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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By activating plasminogen into plasmin, which in turn dissolves fibrin, fibrinolytic agents can dissolve pathologic thrombi. Streptokinase, a fibrinolytic agent derived from group C beta-hemolytic streptococci, is antigenic and can elicit allergic reactions. Urikinase, a fibrinolytic agent obtained by purification from human urine or from human fetal kidney cell culture, is not antigenic, and for this reason can be used repeatedly, if needed, whereas streptokinase cannot be used for retreatment within six months of a course of therapy. Either agent can be introduced into the circulation systemically (intravenously) or locally (via catheter). The indications for systemic therapy include deep-vein thrombosis, pulmonary embolism, and arterial thrombosis and embolism. The indications for local therapy include acute myocardial infarction, arterial thrombosis and embolism, and the clearing of occluded arteriovenous cannulae and access shunts. Contraindications include an actively bleeding lesion, a vascular intracranial disorder, or uncontrolled hypertension; relative contraindications include pregnancy; a recent wound, fracture, surgery, or deep closed biopsy; or a general contraindication to anticoagulation, such as coagulopathy, uremia, or severe liver disease. During thrombolytic therapy, invasive procedures, intramuscular injections, and the use of other anticoagulant or antiplatelet agents should be avoided. Measurement of fibrinogen levels, the titer of fibrin/fibrinogen degradation product, or thrombin time can be used to monitor therapy.
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PMID:Fibrinolysis and its current usage. 634 82

The efficacy of streptokinase was studied in an open trial on 30 consecutive patients with major pulmonary embolism, affecting at least three lobar arteries in pulmonary angiography. Streptokinase was started on average 26 hours from the onset of symptoms and usually given directly to the pulmonary artery. Conventional dosage was used and adjusted by thrombin time. The average treatment period was 32 hours. 26 patients (87%) survived and made a good clinical recovery. Improvement occurred early: signs of improved pulmonary perfusion appeared usually within four hours. Repeat angiograms in 20 patients showed remarkable increase in pulmonary perfusion and partial but not complete lysis of the emboli. Four patients (13%) died, three of them because of no response and one due to late cardiac arrhythmia. Bleeding requiring blood transfusion occurred in four patients, but caused no late sequelae. It is concluded that streptokinase treatment of major pulmonary embolism is effective and safe in rapidly restoring pulmonary perfusion.
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PMID:Experience with streptokinase treatment of major pulmonary embolism. 634 37

Out of 102 patients suffering from deep venous thrombosis of leg and pelvis 46 of them underwent thrombectomy with excellent results in 73.9%; in 23.9% the result was good, one patient came to death due to pulmonary embolism. In no case a postthrombotic syndrome could be traced. 23 patients (22.5%) underwent thrombolysis by Streptokinase. In no case the result was excellent, in 19 patients this treatment showed satisfactory results, 2 patients developed a postthrombotic syndrome, 2 patients died of haemorrhage. 33 patients (32.25%) were treated by a combination of heparin and acetyl-salicylic acid. A good result could only be obtained in 2 patients, a postthrombotic syndrome developed in the remaining 31 cases.
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PMID:[Treatment of thrombotic occlusion of the pelvic and extremity veins. Comparison of three different types of treatment]. 671 Nov 68

Urokinase and streptokinase are the two fibrinolytics approved for clinical use. Streptokinase has the broader application, being used to treat deep vein thrombosis (DVT), pulmonary embolism (PE), arterial thromboembolism, and occluded arteriovenous shunts in renal dialysis. Bleeding, the most significant complication of fibrinolytic therapy, arises mostly from invaded sites and can be significantly reduced by minimizing venipuncture and other invasive procedures.
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PMID:Fibrinolytic guidelines in diabetes. 706 Sep 47

