eMedicine Specialties > Emergency Medicine > Ophthalmology

Retinal Artery Occlusion: Treatment & Medication

Author: Neil Jain, MD, Staff Physician, Yale University School of Medicine, Department of Surgery, Section of Emergency Medicine
Coauthor(s): Pascal SC Juang, MD, FAAEM, FACEP, Medical Director, ED Information Systems, Attending Physician, Department of Emergency Medicine, Hoag Memorial Hospital Presbyterian
Contributor Information and Disclosures

Updated: Jun 30, 2009

Treatment

Prehospital Care

No specific prehospital treatment is available for retinal artery occlusion. The prognosis for visual recovery is related directly to the promptness in treatment; thus, rapid transport to the ED is essential.

Emergency Department Care

The 2 phases of ED care must occur. The first phase involves rapid detection and treatment of visual loss. The second phase involves a thorough investigation for the cause of visual loss.

No randomized controlled trials to support one treatment modality over any others are underway, but anecdotal reports and case series have suggested many modalities of treatment.

  • Immediate lowering of IOP to a target pressure of 15 mm Hg using medical management, ocular massage, and anterior chamber paracentesis
    • Ocular massage
      • Apply direct pressure for 5-15 seconds, then release. Repeat several times.
      • Increased IOP causes a reflexive dilation of retinal arterioles by 16%.
      • A sudden drop in IOP with release increases the volume of flow by 86%.
      • Ocular massage dislodges the embolus to a point further down the arterial circulation and improves retinal perfusion.
    • Anterior chamber paracentesis
      • Advocated when visual loss has been present for less than 24 hours
      • Early paracentesis is associated with increased visual recovery.
      • Slit-lamp removal of 0.1-0.4 mL of aqueous humor via tuberculin syringe and a 27-gauge needle may decrease IOP to 3 mm Hg.
      • Decrease in IOP is thought to allow greater perfusion, pushing emboli further down the vascular tree.
  • Other treatments
    • See Medication for details and mechanisms of action for medications.
    • Start timolol early in the treatment of CRAO, as this is readily available in most emergency departments. Acetazolamide and mannitol should also be used when CRAO is suspected because there are few downsides to starting these medications early.
    • In carbogen therapy (5% carbon dioxide, 95% oxygen), carbon dioxide dilates retinal arterioles, and oxygen increases oxygen delivery to ischemic tissues.
    • Thrombolytics may be useful if initiated within 4-6 hours of visual loss, but they may not be much help if the embolus is cholesterol, talc, or calcific. Thrombolytics are introduced via the proximal ophthalmic artery, delivering increased concentrations directly to the retinal artery and minimizing systemic complications. Results of noncontrolled retrospective studies have been mixed. As of 2007, a European controlled study is underway.1
    • Hyperbaric oxygen (HBO) therapy may be beneficial if initiated within 2-12 hours of onset of symptoms. Institute treatment with other interventions first; transport to a chamber may usurp precious time. Results from noncontrolled studies have been mixed. A 2001 controlled study in Israel showed a benefit in the treatment group.2 In this study, all patients were treated within 8 hours of symptom onset.
    • Treatment with IV thrombolytics as with cerebral infarction has been discussed3 but currently is not the standard of care.

Consultations

  • Ophthalmologist
    • Immediate evaluation is imperative for any patient with acute CRAO.
    • Ophthalmologists can decide with which further treatment (eg, thrombolytics, hyperbaric oxygen, retrobulbar block) to proceed.
    • Early treatment (<2 h from onset of symptoms) with HBO may be associated with increased visual recovery, but HBO can be considered if the duration of visual loss is less than 12 hours. Inhalation of 100% oxygen at 2 atm can provide an arterial pO2 of 1000-1200 mm Hg, resulting in a 3-fold increase in oxygen diffusion distance through ischemic retinal tissues. Some studies show a 40% improvement of 2 or more levels of visual acuity.

Medication

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

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.

Adult

250-500 mg IV; repeat in 2-4 h prn; not to exceed 1 g/d

Pediatric

5-10 mg/kg/dose IV/IM q6h or 10-15 mg/kg/d PO divided q6-8h

Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, 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

Use in impaired hepatic function may lead to coma; may cause substantial increase in blood glucose in some diabetic patients


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.

Adult

1 gtt in affected eye(s) tid

Pediatric

Not established

Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already taking oral CA inhibitors

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 chronic administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy)

Hyperosmotic diuretics

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.

