IOP is not reduced 30 minutes after the second dose of pilocarpine, an osmotic agent must be considered. An oral agent like glycerol can be administered in nondiabetics. In diabetics, oral isosorbide is used to avoid the risk of hyperglycemia associated with glycerol. Patients who are unable to tolerate oral intake or do not experience a decrease in IOP despite oral therapy are candidates for IV mannitol.
Hyperosmotic agents are useful for several reasons. They reduce vitreous volume, which, in turn, decreases IOP. The decreased IOP reverses iris ischemia and improves its responsiveness to pilocarpine and other drugs. Osmotic agents cause an osmotic diuresis and total body fluid reduction. They should not be administered in cardiovascular and renal patients. Choong et el demonstrated that 44% of patients required the addition of an osmotic agent to decrease IOP.7 Repeat doses may be necessary if no effect is seen and if tolerated by the patient.
Laser peripheral iridotomy (LPI), performed 24-48 hours after IOP is controlled, is considered the definitive treatment for AACG. While LPI is the current definitive treatment, there is evidence to suggest that argon laser peripheral iridoplasty (ALPI) and anterior chamber paracentesis (ACP) may have increasing roles in the management of AACG.
In ALPI, burns are made in the peripheral iris resulting in iris contraction and opening of the angle. Some studies suggest ALPI causes a more immediate decrease in IOP, resulting in better outcomes with fewer side effects than systemic therapy.8 Systemic therapy must still be used with ACP, but ACP appears to instantaneously relieve symptoms.
The choice of which therapy to use will be made by an ophthalmologist who will evaluate all patients via gonioscopy with complete inspection of the angle. At institutions where an ophthalmologist is immediately available on staff, initial treatment should be performed in conjunction with the specialist.
If there is a delayed interval between the initial presentation and definitive ophthalmic care, the emergency department physician should begin treatment as described above. After an appropriate reduction in IOP, immediate ophthalmic evaluation must be ensured. If the IOP is unchanged or increased from the time of treatment, further treatment should be discontinued and the attack most likely will terminate only with LPI. Ocular massage through a closed eyelid may be preformed while waiting for ophthalmology if no other treatment reduces IOP.
Consultations
- Ophthalmic consultation should be obtained as soon as possible because acute-angle closure glaucoma is an ophthalmic emergency.
Medication
The goal in treatment of AACG is to reduce IOP. Medical management is the first step. A prompt reduction in IOP using topical and systemic medication decreases the duration of elevated IOP and the potential for visual field loss. IOP reduction is accomplished via suppressing aqueous humor production, eliminating pupillary block, and reversing inflammation. As with any medical intervention, intimate knowledge of the drugs, their indications, contraindications, and potential side effects can aid the physician in providing the best treatment and a favorable outcome.
Carbonic anhydrase inhibitors
These are first-line agents that should be used immediately during the initial intervention. They reduce bicarbonate production in the ciliary epithelium and therefore decrease aqueous formation.
Acetazolamide (Diamox)
Reduces rate of aqueous humor formation by direct inhibition of enzyme carbonic anhydrase (CA) on secretory ciliary epithelium, causing, in turn, a reduction in IOP. More than 90% of CA must be inhibited before IOP reduction can occur. May reduce IOP by 40-60%. Effects are seen in about an hour, they peak in 4 h, and trough in about 12 h. Derived chemically from sulfa drugs. If one form is not well tolerated, another form may be better or lower dose of the drug may better tolerated. IV administration of this medication may be used for rapid relief of increased IOP. A beneficial effect occurs when used with miotics or mydriatics.
Adult
500 mg IV stat, followed by 500 mg PO
Pediatric
5-10 mg/kg/dose IV/IM, then 0-15 mg/kg/d PO divided q6-8h
Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine
Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction
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
Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose level in some diabetic patients
Methazolamide (Neptazane)
Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.
Adult
50-100 mg PO bid/tid
Pediatric
Not established
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
Documented hypersensitivity; renal impairment
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
Beta-adrenergic blockers
These agents may lower IOP via their suppression of aqueous humor production and probably not through any affects on the pupil.
Timolol (Timoptic, Timoptic XE)
Reduces elevated and normal IOP by reducing aqueous humor production or possibly the outflow.