A case study report is presented of a 20 year old black woman with a past history of oral contraceptive (OC) use who developed Budd-Chiari syndrome (hepatic vein thrombosis) associated with decreased levels of antithrombin 3. This combination has not been previously reported. The woman presented on December 28, 1979 with midepigastric pain. She had no previous illnesses, but OCs had been used up to 2 years prior to admission. Shortly after admission the patient became hypotensive, developed oliguric renal failure, and began to rapidly accumulate ascites. During this admission, the patient's transaminase levels abruptly declined. A percutaneous liver biopsy obtained on January 9, 1980 showed centrilobular hemorrhagic necrosis of a severe degree. An inferior vena cavagram was repeated on January 14, 1980 demonstrating hepatic vein thrombosis. Streptokinase, followed by heparinization, was given in an effort to lyse the thrombi, but repeat inferior cavagram on January 24th proved this to be unsuccessful. Thrombosis of the left iliac and left femoral vein then appeared. Because of her apparent "hypercoagulable state," the antithrombin 3 level was measured on January 31st and found to be 27%. A simultaneous serum fibrinogen was 255 mg/dl. Family members (father, mother, and 4 children) were studied. All had normal antithrombin 3 levels, thus excluding a familial defect. The patient gradually improved and was discharged on February 25, 1980 on Coumadin, diuretics, and a 3 g sodium diet. Because of ascites and peripheral edema, a LeVeen shunt was placed on March 25, 1980. At surgery, she was noted to have obstruction of the right internal jugular and right cephalic veins. Because of possible thrombosis in the superior inferior vena cava branches, venography was performed on March 31st and demonstrated thrombosis of the right subclavian, inferior vena cava, and internal iliac veins. Despite the therapy, patient again began to reaccumulate ascites and was readmitted on May 17th. The then nonfunctioning shunt was repositioned in the patient's right atrium. Postoperatively, the patient's course was complicated by DIC. Because heparin induced thromboycytopenia was suspected, heparin was discontinued and Coumadin begun. On June 6th the patient became suddenly short of breath. A lung scan was consistent with pulmonary embolism. She could not be adequately ventilated and died on June 8th. Although the patient discontinued OC use 2 years prior to initial presentation of the disease, the morphologic features of the venous thrombosis and hepatic damage were indicative of a chronic, ongoing process of longer than 6 months' duration, thus raising the possibility of a cause-effect relationship between the OC and thrombotic process. Prospective studies are needed to substantiate the view of a relationship between OC use, antithrombin 3 deficiency, and the Budd-Chiari syndrome.
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PMID:Budd-Chiari Syndrome and antithrombin III deficiency. 710 23

Streptokinase was infused for 103 +/- 25 hrs. in 27 patients (6 with deep vein thrombosis of the leg, 7 with thrombosis of Vv. axillaris and subclavia, 9 with acute massive pulmonary embolism, 3 with chronic artery occlusion, 2 with thrombosis of the retinal vein). Blood coagulation studies were performed repeatedly. Anticoagulation (prolongation of thrombin time to 1 1/2-2 1/2 of normal) could be achieved without additional heparin by reduction of streptokinase to doses as low as 20 000 U/h. Reptilase time correlated significantly with thrombin times. Following 24 hrs. of infusion, PTT was less than 50 sec. and Quick test less than 50% of normal in most instances. No correlation was found between PTT or Quick test and factor II, V, VI, X activities during streptokinase infusion. Bleeding was observed in 18 patients. The infusion was stopped because of bleeding in 3 cases. None of the coagulation tests performed in this study correlated with the incidence of bleeding. Hemoglobin concentration decreased 2,6 +/- 1,6 gr% and this decrease could no be explained by blood lesses.
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PMID:[Control of blood coagulation and complications in long-term streptokinase therapy]. 719 87

Streptokinase (290 000 U/2 h) was directly infused under angiographic control into the predominantly affected right pulmonary artery in a 71-year-old patient with acute pulmonary embolism and persistent shock. This led to immediate complete remission of shock symptoms and lasting stabilisation of the patient. If, as this case demonstrates, embolectomy is not possible and high-dose intravenous streptokinase is contraindicated, localised use of streptokinase in low dosage offers a possibility for treatment of life-threatening pulmonary embolism.
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PMID:[Local streptokinase treatment in acute pulmonary embolism with shock (author's transl)]. 744 35

