eMedicine Specialties > Ophthalmology > Hematologic & Cardiovascular Disorders

Ocular Ischemic Syndrome: Treatment & Medication

Author: Igal Leibovitch, MD, Oculoplastic and Orbital Devision, Department of Ophthalmology, Tel-Aviv Medical Center, Tel-Aviv, Israel
Coauthor(s): Diego Calonje, MD, Consulting Staff, Department of Ophthalmology, Private Practice; Sherif M El-Harazi, MD, MPH, Consulting Staff, Department of Ophthalmology, Sherif El-Harazi, MD
Contributor Information and Disclosures

Updated: May 13, 2009

Treatment

Medical Care

  • Ocular treatments2,19,20
    • Panretinal photocoagulation to treat neovascularization of the iris, optic nerve, or retina. It was reported to cause regression of neovascularization in about one third of patients with ocular ischemic syndrome (OIS).
    • Topical medication to lower intraocular pressure
    • Cyclodiathermy and cyclocryotherapy to lower intraocular pressure
    • Intravitreal steroids - Possible adjunct therapy in cases of recurrent cystoid macular edema in OIS21
    • Ocular filtering procedures and implantation of glaucoma drainage valves to treat neovascular glaucoma
  • Systemic treatments
    • Antiplatelet therapy
    • Thrombolytic therapy: Potential benefits of thrombolytic therapy include fast dissolution of physiologically compromising pulmonary emboli, faster recovery, prevention of recurrent thrombus formation, and rapid restoration of hemodynamic disturbances.
    • Steroids (when giant cell arteritis is suspected)

Surgical Care

  • Carotid endarterectomy22
    • A small number of publications have reported on the ophthalmic outcome of carotid endarterectomy in patients with OIS, and the data presented are not conclusive.
    • Carotid endarterectomy has been shown to benefit symptomatic patients with a nondisabling stroke, amaurosis fugax, and a hemispheric transient ischemic attack whose carotid stenosis is 70-99%.
    • The North American Symptomatic Carotid Endarterectomy Trial Collaborators found a 2-year stroke rate of 9% in such patients who underwent endarterectomy versus a 26% rate in those treated with antiplatelet therapy alone. Stabilization or improvement of visual acuity occurs in about 25% of eyes following endarterectomy.23
  • Superficial temporal artery to middle cerebral artery anastomoses - Bypass procedures, such as superficial temporal artery to middle cerebral artery anastomoses (STA-MCA), have been tried in patients with 100% carotid obstruction in whom a thrombus has propagated distally and an endarterectomy is precluded.

Consultations

  • Cardiology
  • Cardiovascular surgery
  • Neurology

Diet

A strict, low-fat diet is recommended. A low-salt and low-sugar diet is recommended for patients with hypertension and diabetes.

Medication

Medications include antiplatelet therapy and anticoagulant therapy.

Antiplatelets

Inhibit platelet function by blocking cyclooxygenase and subsequent aggregation.


Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Odorless white powdery substance available in 81 mg, 325 mg, and 500 mg for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids.
Stronger inhibitor of both prostaglandin synthesis and platelet aggregation than other salicylic acid derivatives. Acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.

Adult

325 mg PO qd

Pediatric

Not established

May decrease hyponatremic and hypotensive effects of ACE inhibitors due to direct effect on renin-angiotensin conversion pathway; concurrent use of aspirin and acetazolamide can lead to high serum concentrations of acetazolamide (and toxicity) due to competition at renal tubules for secretion; effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses greater than 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; because of association of aspirin with Reye syndrome, do not use in children ( <16 y) with flu

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Use during third trimester of pregnancy should be avoided; may cause severe urticaria, angioedema, or bronchospasm; may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants


Ticlopidine (Ticlid)

Platelet aggregation inhibitor. Causes a time and dose-dependent inhibition of both platelet aggregation and release of platelet granule constituents. After oral ingestion, interferes with platelet membrane function by inhibiting ADP-induced platelet-fibrinogen binding and subsequent platelet-platelet interactions. Tablets for oral administration are sold as white, oval, film-coated tablets.

