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

Venous thromboembolism is usually treated with heparin followed by oral anticoagulants for approximately 3 months. The optimal length of heparin therapy is uncertain. There is now good evidence that treatment failures are associated with inadequate heparin effects. Heparin can be administered with similar safety and effectiveness by either intravenous infusion or 2 hourly subcutaneous injection. Oral anticoagulant therapy is effective and safe if given in a dose which prolongs the prothrombin time to an international normalized ratio of 2.0 to 2.5. Thrombolytic therapy is indicated in patients with major pulmonary embolism and in selected patients with recent acute venous thrombosis. Vena caval interruption is usually confined to patients who have contraindications to anticoagulant therapy. Surgical removal of thromboembolic obstruction should be considered in selected patients with thromboembolic pulmonary hypertension.
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PMID:The treatment of venous thromboembolism. 304 68

Intravenous heparin is the initial treatment of choice for most patients with acute pulmonary embolism or proximal deep vein thrombosis. The primary objective of initial heparin therapy in such patients is to prevent recurrent venous thromboembolism. The efficacy of intravenous heparin for this purpose has been established by randomized clinical trials in patients with pulmonary embolism, and more recently, in patients with proximal vein thrombosis. Heparin is given as an initial intravenous bolus of 5000 units, followed by a maintenance dose of 30,000-40,000 units per 24 h by continuous intravenous infusion. A recent randomized trial in patients with proximal vein thrombosis indicates that failure to achieve an adequate anticoagulant response (APTT greater than 1.5 times control) is associated with a high risk (25%) of recurrent venous thromboembolism. Intravenous heparin administered in doses that prolong the activated partial thromboplastin time (APTT) to 1.5 or more times the control value is highly effective, and associated with a low frequency (2%) of recurrent venous thromboembolism. Heparin is continued for 7-10 days, overlapped with warfarin sodium during the last 4-5 days. Multiple randomized clinical trials indicate that this approach is highly effective. An alternative approach is to commence heparin and oral anticoagulants together at the time of diagnosis, and to discontinue heparin on the fourth or fifth day. A recent randomized trial in patients with submassive venous thrombosis or pulmonary embolism suggests that 4-5 days of initial heparin therapy is effective and safe, but this approach must be evaluated by further randomized trials before it is recommended for patients with extensive proximal vein thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin therapy for venous thrombosis and pulmonary embolism. 306 31

A prospective randomized pilot study of subcutaneous low-dose heparin in the prevention of deep-vein thrombosis and pulmonary embolism was carried out in patients admitted to hospital after intracerebral hemorrhage. A high incidence of deep-vein thrombosis and lung embolism was detected by phleboscintigraphy and lung perfusion scintigraphy, respectively. There was no significant reduction of deep-vein thrombosis and pulmonary embolism in the therapy group. Heparin did not increase the risk of rebleeding.
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PMID:Heparin therapy, deep-vein thrombosis and pulmonary embolism after intracerebral hemorrhage. 306 68

The incidence and mortality of acute pulmonary embolism (PE) remain ill defined, particularly in the setting of the emergency department. However, high-risk groups can be identified based on medical conditions known to predispose patients to venous thrombosis. Recent research into the physiologic regulation of coagulation and thrombolysis reveals that recurrent venous thrombosis and PE may be caused by heritable deficiencies and abnormalities of plasma proteins. To decide among options for evaluation and treatment of patients suspected of PE, physicians combine clinical assessment with patterns observed on radionuclide ventilation-perfusion (V/Q) scans. However, the prevalence of PE among patients with "low probability" V/Q scans suggests that current physician behavior may be imprudent. Heparin anticoagulation continues to be standard therapy for acute PE, but newer clot-specific thrombolytic drugs may offer superior benefits with acceptable complication rates in carefully selected patients.
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PMID:Pulmonary embolism. 327 57

Pulmonary embolism remains a challenging problem in diagnosis and management for the emergency physician. Although its clinical presentation is protean and often ambiguous, risk stratification can be accomplished based on the predictive power of a limited number of physical and historical characteristics. Ventilation-perfusion lung scanning occupies a central position in the work-up of suspected PE; however, evidence exists that it may be misused by many physicians. A low probability V-Q scan does not exclude the diagnosis of PE. Patients with other than normal- or high-probability patterns of pulmonary ventilation and perfusion on lung scanning require further investigation. Noninvasive venous studies are useful when indicative of proximal deep venous thrombosis, but are normal in many patients with acute PE. Heparin remains the standard of treatment for most patients with PE. Vena cava filters effectively reduce the incidence of recurrent PE in patients with contraindications to anticoagulation. Thrombolytic therapy offers potential advantages in the treatment of patients with shock due to their PE. Case reports of PE treated with tissue-type plasminogen activator, a new thrombus-specific fibrinolytic agent, are encouraging but preliminary.
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PMID:Pulmonary embolism. 328 Mar 1