Adult
1 gtt of 0.25% or 0.5% solution in affected eye(s) bid; if IOP is maintained at satisfactory levels, reduce dosage to 1 gtt qd in affected eye(s)
Pediatric
Not established
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock
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; may exacerbate or precipitate heart block, asthma, chronic obstructive pulmonary disease, mental changes (especially in the elderly persons)
Carteolol (Ocupress)
Nonselective beta-adrenergic receptor. Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic activity (ISA), with possibly fewer cardiac and lipid profile adverse effects. Precise mechanism by which carteolol decreases IOP is thought to be through reduction of aqueous formation.
Adult
1 gtt in affected eye(s) bid
Pediatric
Not established
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Documented hypersensitivity; congestive heart failure; asthma; cardiac conduction defects; breastfeeding
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 certain susceptible persons
Levobetaxolol (Betaxon)
Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.
Adult
1 gtt in affected eye(s) bid
Pediatric
Not established
May have additive systemic effects if patient is already on systemic beta-blockers
Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock
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
Levobunolol (AKBeta, Betagan)
Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and may increase outflow of aqueous humor.
Dosages of more than 1 gtt of 0.5% levobunolol twice daily have not been shown to be more effective. If IOP not at satisfactory level on this regimen, concomitant therapy can be instituted. However, do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously.
Adult
0.5% solution: 1-2 gtt in affected eye(s) qd
0.25% solution: 1-2 gtt in affected eye(s) bid
Severe or uncontrolled glaucoma: 0.5% solution bid; closely monitor patient
>1 gtt (0.5% levobunolol) bid not shown to be more effective; if IOP not at satisfactory level on this regimen, concomitant therapy can be instituted; do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously
Pediatric
Not established
May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)
Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock
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
Alpha-adrenergic agonists
These agents are used as adjunct agents to further decrease IOP secondary to their affect on aqueous humor production.
Apraclonidine (Iopidine)
Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Suppresses aqueous production. Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. Apraclonidine is relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.
Adult
1 gtt of 0.5% or 1% in affected eye(s) tid
Pediatric
Not established
Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAO inhibitors
Documented hypersensitivity; patients on MAO inhibitors or have taken them in the past 14 d
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
May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy
Brimonidine (Alphagan, Alphagan-P)
Selective alpha2 receptor that may reduce aqueous humor formation, may decrease inflow, or may increase uveoscleral outflow.
Adult
1 gtt in affected eye tid
Pediatric
Not established
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
Documented hypersensitivity; patients receiving MAO inhibitor therapy
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy
Corticosteroids
These agents reduce ocular inflammation thereby providing symptomatic relief and augmenting the affects of other medications.
Prednisolone (AK-Pred, Econopred)
Used in treatment of acute inflammations following eye surgery or other insults to the eye.
In cases of bacterial infections, concomitant use of anti-infective agents is mandatory. If signs and symptoms do not improve after 2 d, reevaluate the patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.
Adult
Solution: 1-2 gtt of solution into conjunctival sac up to q1h during day and q2h at night prn
When a favorable response observed, reduce dosage to 1 gtt q4h; further reduction in dosage to 1 gtt tid/qid may suffice to control symptoms
Susp: Shake well before using; 1-2 gtt into conjunctival sac bid/qid; during initial 24-48 h, dosing frequency may be increased prn
Pediatric
Not established
Decreases effects of salicylates and toxoids (for immunizations); phenytoin, carbamazepine, barbiturates, and rifampin decrease effects of corticosteroids
Documented hypersensitivity; viral, fungal, or tubercular skin lesions
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 hyperthyroidism, osteoporosis, cirrhosis, nonspecific ulcerative colitis, peptic ulcer, diabetes, and myasthenia gravis
Ophthalmic agents, miotic
These agents pull the peripheral iris tissue away from the trabecular meshwork helping to eliminate obstructed aqueous humor flow. They are ineffective during the initial period due to the ischemic paralysis of the iris. Miotics should be used after the immediate management and initial reduction of IOP.
Pilocarpine (Pilagan, Pilocar, Pilostat)
Patients may be maintained on pilocarpine as long as IOP is controlled and no deterioration in visual fields is present. May be used alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.
Frequency of instillation and concentration are determined by patient's response. Individuals with heavily pigmented irides may require higher strengths.