Adult

250 mg PO bid

Pediatric

Not established

Potentiates effect of aspirin or other NSAIDs on platelet aggregation; antacids decrease levels of ticlopidine; cimetidine increases ticlopidine serum levels; ticlopidine decreases digoxin plasma levels; concomitant administration of ticlopidine resulted in a significant increase in theophylline elimination half-time

Documented hypersensitivity; hematopoietic disorders, such as neutropenia and thrombocytopenia; hemostatic disorder or active pathological bleeding; severe liver impairment

Pregnancy

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

Precautions

Recommended to help reduce risk of having stroke, for patients who have had a stroke or early warning symptoms while on aspirin; not for use in those who can take aspirin to prevent stroke because ticlopidine can cause life-threatening blood problems; neutropenia occurs in about 2.4% of people on ticlopidine


Clopidogrel (Plavix)

Inhibitor of platelet aggregation. Selectively inhibits binding of ADP to platelet receptor, thereby inhibiting platelet aggregation.

Adult

75 mg PO qd

Pediatric

Not established

Concomitant administration of aspirin and clopidogrel not established; concomitant use with heparin should be undertaken with caution; concomitant administration with NSAIDs associated with increased occult GI blood loss; safety of coadministration with warfarin not established

Documented hypersensitivity; active pathological bleeding such as peptic ulcer or intracranial hemorrhage

Pregnancy

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

Precautions

Use during pregnancy only if clearly needed; in breastfeeding, decision should be made whether to discontinue breastfeeding or discontinue drug, taking into account importance of drug to breastfeeding women

Anticoagulant therapy

Prevent recurrent or ongoing thromboembolic occlusion of vertebrobasilar circulation.


Warfarin (Coumadin)

Acts by inhibiting synthesis of vitamin K-dependent clotting factors. Believed to interfere with clotting factor synthesis by inhibiting regeneration of vitamin K-1 epoxide. Degree of depression is dependent upon dose administered.

Adult

5-15 mg/d PO qd for 2-5 d; adjust dose according to desired INR

Pediatric

Not established

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate; medications that may increase anticoagulant effects of warfarin include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Anticoagulation is contraindicated in any localized or general physical condition or personal circumstance in which the hazard of hemorrhage might be greater than the potential clinical benefits of anticoagulation, such as pregnancy; hemorrhagic tendencies or blood dyscrasias; recent or completed surgery of central nervous system, eye, or traumatic surgery resulting in large open surfaces; bleeding tendencies associated with active ulceration; threatened abortion; unsupervised patients with senility; spinal puncture

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Perform periodic determination of PT/INR or other suitable coagulation test; numerous factors, alone or in combination, including travel, changes in diet, environment, physical state, and medication may influence response of patient to anticoagulants; generally a good practice to monitor patient's response with additional PT/INR determinations in period immediately after discharge from hospital


Heparin

Inhibits reactions that lead to clotting of blood and formation of fibrin clots in vitro and in vivo. Acts at multiple sites in normal coagulation system. Prevents formation of stable fibrin clot by inhibiting activation of fibrin-stabilizing factor. Dosage adequate when activated partial thromboplastin time (aPTT) is 1.5-2 times normal or when whole-blood clotting time is elevated approximately 2.5-3 times control value.

