Medscape is available in 5 Language Editions – Choose your Edition here.


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.


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.


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.



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.


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.



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.


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.

Contributor Information and Disclosures

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.


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.


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.

  1. Youm DJ, Ha MM, Chang Y, Song SJ. Retinal vessel caliber and risk factors for branch retinal vein occlusion. Curr Eye Res. 2012 Apr. 37(4):334-8. [Medline].

  2. Klein R, Klein BE, Moss SE, Meuer SM. Retinal emboli and cardiovascular disease: the Beaver Dam Eye Study. Arch Ophthalmol. 2003 Oct. 121(10):1446-51. [Medline].

  3. Ratra D, Dhupper M. Retinal arterial occlusions in the young: Systemic associations in Indian population. Indian J Ophthalmol. 2012 Mar. 60(2):95-100. [Medline].

  4. Biousse V, Calvetti O, Bruce BB, Newman NJ. Thrombolysis for central retinal artery occlusion. J Neuroophthalmol. 2007 Sep. 27(3):215-30. [Medline].

  5. Beiran I, Goldenberg I, Adir Y, Tamir A, Shupak A, Miller B. Early hyperbaric oxygen therapy for retinal artery occlusion. Eur J Ophthalmol. 2001 Oct-Dec. 11(4):345-50. [Medline].

  6. Hattenbach LO, Kuhli-Hattenbach C, Scharrer I, Baatz H. Intravenous thrombolysis with low-dose recombinant tissue plasminogen activator in central retinal artery occlusion. Am J Ophthalmol. 2008 Nov. 146(5):700-6. [Medline].

  7. Nowak RJ, Amin H, Robeson K, Schindler JL. Acute Central Retinal Artery Occlusion Treated with Intravenous Recombinant Tissue Plasminogen Activator. J Stroke Cerebrovasc Dis. 2012 Feb 18. [Medline].

  8. Cohen JE, Moscovici S, Halpert M, Itshayek E. Selective thrombolysis performed through meningo-ophthalmic artery in central retinal artery occlusion. J Clin Neurosci. 2012 Mar. 19(3):462-4. [Medline].

  9. Atebara NH, Brown GC, Cater J. Efficacy of anterior chamber paracentesis and Carbogen in treating acute nonarteritic central retinal artery occlusion. Ophthalmology. 1995 Dec. 102(12):2029-34; discussion 2034-5. [Medline].

  10. Augsburger JJ, Magargal LE. Visual prognosis following treatment of acute central retinal artery obstruction. Br J Ophthalmol. 1980 Dec. 64(12):913-7. [Medline].

  11. Beiran I, Reissman P, Scharf J, et al. Hyperbaric oxygenation combined with nifedipine treatment for recent-onset retinal artery occlusion. Eur J Ophthalmol. 1993 Apr-Jun. 3(2):89-94. [Medline].

  12. Brown GC. Retinal artery obstructive disease. Ryan SJ, ed. Retina. St. Louis: Mosby; 1994. Vol 2: 1361-77.

  13. Brown GC, Magargal LE, Shields JA, et al. Retinal arterial obstruction in children and young adults. Ophthalmology. 1981 Jan. 88(1):18-25. [Medline].

  14. Butz B, Strotzer M, Manke C, et al. Selective intraarterial fibrinolysis of acute central retinal artery occlusion. Acta Radiol. 2003 Nov. 44(6):680-4. [Medline].

  15. Cella W, Avila M. Optical coherence tomography as a means of evaluating acute ischaemic retinopathy in branch retinal artery occlusion. Acta Ophthalmol Scand. 2007 Nov. 85(7):799-801. [Medline].

  16. Ffytche TJ, Bulpitt CJ, Kohner EM, et al. Effect of changes in intraocular pressure on the retinal microcirculation. Br J Ophthalmol. 1974 May. 58(5):514-22. [Medline].

  17. Fraser S, Siriwardena D. Interventions for acute non-arteritic central retinal artery occlusion. Cochrane Database Syst Rev. 2002. CD001989. [Medline].

  18. Hayreh SS, Kolder HE, Weingeist TA. Central retinal artery occlusion and retinal tolerance time. Ophthalmology. 1980 Jan. 87(1):75-8. [Medline].

  19. Hertzog LM, Meyer GW, Carson S, et al. Central retinal artery occlusion treated with hyperbaric oxygen. J Hyperbaric Med. 1992. 7:33-42.

  20. Knoop K, Trott A. Ophthalmologic procedures in the emergency department--Part I: Immediate sight-saving procedures. Acad Emerg Med. 1994 Jul-Aug. 1(4):408-12. [Medline].

  21. Lacy C, Armstrong LL, Ingram N, et al. Drug Information Handbook. 4th ed. Hudson, Cleveland: Lexi-Comp Inc; 1996.

  22. Magargal LE, Goldberg RE. Anterior chamber paracentesis in the management of acute nonarteritic central retinal artery occlusion. Surg Forum. 1977. 28:518-21. [Medline].

  23. Mangat HS. Retinal artery occlusion. Surv Ophthalmol. 1995 Sep-Oct. 40(2):145-56. [Medline].

  24. Mead GE, Lewis SC, Wardlaw JM, Dennis MS. Comparison of risk factors in patients with transient and prolonged eye and brain ischemic syndromes. Stroke. 2002 Oct. 33(10):2383-90. [Medline].

  25. Miyake Y, Horiguchi M, Matsuura M, et al. Hyperbaric oxygen therapy in 72 eyes with retinal arterial occlusion. 9th International Symposium on Underwater and Hyperbaric Physiology. 1987. 949-53.

  26. Rumelt S, Brown GC. Update on treatment of retinal arterial occlusions. Curr Opin Ophthalmol. 2003 Jun. 14(3):139-41. [Medline].

  27. Schmidt D, Schumacher M, Wakhloo AK. Microcatheter urokinase infusion in central retinal artery occlusion. Am J Ophthalmol. 1992 Apr 15. 113(4):429-34. [Medline].

  28. Schmidt DP, Schulte-Monting J, Schumacher M. Prognosis of central retinal artery occlusion: local intraarterial fibrinolysis versus conservative treatment. AJNR Am J Neuroradiol. 2002 Sep. 23(8):1301-7. [Medline].

  29. Suri MF, Nasar A, Hussein HM, Divani AA, Qureshi AI. Intra-arterial thrombolysis for central retinal artery occlusion in United States: Nationwide In-patient Survey 2001-2003. J Neuroimaging. 2007 Oct. 17(4):339-43. [Medline].

  30. Wray SH. The management of acute visual failure. J Neurol Neurosurg Psychiatry. 1993 Mar. 56(3):234-40. [Medline].

The cherry red spot of central retinal artery occlusion.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.