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Acute Angle-Closure Glaucoma Medication

  • Author: Joseph Freedman, MD; Chief Editor: Steven C Dronen, MD, FAAEM  more...
 
Updated: Oct 27, 2015
 

Medication Summary

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.

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Carbonic anhydrase inhibitors

Class Summary

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.

Methazolamide (Neptazane)

 

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

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Beta-adrenergic blockers

Class Summary

These agents may lower IOP via their suppression of aqueous humor production and probably not through any affects on the pupil.

Timolol ophthalmic (Timoptic, Timoptic XE)

 

Reduces elevated and normal IOP by reducing aqueous humor production or possibly the outflow.

Carteolol ophthalmic (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.

Levobetaxolol (Betaxon)

 

Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.

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.

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Alpha-adrenergic agonists

Class Summary

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.

Brimonidine (Alphagan, Alphagan-P)

 

Selective alpha2 receptor that may reduce aqueous humor formation, may decrease inflow, or may increase uveoscleral outflow.

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Corticosteroids

Class Summary

These agents reduce ocular inflammation thereby providing symptomatic relief and augmenting the affects of other medications.

Prednisolone ophthalmic (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.

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Ophthalmic agents, miotic

Class Summary

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 ophthalmic (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.

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Hyperosmotics

Class Summary

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.

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.

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.

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Contributor Information and Disclosures
Author

Joseph Freedman, MD Resident Physician, Department of Emergency Medicine, State University of New York Downstate, King's County Hospital Center

Joseph Freedman, MD is a member of the following medical societies: Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Coauthor(s)

Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Vice-Chair in Charge of Research, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Andrew Aherne, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital Center, University Hospital of Brooklyn

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

Douglas Lavenburg, MD Clinical Professor, Department of Emergency Medicine, Christiana Care Health Systems

Douglas Lavenburg, MD is a member of the following medical societies: American Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Ayim K Darkeh, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center

Ayim K Darkeh is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, National Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Michelle Ervin, MD Chair, Department of Emergency Medicine, Howard University Hospital

Michelle Ervin, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, National Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD, MMB, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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