Adult

1.5-2 g/kg IV as a 20% solution (7.5-10 mL/kg) or as a 15% solution (10-13 mL/kg) over a period as short as 30 min

Pediatric

0.5-1 g/kg IV initial; then 0.25-0.5 g/kg IV q4-6h maintenance dose

Documented hypersensitivity; anuria; severe pulmonary congestion; severe dehydration; active intracranial bleeding; progressive renal damage; 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 because 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


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.

Adult

1-2 g/kg PO; repeat q5h prn; alternatively, 1 mL/kg PO as a 50% solution in juice

Pediatric

Administer as in adults

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

For oral use only; never administer parenterally; 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 persons with cardiac, renal, or hepatic disease

Sympathomimetics

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.

Adult

Solution (0.5%): 1-2 gtt in affected eye(s) tid; since apraclonidine 0.5% is used with other ocular glaucoma therapies, use an approximate 5-min interval between instillation of each medication to prevent washout of previous dose; do not inject into the eye
Solution (1%): 1 gtt in affected eye 1 h before initiating anterior segment laser surgery; second gtt into the same eye immediately upon completion of surgery

Pediatric

Not established

Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAOIs

Documented hypersensitivity; patients using MAOIs or those who 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

Caution in coronary insufficiency, chronic renal failure, recent myocardial infarction, cerebrovascular disease, Raynaud disease, thromboangiitis obliterans, and depressed patients


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.

Adult

1 gtt into eye(s) q12h

Pediatric

Not established

Increased or synergistic effects when used concurrently with agents that lower IOP

Documented hypersensitivity; narrow-angle glaucoma; dilation of pupil may predispose patient to attack of angle-closure glaucoma

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Macular edema occurs in up to 30% of aphakic patients treated with epinephrine; discontinuation of treatment generally results in reversal of maculopathy; caution in vascular hypertension

Cholinergic/miotic agents

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 (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.

Adult

Solution: 1 or 2 gtt tid/qid
Gel: Apply a 0.5-inch ribbon in the lower conjunctival sac of affected eye(s) hs

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, hypertension, or hypotension

Corticosteroids

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.

Adult

Not to exceed 80 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve

Pediatric

4-5 mg/m2/d PO
Alternative: 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; fungal, viral, connective tissue, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction; GI disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in hypertension; known to cause cataract formation with long-term use; in prolonged use, withdraw treatment by gradually decreasing frequency of applications to avoid adrenal insufficiency

Beta-adrenergic blocking agents

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 (Timoptic)

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

Adult

1 gtt of 0.25% or 0.5% in affected eye(s) bid; if IOP is maintained at satisfactory levels, change the dosage to 1 gtt in affected eye(s) qd; if clinical response is not adequate, change dosage to 1 gtt of 0.5% solution in affected eye(s) bid; if IOP is still not at a satisfactory level, consider concomitant therapy

Pediatric

Administer as in adults

Coadministration of ophthalmic timolol may cause bradycardia and asystole when used in combination with systemic beta-blockers; rechallenge studies have confirmed these effects; use topical beta-blockers with caution if the patient is already taking systemic beta-blockers

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

May contain sulfites, which may cause allergic-type reactions in susceptible patients

More on Retinal Artery Occlusion

Overview: Retinal Artery Occlusion
Differential Diagnoses & Workup: Retinal Artery Occlusion
Treatment & Medication: Retinal Artery Occlusion
Follow-up: Retinal Artery Occlusion
Multimedia: Retinal Artery Occlusion
References
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References

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

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

  3. 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. Nov 2008;146(5):700-6. [Medline].

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

  21. 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.

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

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

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

  25. 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. Oct 2007;17(4):339-43. [Medline].

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

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Further Reading

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Keywords

retinal artery occlusion, RAO, branch retinal artery occlusion, BRAO, central retinal artery occlusion, CRAO, retinal disease, arterial occlusive disease, ocular stroke, embolism of the retinal artery, retinal artery emboli, loss of vision

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Contributor Information and Disclosures

Author

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 and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Pascal SC Juang, MD, FAAEM, FACEP, Medical Director, ED Information Systems, Attending Physician, Department of Emergency Medicine, Hoag Memorial Hospital Presbyterian
Pascal SC Juang, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Assaad J Sayah, MD, Chief, Department of Emergency Medicine, Cambridge Health Alliance
Assaad J Sayah, MD is a member of the following medical societies: National Association of EMS Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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 College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

 
 
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