The history and physical examination were assessed in 215 patients with acute pulmonary embolism uncomplicated by preexisting cardiac or pulmonary disease. The patients had been included in the Urokinase Pulmonary Embolism Trial or the Urokinase-Streptokinase Embolism Trial. Presenting syndromes were (1) circulatory collapse with shock (10 percent) or syncope (9 percent); (2) pulmonary infarction with hemoptysis (25 percent) or pleuritic pain and no hemoptysis (41 percent); (3) uncomplicated embolism characterized by dyspnea (12 percent) or nonpleuritic pain usually with tachypnea (3 percent) or deep venous thrombosis with tachypnea (0.5 percent). The most frequent symptoms were dyspnea (84 percent), pleuritic pain (74 percent), apprehension (63 percent) and cough (50 percent). Hemoptysis occurred in only 28 percent. Dyspnea, hemoptysis or pleuritic pain occurred separately or in combination in 94 percent. All three occurred in only 22 percent. The most frequent signs were tachypnea (respiration ate 20/min or more) (85 percent), tachycardia (heart rate 100 beats/min or more) (58 percent), accentuated pulmonary component of the second heart sound (57 percent) and rales (56 percent). Signs of deep venous thrombosis were present in only 41 percent and a pleural friction rub was present in only 18 percent. Either dyspnea or tachypnea occurred in 96 percent. Dyspnea, tachypnea or deep venous thrombosis occurred in 99 percent. As a group, the identified clinical manifestations, although nonspecific, are strongly suggestive of acute pulmonary embolism. Conversely, acute pulmonary embolism was rarely identified in the absence of dyspnea, tachypnea or deep venous thrombosis.
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PMID:History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. 746 69

Intravenous heparin is still the basic treatment of deep vein thrombosis in the lower limbs. However, its weak action on the blood clot and its poor efficiency in the prevention of functional sequelae have resulted in its replacement by thrombolytic agents. Streptokinase produces a more than 50 percent lysis of the thrombus 4 times more frequently than heparin, but the result depends on the degree of venous occlusion and on the site and duration of the thrombosis. The risk of pulmonary embolism does not seem to be increased, but haemorrhagic accidents are 3 times more frequent than with heparin. The long-term benefit on functional venous sequelae is questionable, the best results being obtained by an early treatment with complete recanalization of the vein and absence of recurrence. The value of thrombolytic agents in the treatment of deep vein thrombosis has therefore not been demonstrated, but they can reasonably be prescribed to young patients with recent proximal and non-occlusive phlebitis.
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PMID:[Thrombolytic therapy in deep vein phlebitis of the lower limbs]. 817 45

The 4 widely available thrombolytic agents, alteplase (recombinant tissue plasminogen activator, rt-PA), anisoylated plasminogen streptokinase activator complex (APSAC; anistreplase), streptokinase and urokinase have revolutionised the treatment of acute myocardial infarction and are also effective in treating pulmonary embolism and peripheral arterial thrombosis. Therapeutic efficacy of the agents appears to be similar. Choice of a thrombolytic agent depends more on patient characteristics, availability and familiarity with the drug, cost and differences in tolerability. While overall thrombolytic therapy is relatively safe, these 4 agents differ in their tolerability profiles. Streptokinase has the lowest cerebral haemorrhage rate, anistreplase an intermediate and alteplase the highest rate. The incidence of total stroke is also higher with alteplase and anistreplase than with streptokinase, translating to an actual difference in patient risk of 4 extra strokes per 1000 patients treated. Risk of major bleeding is dependent on predisposing factors and seems to be similar with each agent. The incidence of hypotension with alteplase (4.3% in ISIS-3) is less than with streptokinase or anistreplase (6.8 and 7.2%, respectively in ISIS-3). The incidence of major anaphylactic reactions with streptokinase and anistreplase is low (< 1%). Urokinase and alteplase may be preferred for readministration of thrombolytic therapy and anistreplase is the agent of choice where rapid completion of therapy is desirable. The various agents may have different tolerability profiles with different adjunctive therapies and further data are therefore required.
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PMID:Comparative tolerability profiles of thrombolytic agents. A review. 847 Nov 85


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