You are in: eMedicine Specialties > Ophthalmology > HEMATOLOGIC AND CARDIOVASCULAR DISORDERS Ocular Ischemic SyndromeArticle Last Updated: Jun 26, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 10
  Author: Igal Leibovitch, MD, Oculoplastic and Orbital Devision, Department of Ophthalmology, Tel-Aviv Medical Center, Tel-Aviv, Israel Igal Leibovitch is a member of the following medical societies: American Academy of Ophthalmology 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 Editors: Vytautas A Pakainis, MD, Chief of Ophthalmology, Dorn Veterans Administration Medical Center, Professor of Ophthalmology, Ophthalmology, University of South Carolina School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Steve Charles, MD, Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri; Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences Author and Editor Disclosure Synonyms and related keywords: OIS, venous stasis retinopathy, ischemic ocular inflammation, ischemic oculopathy, carotid occlusive disease INTRODUCTIONSection 2 of 10
  BackgroundOcular ischemic syndrome (OIS) encompasses the ocular signs and symptoms that result from chronic vascular insufficiency. Common anterior segment findings include advanced cataract, anterior segment inflammation, and iris neovascularization. Posterior segment signs include narrowed retinal arteries, dilated but nontortuous retinal veins, midperipheral dot-and-blot retinal hemorrhages, cotton-wool spots, and optic nerve/retinal neovascularization. The presenting symptoms include ocular pain and abrupt or gradual visual loss. PathophysiologyThe most common etiology of OIS is severe unilateral or bilateral atherosclerotic disease of the internal carotid artery or marked stenosis at the bifurcation of the common carotid artery. OIS may also be caused by giant cell arteritis (GCA). It is postulated that the decreased vascular perfusion results in tissue hypoxia and increased ocular ischemia, leading to neovascularization. FrequencyUnited StatesThe true incidence of OIS is unknown. It is estimated that approximately 5% of patients with marked carotid artery stenosis present with OIS. By extrapolating data from previous studies, and applying it to the population of the US, approximately 1800 new cases (7.5 per million) are encountered per year. Mortality/MorbidityThe 5-year mortality rate in patients with OIS is about 40%. The leading cause of death is cardiac disease, followed by stroke and cancer. Predisposing risk factors for atherosclerosis (eg, hypertension, diabetes mellitus) have a higher prevalence in patients with OIS than in age-matched populations. SexMales are affected more frequently than females, by a ratio of approximately 2:1. AgeOIS mainly affects elderly patients. The age range is 50-80 years, with a mean age range of 65-68 years. OIS is uncommon in patients younger than 50 years. CLINICALSection 3 of 10
HistorySymptoms can include amaurosis fugax, gradual or sudden visual loss, and pain. The diagnosis of OIS should always be suspected in elderly patients with asymmetric anterior uveitis, hypotony, neovascularization cataract, and retinopathy.
PhysicalArm pulses, cardiac auscultation, and carotid auscultation
Causes
DIFFERENTIALSSection 4 of 10
Central Retinal Vein Occlusion Retinopathy, Diabetic, Background Retinopathy, Diabetic, Proliferative
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| Drug Name | Aspirin (Anacin, Ascriptin, Bayer Aspirin) |
|---|---|
| Description | 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 Dose | 325 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | 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 |
| Interactions | 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 |
| Pregnancy | D - Unsafe in pregnancy |
| 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 |
| Drug Name | Ticlopidine (Ticlid) |
|---|---|
| Description | 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 Dose | 250 mg PO bid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; hematopoietic disorders, such as neutropenia and thrombocytopenia; hemostatic disorder or active pathological bleeding; severe liver impairment |
| Interactions | 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 |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| 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 |
| Drug Name | Clopidogrel (Plavix) |
|---|---|
| Description | Inhibitor of platelet aggregation. Selectively inhibits binding of ADP to platelet receptor, thereby inhibiting platelet aggregation. |
| Adult Dose | 75 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; active pathological bleeding such as peptic ulcer or intracranial hemorrhage |
| Interactions | 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 |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| 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 |
Prevent recurrent or ongoing thromboembolic occlusion of vertebrobasilar circulation.
| Drug Name | Warfarin (Coumadin) |
|---|---|
| Description | 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 Dose | 5-15 mg/d PO qd for 2-5 d; adjust dose according to desired INR |
| Pediatric Dose | Not established |
| Contraindications | 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 |
| Interactions | 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 |
| Pregnancy | X - Contraindicated in pregnancy |
| 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 |
| Drug Name | Heparin |
|---|---|
| Description | 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 Dose | 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 Dose | Not established |
| Contraindications | Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia |
| Interactions | Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| 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 |
Ocular Ischemic Syndrome excerpt
Article Last Updated: Jun 26, 2006