Adult
Solution: 1-2 gtt tid/qid
Gel: Apply 0.5-inch ribbon in the lower conjunctival sac of affected eye(s) hs
If another glaucoma medication being used hs, use gtt at least 5 min before gel
Pediatric
Not established
May be ineffective when used concomitantly with nonsteroidal anti-inflammatory agents
Documented hypersensitivity; acute inflammatory disease of anterior chamber
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 acute cardiac failure, peptic ulcer, hyperthyroidism, GI spasm, bronchial asthma, Parkinson disease, recent MI, urinary tract obstruction, and hypertension or hypotension
Hyperosmotics
Hyperosmotic agents increase serum osmolarity and cause a fluid shift from the eye into the vascular space. The subsequent osmotic diuresis reduces IOP.
Glycerin (Osmoglyn)
Used in glaucoma to interrupt acute attacks. Reduces IOP through its diuretic effects. Adds to tonicity of blood until metabolized and eliminated by kidneys. Maximal reduction of IOP occurs 1 h after glycerin administration. The effect lasts approximately 5 h.
Adult
1-2 g/kg PO and repeat q5h prn; alternatively, 1 mL/kg PO as a 50% solution in juice
Pediatric
Administer as in adults
None reported
Documented hypersensitivity; frank or impending acute pulmonary edema, anuria, severe dehydration, and severe cardiac decompensation
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
Administer orally, never parenterally; for oral use only; avoid in acute urinary retention in preoperative period; continued use may result in weight gain; caution in hypervolemia, diabetes, severely dehydrated individuals, confused mental states, congestive heart disease, and cardiac, renal, or hepatic disease
Isosorbide (Ismotic)
In the eyes, creates an osmotic gradient between plasma and ocular fluids. Induces diuresis by elevating osmolarity of glomerular filtrate, thereby hindering tubular reabsorption of water. May be used to interrupt an acute attack of glaucoma. Use when less risk of nausea and vomiting, compared with other oral hyperosmotic agents, is needed.
Adult
1.5 g/kg PO initially, followed by 1-3 g/kg PO bid/qid prn
Pediatric
Not established
None reported
Documented hypersensitivity; anuria, severe dehydration, frank or impending acute pulmonary edema, and severe cardiac decompensation
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
Use repetitive doses with caution, particularly in patients with diseases associated with salt retention
Mannitol (Osmitrol)
Reduces elevated IOP when pressure cannot be lowered by other means.
Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h.
In children, assess for adequate renal function by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 1 mL/h over 1-3 h.
Adult
1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over a period as short as 30 min
Pediatric
Not established
May decrease serum lithium levels
Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure
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
Carefully evaluate cardiovascular status before rapid administration of mannitol since a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood
More on Glaucoma, Acute Angle-Closure |
| Overview: Glaucoma, Acute Angle-Closure |
| Differential Diagnoses & Workup: Glaucoma, Acute Angle-Closure |
 Treatment & Medication: Glaucoma, Acute Angle-Closure |
| Follow-up: Glaucoma, Acute Angle-Closure |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
Berkoff DJ, Sanchez LD. An uncommon presentation of acute angle closure glaucoma. J Emerg Med. Jul 2005;29(1):43-4. [Medline].
Yip LW, Aquino MC, Chew PT. Measurement of anterior lens growth after acute primary angle-closure glaucoma. Can J Ophthalmol. Apr 2007;42(2):321-2. [Medline].
Ang LP, Ang LP. Current understanding of the treatment and outcome of acute primary angle-closure glaucoma: an Asian perspective. Ann Acad Med Singapore. Mar 2008;37(3):210-5. [Medline].
Rahim SA, Sahlas DJ, Shadowitz S. Blinded by pressure and pain. Lancet. Jun 25-Jul 1 2005;365(9478):2244. [Medline].
Cholongitas E, Pipili C, Dasenaki M. Acute angle closure glaucoma presented with nausea and epigastric pain. Dig Dis Sci. May 2008;53(5):1430-1. [Medline].
Croos R, Thirumalai S, Hassan S, Davis Jda R. Citalopram associated with acute angle-closure glaucoma: case report. BMC Ophthalmol. Oct 4 2005;5:23. [Medline].
Choong YF, Irfan S, Menage MJ. Acute angle closure glaucoma: an evaluation of a protocol for acute treatment. Eye. Oct 1999;13 (Pt 5):613-6. [Medline].