The efficacy of low-dose, locally administered streptokinase (SK) combined with full therapeutic systemic doses of heparin was investigated. Seven patients with angiographically proven massive acute pulmonary embolism were treated. Streptokinase, 10,000-20,000 units/hour, was administered directly into the left or right pulmonary artery for 9 to 24 hours. Heparin was administered concurrently. The number of unperfused segments of the infused lung shown on the lung scan decreased from 5 +/- 2 to 2 +/- 1 after 12-24 hours (p less than .01). No change was shown in the contralateral lung. The angiographic index of severity score in the infused lung decreased from 16 +/- 1 to 9 +/- 4 (p less than .01). The partial pressure of oxygen in arterial blood improved within four hours. In spite of the low doses of streptokinase, however, two major bleeding episodes occurred that required blood transfusion. In conclusion, low dose intrapulmonary streptokinase, combined with intravenous heparin, may provide a therapeutic option in patients with life-threatening massive acute pulmonary embolism in whom full dose lytic therapy may be hazardous, although even low dose lytic therapy was associated with risk.
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PMID:Treatment of massive acute pulmonary embolism. The use of low doses of intrapulmonary arterial streptokinase combined with full doses of systemic heparin. 333 89

Use of urokinase to treat heparin-associated thrombocytopenia and thrombosis in one patient is described, and various treatments proposed for this syndrome are discussed. A 56-year-old man received an intravenous bolus dose of heparin sodium at his local hospital and was transferred to another institution for treatment of suspected pulmonary embolism; he had received heparin two weeks earlier during coronary angiography. The patient's platelet count was reported to be normal before heparin administration. When embolism was confirmed, heparin was discontinued and streptokinase was given for 24 hours. Heparin infusion was then restarted at 1000 units/hr and continued for four days. Platelet count on admission to the second hospital was 47,000/cu mm; 12 hours later it was 19,000/cu mm, and it remained low despite platelet transfusions. Five days after admission, deep-vein thrombosis developed in the left leg. Heparin was discontinued and urokinase and warfarin were started. Urokinase was infused at 320,000 IU/hr for 12 hours and continued at dosages of 160,000-320,000 IU/hr for a total of 40 hours. The initial warfarin sodium dose was 15 mg, followed by a dosage of 10 mg/day. Symptoms of deep-vein thrombosis improved within 12 hours and platelet count increased after heparin was discontinued. If it is recognized early enough, heparin-associated thrombocytopenia can be reversed by discontinuation of heparin. Transfusions of platelets are of little benefit. Dipyridamole, cyclo-oxygenase inhibitors such as aspirin, and protamine sulfate may be useful. Long term anticoagulation with warfarin is recommended to prevent recurrent thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thrombolytic therapy in heparin-associated thrombocytopenia with thrombosis. 348 69

Protein C is, after activation by thrombin, a potent inhibitor of blood coagulation. An isolated deficiency of protein C increases the risk of thrombosis. The two forms of protein C deficiency, the heterozygous and the homozygous deficiency state, have different clinical features. Patients with heterozygous protein C deficiency are at a high risk to develop venous thrombosis and pulmonary embolism. In newborns with homozygous protein C deficiency with very low protein C levels (1%) a purpura fulminans like syndrome was observed. Heparin and coumarin derivatives are effective drugs in heterozygous protein C deficiency, homozygous patients may be treated either by replacement of protein C or coumarin derivatives. Decreased protein C levels were observed in various other diseases: Chronic and acute liver disease, disseminated intravascular coagulation, malignancy, postoperatively and during treatment with asparaginase. The role of protein C in these diseases to trigger thrombosis is not yet established.
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PMID:Clinical relevance of protein C. 352 11

Heparin (Lipo-Hepin, Liquaemin Sodium) and warfarin sodium (Coumadin, Panwarfin) are the classic anticoagulants in use for venous thromboembolic disease. They work by modifying the coagulation mechanism, heparin having an immediate effect and warfarin having a more delayed effect. The most common adverse effects of anticoagulation therapy are hemorrhagic complications. Thrombolytic therapy should be considered in all patients with massive pulmonary embolism with hypotension and in patients with deep venous thrombosis in the popliteal area or higher. Such therapy has been shown to help preserve the pulmonary microcirculation after pulmonary embolism and to decrease the incidence of the postthrombotic syndrome following deep venous thrombosis. If certain clinical guidelines are followed rigidly, the incidence of significant bleeding complications is low. Although the use of tissue plasminogen activator in venoocclusive disease has been limited to isolated cases, results have been very promising.
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PMID:Treatment of venous thromboembolic disease. A pragmatic approach to anticoagulation and thrombolysis. 370 54

Eighteen patients with femoral and iliofemoral venous thrombosis were treated surgically. Five of the patients had a moderate degree of venous congestion and were classified as having phlegmasia alba dolens and 13 patients had phlegmasia cerulea dolens. The mean age was 39 years, range 18-60 years; 6 were men and 12 women. Thrombectomy was performed with a Fogarty venous thrombectomy catheter. In all cases the thrombosis was verified by phlebography. Pre- and postoperative phlebography was used in all cases to show the patency of the femoral and iliofemoral segment. There was no operative pulmonary embolism or mortality. Heparin infusion was continued in the thrombectomized segment for 10 days followed by phenprocumone treatment. The patients were followed from 6 to 8 months, postoperatively. The operation was performed in the acute stage and the late results are as follows: 4 limbs good, 6 limbs fair and 8 limbs poor. The best results were obtained when the latency period was 24 to 72 hours. Postthrombotic sequelae could not be prevented in about 44% of all patients despite venous thrombectomy.
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PMID:Femoral and iliofemoral thrombectomy to prevent chronic venous insufficiency. Follow-up of 18 patients. 372 47


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