Embolization peripheral

Prophylaxis and treatment Prophylaxis and treatment of venous thrombosis and its extension pulmonary embolism peripheral arterial embolism atrial fibrillation with embolization. 

Treatment of venous thrombosis, pulmonary embolism, peripheral arterial embolism, atrial fibrillation with embolism Intermittently Initially, 10,000 units, then 50-70 units/kg (5000-10,000 units) q4 6h. IV Infusion Loading dose 80 units/kg, then 18 units/kg/hr, with adjustments based on aPTT. Range 10-30 units/kg/hr. 

Prevention of venous thrombosis, pulmonary embolism, peripheral arterial embolism, atrial fibrillation with embolism Subcutaneous 5000 units q8-12h. 

The more peripheral the embolization is to the tumor, the less the opportunity for collateral circulation and the greater likelihood of tumor necrosis. While tumor necrosis is a desired effect, necrosis of adjacent non-targeted tissue is not. Microcatheter coaxial systems allow subselective or superselective embolizations to access tumor vessels and avoid non-targeted embolization. Peripheral embolization produces small vessel occlusion without sacrificing the main arteries, allowing future re-embolization when necessary. 

Treatment of coronary occlusion, acute MI, and peripheral arterial embolism ... 

Many serious health problems result from abnormally located blood clots heart attacks (clots in coronary arteries), pulmonary embolism (clots in the lungs), and peripheral arterial occlusion and deep vein thrombosis (clots in the limbs). Each year heart attacks alone afflict over a million people in the United States, and almost half of them die as a result. 

It is indicated in the prophylaxis and treatment of deep vein thrombosis in major surgery and pulmonary embolism, treatment of atrial fibrillation with embolisation, prophylaxis and treatment of peripheral arterial embolism. 

Papaverine, because of its general depressant effect on smooth muscle, has been used in doses of 30 to 60 mg, subcutaneously and intravenously, in peripheral thrombosis and embolism, acute myocardial infarction, angina pectoris, bronchial asthma, renal and biliary colic, and other conditions in which relaxation of smooth muscle is desired. However, the therapeutic effectiveness of papaverine is questionable, and there is no established indication for its use. 

Falk E, Unstable angina with fatal outcome dynamic coronary thrombosis leading to infarction and/or sudden death autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion, Circulation 1985 71 699-708. 

Urokinase is intended for intravenous use only and indicated for the treatment of pulmonary embolism, coronary artery thrombosis, and intravenous catheter clearance. Typical dosages in peripheral arterial disease consist of an infusion at a rate ranging from 60,000 lU/hr to 240,000 lU/hr infused directly into the thrombus. 

Alteplase was the first commercially available recombinant tissue-type plasminogen activator (rt-PA) (25), It has a plasma half-life of less than five minutes and is metabolized by the liver, This agent was initially hailed as fibrin-specific unlike its precursors (urokinase and streptokinase). It was thought that this would result in a better safety profile, but this has not been born out in either the coronary or the peripheral experience, where actually there may be a higher bleeding risk as infusion time increases. Alteplase is currently indicated for use in the treatment of myocardial infarction, acute ischemic stroke, and pulmonary embolism. 

Therapeutic uses Originally used for the treatment of deep-vein thrombosis and serious pulmonary embolism, thrombolytic drugs are now being used with increasing frequency to treat acute myocardial infarction and peripheral arterial thrombosis and emboli, and for unclotting catheters and shunts. 

Thrombophilias and other causes of hypercoagulability are rare causes of stroke (Matijevic and Wu 2006). Antithrombin III deficiency, protein C deficiency, activated protein C resistance owing to factor V Leiden mutation, protein S deficiency and plasminogen abnormality or deficiency can all cause peripheral and intracranial venous thrombosis. Thrombosis is usually recurrent and there is often a family history. Thrombophilia may cause arterial thrombosis, although the alternative diagnosis of paradoxical embolism should always be considered in patients with these disorders. It should be noted that deficiencies in any one of the factors associated with thrombophilia may be an incidental finding and cannot necessarily be assumed to be the cause of stroke. 

