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Retinal Artery Occlusion Medication

  • Author: Benjamin Feldman, MD; Chief Editor: Robert E O'Connor, MD, MPH  more...
 
Updated: Dec 14, 2015
 

Medication Summary

Medical therapy for retinal artery occlusion is directed toward lowering IOP, increasing retinal perfusion, and increasing oxygen delivery to hypoxic tissues. The first goal is accomplished by using the same drugs that are used in acute closed-angle glaucoma. Retinal perfusion may be increased by vasodilatory drugs, increasing arterial pCO2, or by giving peripheral thrombolytics to remove the offending embolus. Oxygen delivery is improved by breathing higher concentrations of oxygen or with hyperbaric oxygen.

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Carbonic anhydrase inhibitors

Class Summary

Carbonic anhydrase (CA) is an enzyme found in many tissues of the body, including the eye. The reversible reaction it catalyzes involves the hydration of carbon dioxide and the dehydration of carbonic acid.

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)

 

Reduces rate of aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP. Used most frequently as single diuretic agent in acute management of CRAO. Other diuretics may be added if sufficient decrease in IOP not attained.

Dorzolamide (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 carbonic anhydrase, reducing hydrogen ion secretion at renal tubules and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

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Hyperosmotic diuretics

Class Summary

Lower IOP by creating an osmotic gradient between the ocular fluids and plasma (not for long-term use).

Mannitol (Osmitrol)

 

Reduces elevated IOP when the pressure cannot be lowered by other means.

Initially assess for adequate renal function in adults by administering 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 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.

Glycerin (Ophthalgan)

 

Used in glaucoma to interrupt acute attacks. Oral osmotic agent for reducing IOP. Able to increase tonicity of blood until finally metabolized and eliminated by kidneys. Maximum reduction of IOP usually occurs 1 h of glycerin administration. Effect usually lasts approximately 5 h.

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Sympathomimetics

Class Summary

Lower IOP mainly by increasing outflow and reducing the production of aqueous humor. The combination of a miotic and a sympathomimetic has additive effects in lowering IOP. Each may be added in rotation after 5-minute intervals until target IOP is reached.

Apraclonidine (Iopidine)

 

Reduces elevated (and normal) IOP, whether accompanied by glaucoma or not. Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

Dipivefrin (AKPro, Propine)

 

Converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by decreasing aqueous production and enhancing outflow facility. Has same therapeutic effect as epinephrine with fewer local and systemic adverse effects. May be used as initial therapy or as adjunct with other antiglaucoma agents for control of IOP.

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Cholinergic/miotic agents

Class Summary

These direct-acting agents used to be considered the first step in the treatment of glaucoma; however, they have now yielded to the beta-blockers. DOC in this category is pilocarpine; a useful adjunctive agent that is additive to the effects of beta-blockers, carbonic anhydrase inhibitors, or sympathomimetics. Individualize dosage and frequency of administration. Patients with darkly pigmented irides may require higher strengths of pilocarpine.

Pilocarpine ophthalmic (Ocusert Pilo-40, Pilagan, Isopto, Pilostat)

 

Directly stimulates cholinergic receptors in the eye, decreasing resistance to aqueous humor outflow.

Instillation frequency and concentration are determined by patient's response.

If other glaucoma medication also is being used, at bedtime, use gtt at least 5 min before gel.

Patients may be treated with pilocarpine as long as IOP is controlled and no deterioration in the visual fields occurs.

May use alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.

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Corticosteroids

Class Summary

Used in arterial occlusion only when temporal arteritis is the suspected or if etiology is confirmed.

Prednisone (Deltasone, Orasone, Sterapred)

 

Useful in the treatment of inflammatory and allergic reactions. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

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Beta-adrenergic blocking agents

Class Summary

Lower IOP by decreasing the rate of aqueous humor production and possibly outflow. May be more effective than pilocarpine or epinephrine alone and have the advantage of not affecting pupil size or accommodation.

Timolol ophthalmic (Timoptic)

 

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

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Contributor Information and Disclosures
Author

Benjamin Feldman, MD Resident Physician, Department of Emergency Medicine, University of California, Irvine, School of Medicine

Benjamin Feldman, MD is a member of the following medical societies: American Academy of Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Coauthor(s)

Pascal SC Juang, MD Medical Director, ED Information Systems, Department of Emergency Medicine, Hoag Memorial Hospital Presbyterian

Pascal SC Juang, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

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

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Heart Association, Medical Society of Delaware, Society for Academic Emergency Medicine, Wilderness Medical Society, American Medical Association, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Additional Contributors

Assaad J Sayah, MD, FACEP Chief, Department of Emergency Medicine; Senior Vice President, Primary and Emergency Care, Cambridge Health Alliance

Assaad J Sayah, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, Massachusetts Medical Society, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Neil Jain, MD Staff Physician, Yale University School of Medicine, Department of Surgery, Section of Emergency Medicine

Neil Jain, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Kilbourn Gordon III, MD, and Enoch Huang, MD, to the development and writing of this article.

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The cherry red spot of central retinal artery occlusion.
 
 
 
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