Adult

Initial dose: 40-70 U/kg IV
Maintenance infusion: 18 U/kg/h IV
Alternatively, 50 U/kg/h IV initially, followed by continuous infusion of 15-25 U/kg/h and increase dose by 5 U/kg/h q4h prn using PTT results

Pediatric

Not established

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity

Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia

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 on heparin may develop new thrombus formation in association with thrombocytopenia, resulting from irreversible aggregation of platelets induced by heparin, the so-called white-dot syndrome; increased resistance to heparin frequently is encountered in fever, thrombosis, thrombophlebitis, infections with thrombosing tendencies, myocardial infarction, cancer, and postsurgical patients
Increased risk in older women: A higher incidence of bleeding has been reported in women >60 y

More on Ocular Ischemic Syndrome

Overview: Ocular Ischemic Syndrome
Differential Diagnoses & Workup: Ocular Ischemic Syndrome
Treatment & Medication: Ocular Ischemic Syndrome
Follow-up: Ocular Ischemic Syndrome
References

References

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  2. Brown GC. Ocular ischemic syndrome. In: Retina. 2nd ed. Mosby;1994: 1515-27.

  3. Kahn M, Green WR, Knox DL, et al. Ocular features of carotid occlusive disease. Retina. Winter 1986;6(4):239-52. [Medline].

  4. Kearns TP, Hollenhurst RW. Venous-stasis retinopathy of occlusive disease of the carotid artery. Proc Staff Meet Mayo Clin. Jul 17 1963;38:304-12. [Medline].

  5. Eugene JR, Abdallah M, Miglietta M, et al. Carotid occlusive disease: primary care of patients with or without symptoms. Geriatrics. May 1999;54(5):24-6, 29-30, 33 passim. [Medline].

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  8. Smith VH. Pressure changes in the ophthalmic artery after carotid occlusion (an experimental study in the rabbit). Br J Ophthalmol. 1961;45:1-26.

  9. Takaki Y, Nagata M, Shinoda K, et al. Severe acute ocular ischemia associated with spontaneous internal carotid artery dissection. Int Ophthalmol. Dec 2008;28(6):447-9. [Medline].

  10. Kubicka-Trzaska A, Romanowska-Dixon B. Non-malignant uveitis masquerade syndromes. Klin Oczna. 2008;110(4-6):203-6. [Medline].

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  12. Hollenhorst RW, Svien HJ, Benoit CF. Unilateral blindness occurring during anaesthesia for neuro- surgical operations. Arch Ophthalmol. 1954;52:819-30.

  13. Leibovitch I, Casson R, Laforest C, et al. Ischemic orbital compartment syndrome as a complication of spinal surgery in the prone position. Ophthalmology. Jan 2006;113(1):105-8. [Medline].

  14. Casson RJ, Fleming FK, Shaikh A, et al. Bilateral ocular ischemic syndrome secondary to giant cell arteritis. Arch Ophthalmol. Feb 2001;119(2):306-7. [Medline].

  15. Hwang JM, Girkin CA, Perry JD, et al. Bilateral ocular ischemic syndrome secondary to giant cell arteritis progressing despite corticosteroid treatment. Am J Ophthalmol. Jan 1999;127(1):102-4. [Medline].

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  17. Ho AC, Lieb WE, Flaharty PM, et al. Color Doppler imaging of the ocular ischemic syndrome. Ophthalmology. Sep 1992;99(9):1453-62. [Medline].

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Further Reading

Keywords

ocular ischemic syndrome, OIS, venous stasis retinopathy, ischemic ocular inflammation, ischemic oculopathy, carotid occlusive disease

Contributor Information and Disclosures

Author

Igal Leibovitch, MD, Oculoplastic and Orbital Devision, Department of Ophthalmology, Tel-Aviv Medical Center, Tel-Aviv, Israel
Igal Leibovitch, MD is a member of the following medical societies: American Academy of Ophthalmology
Disclosure: Nothing to disclose.

Coauthor(s)

Diego Calonje, MD, Consulting Staff, Department of Ophthalmology, Private Practice
Disclosure: Nothing to disclose.

Sherif M El-Harazi, MD, MPH, Consulting Staff, Department of Ophthalmology, Sherif El-Harazi, MD
Sherif M El-Harazi, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, and International Society of Refractive Surgery
Disclosure: Nothing to disclose.

Medical Editor

V Al Pakalnis, MD, PhD, Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center
V Al Pakalnis, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and South Carolina Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Steve Charles, MD, Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians & Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong
Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Consulting

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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