Peripheral arterial occlusion. Heparin may prevent extension of a thrombus and hasten its recanalisation it is commonly used in the acute phase following thrombosis or embolism. There is no case for treating ischaemic peripheral vascular disease with an oral anticoagulant (for prevention, see Antiplatelet drugs). 

Thrombosis occurred during celecoxib therapy (400 mg/day) in four women (aged 37-56 years) with connective tissue diseases and conditions that predisposed them to thrombosis, including Raynaud s phenomenon, raised anticardiolipin antibody titers, and a previous history of thrombosis. Peripheral artery thrombosis (three patients) and pulmonary embolism (one patient) were documented after starting celecoxib. Symptoms of thrombosis began to appear within 1 week of starting celecoxib in three patients and 2 months after starting celecoxib in the fourth patient. 

Aberrant thrombus formation and deposition on blood vessel walls imderlies the pathogenesis of acute cardiovascular disease states which remain the principal cause of morbidity and mortality in the industrialized world [1,2,3]. Plasma proteins, proteases and specific cellular receptors that participate in hemostasis have emerged as important risk considerations in thrombosis and thromboembolic disorders. The clinical manifestations of the above disease states include acute coronary artery and cerebrovascular syndromes, peripheral arterial occlusion, deep vein thrombosis and pulmonary/renal embolism [3]. The most dilabilitating acute events precipitated by these disorders are myocardial infarction and stroke. In addition, the interplay between hemostatic factors and hypertension (4) or atherosclerosis (5) dramatically enhances the manifestation of these pathologic states. 

Clinical uses include treatment of acute myocardial infarction, pulmonary embolism and peripheral thromboembolism and in the restoration of circulation through arterial grafts and intravenous catheters. 

There are additional indications for PAs. These may include pulmonary embolism, deep vein thrombosis, acute thromboembolism of peripheral arteries, thromboses precipitated by prosthetic heart valves, and other occlusions. Some of the applications are still investigational. 

Heparin is an anticoagulant that inhibits reactions that lead to clotting. It is indicated in prophylaxis and treatment of venous thrombosis and its extensions, pulmonary embolism (PE), peripheral arterial embolism, and atrial fibrillation with embolization diagnosis and treatment of acute and chronic consumption coagulopathies (DIC) and prevention of postoperative deep venous thrombosis. 

Interest in thrombolytic therapy for acute ischemic stroke re-emerged with reports of successful thrombolysis for arterial thrombosis in the peripheral vascular system. Local lA infusion was found to have higher rates of recanalization compared with systemic IV delivery of thrombolytics without increased levels of hemorrhagic complications IV use of UK and SK was found to provide clinical benefit in patients with pulmonary embolism [5, 6]. In the early 1980s, lA infusion of UK or SK for acute MI was shown to be highly effective [5, 6]. At the same time, technical advances in endovascnlar microcatheter and microguidewire design made access to the intracranial vessels safer... 

Early application of reperfusion therapy with thrombolytic agents has significantly improved the outcomes of acute myocardial infarction and other conditions, such as pulmonary embolism, DVT, arterial thrombosis, acute thrombosis of retinal vessel, extensive coronary emboli, and peripheral vascular thromboembolism (124). 

Clinically, papaverine is used as an antispasmodic, and is given by mouth or by vein in doses of 30 to 80 mg. It has been found useful in the treatment of spastic conditions of the stomach and intestines caused by hyperacidity and duodenal ulcers. Other applications, such as in the treatment of biliary colic, asthma, vascular spasms, including angina pectoris, spasm secondary to embolic phenomena, and peripheral vascular diseases, have been more or less abandoned, and several synthetic antispasmodics have made inroads on the fields formerly reserved for papaverine. However, a shortage of papaverine developed when its usefulness was at a peak, and several methods were developed for the industrial synthetic production of the alkaloid to take care of this condition (see p. 43). A brief selected bibliography may serve as a guide to the literature concerning the clinical application of papaverine (68). 

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