Mansouri K, Ravinet E. Argon-laser iridoplasty in the management of uveitis-induced acute angle-closure glaucoma. Eur J Ophthalmol. Mar-Apr 2009;19(2):304-6. [Medline].
Ang LP, Aung T, Chua WH, Yip LW, Chew PT. Visual field loss from primary angle-closure glaucoma: a comparative study of symptomatic and asymptomatic disease. Ophthalmology. Sep 2004;111(9):1636-40. [Medline].
Aung T, Friedman DS, Chew PT, Ang LP, Gazzard G, Lai YF, et al. Long-term outcomes in Asians after acute primary angle closure. Ophthalmology. Aug 2004;111(8):1464-9. [Medline].
Aung T, Oen FT, Wong HT, et al. Randomised controlled trial comparing the effect of brimonidine and timolol on visual field loss after acute primary angle closure. Br J Ophthalmol. Jan 2004;88(1):88-94. [Medline].
Blake DR, Nathan DM. Acute angle closure glaucoma following rapid correction of hyperglycemia. Diabetes Care. Nov 2003;26(11):3197-8. [Medline].
Bonomi L, Marchini G, Marraffa M, et al. Epidemiology of angle-closure glaucoma: prevalence, clinical types, and association with peripheral anterior chamber depth in the Egna-Neumarket Glaucoma Study. Ophthalmology. May 2000;107(5):998-1003. [Medline].
Fourman S. Diagnosing acute angle-closure glaucoma: a flowchart. Surv Ophthalmol. May-Jun 1989;33(6):491-4. [Medline].
Fricke TR, Mantzioros N, Vingrys AJ. Management of patients with narrow angles and acute angle-closure glaucoma. Clin Exp Optom. Nov 1998;81(6):255-266. [Medline].
Gohdo T, Tsumura T, Iijima H, Kashiwagi K, Tsukahara S. Ultrasound biomicroscopic study of ciliary body thickness in eyes with narrow angles. Am J Ophthalmol. Mar 2000;129(3):342-6. [Medline].
Kramer P, Ritch R. The treatment of acute angle-closure glaucoma revisited. Ann Ophthalmol. Dec 1984;16(12):1101-3. [Medline].
Lam D, Tham C, Lai J, et al. Current approaches to management of acute primary angle closure. Curr Opinion Ophthalmol. 2001;18:146-151.
Lim LS, Aung T, Husain R, Wu YJ, Gazzard G, Seah SK. Acute primary angle closure: configuration of the drainage angle in the first year after laser peripheral iridotomy. Ophthalmology. Aug 2004;111(8):1470-4. [Medline].
Lowe RF. Aetiology of the anatomical basis for primary angle-closure glaucoma. Biometrical comparisons between normal eyes and eyes with primary angle-closure glaucoma. Br J Ophthalmol. Mar 1970;54(3):161-9. [Medline].
MacCumber M. Management of Ocular Injuries and Emergencies. 1998:237-240.
Markowitz SN, Morin JD. Angle-closure glaucoma: relation between lens thickness, anterior chamber depth and age. Can J Ophthalmol. Dec 1984;19(7):300-2. [Medline].
Ritch R. Assessing the treatment of angle closure. Ophthalmology. Oct 2003;110(10):1867-8. [Medline].
Salmon JF. The management of acute angle-closure glaucoma. Eye. Oct 1999;13 (Pt 5):609-10. [Medline].
Saw SM, Gazzard G, Friedman DS. Interventions for angle-closure glaucoma: an evidence-based update. Ophthalmology. Oct 2003;110(10):1869-78; quiz 1878-9, 1930. [Medline].
Further Reading
Related eMedicine topics
Glaucoma, Angle Closure, Acute (from Ophthalmology)
Glaucoma, Drug-Induced (Ophthalmology)
Sudden Visual Loss (from Ophthalmology)
Guidelines
Primary Angle Closure
Glaucoma
Clinical studies
ALPI vs Medical Therapy Effects on Optic Nerve Structure & Function (Iridoplasty)
Keywords
acute angle-closure glaucoma, acute angle closure glaucoma, acute angle closure, AACG, primary angle closure, primary angle-closure glaucoma, increased intraocular pressure, decreased visual acuity, increased IOP
