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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 produces chronic sequelae in the legs and occasional immediate mortality due to pulmonary embolism. Because it occurs in certain high risk situations (for example, after surgery) its prevention is a practical proposition. This has been attempted using many different approaches. Administration of low dose heparin with or without dihydroergotamine to enhance venous return has been one of the most widely tested regimens. There is little doubt that this can prevent, in many patient groups, postoperative deep venous thrombosis and fatal pulmonary embolism, with a low incidence of adverse reactions. Some particularly high risk postoperative patient groups (for example, those undergoing hip surgery) warrant more aggressive measures to prevent thrombosis. Surveys have shown that increasing use is being made of this approach, and it is hoped that all surgeons will adopt a policy that will reduce postoperative venous thrombosis and pulmonary embolism. A reduction in the incidence of venous thromboembolism in large acute myocardial infarction is achieved by low dose heparin, although early mobilization is important. In addition, many of the patients at risk merit full dose anticoagulation to prevent intracardiac thromboembolism. Established venous thrombosis is treated effectively by intravenous heparin, followed by warfarin to keep the prothrombin time at 1.2 to 1.5 times control, as assessed using rabbit thromboplastin; most patients need three months of treatment. Anticoagulation is warranted for pulmonary embolism, with fibrinolytic therapy reserved for patients with massive embolism and hemodynamic compromise. Embolectomy is a heroic measure, which may occasionally be lifesaving.
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PMID:Preventive and therapeutic approach to venous thromboembolic disease and pulmonary embolism--can death from pulmonary embolism be prevented? 353 67

A 57 year old man presented with apparently spontaneous lower extremity deep vein thrombosis and pulmonary embolism. He was treated in conventional fashion with intravenous heparin and oral warfarin. After 4 daily doses of warfarin the prothrombin and proconvertin (P+P) time was within therapeutic range, and heparin was stopped. Over the next six hours complete defibrination occurred, associated with severe bleeding complications. Functional protein C measured after normalization of routine coagulation tests averaged 40% of normal, and was only 3.5% of normal immediately prior to the episode of defibrination. We conclude that the very low functional protein C levels seen immediately prior to defibrination were caused by a combination of pre-existent protein C deficiency and warfarin therapy, and directly predisposed to defibrination once heparin was stopped, despite "therapeutic" warfarin anticoagulation. Exacerbation of intravascular coagulation should be considered a potential prothrombotic effect of warfarin therapy in protein C deficient individuals.
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PMID:Defibrination during warfarin therapy in a man with protein C deficiency. 383 6

The pathophysiology of deep-vein thrombosis (DVT) and pulmonary embolism (PE) is briefly discussed, and the efficacy, dosage and administration, laboratory monitoring, and adverse effects of thrombolytic agents, heparin, and warfarin are reviewed. Acute therapy of DVT and PE is usually initiated with intravenous heparin; however, thrombolytic agents such as streptokinase and urokinase may be preferred in patients with massive PE or severe DVT when clot lysis rather than clot stabilization is deemed necessary. For DVT or PE, an intravenous loading dose of streptokinase or urokinase is given, followed by a continuous infusion of the drug. Therapy with streptokinase is continued for 24 hours in patients with PE and for 72 hours in those with DVT; urokinase is continued for 12 hours in patients with PE. Monitoring of blood coagulation tests during thrombolytic therapy is recommended primarily for ensuring that a lytic state is achieved. Intravenous heparin is preferred for acute treatment of DVT or PE; controversy exists regarding whether administration by continuous infusion or intermittent bolus injection is superior. Heparin dosage is usually adjusted to maintain the activated partial-thromboplastin time (APTT) ratio between 1.5 and 2.5; however, the ideal therapeutic range has never been firmly established. After acute treatment with heparin, most patients should continue to receive either warfarin or subcutaneous heparin for several months to prevent recurrent thromboembolism. Bleeding is the major adverse effect of thrombolytic agents and anticoagulants. The risk of bleeding with heparin and warfarin therapy increases with excessive prolongation of the APTT and prothrombin time (PT), respectively. Future clinical trials should further define the role of thrombolytic agents in the treatment of DVT and PE and the efficacy of less-intense warfarin therapy for pulmonary embolism or arterial thromboembolic events.
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PMID:Pathophysiology and treatment of deep-vein thrombosis and pulmonary embolism. 389 Dec

A piroxicam-warfarin interaction is presented with a discussion of the possible mechanism of action. A 60-year-old white male on warfarin therapy for recurrent pulmonary embolism and deep venous thrombophlebitis showed a decrease in his previously therapeutic and stable prothrombin time when piroxicam was discontinued from his drug regimen. On two rechallenges over a ten-month period, his prothrombin times showed consistent and clinically significant fluctuations as piroxicam was added and deleted from his drug regimen.
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PMID:A warfarin-piroxicam drug interaction. 402 61

Use of a protocol for pharmacist determination of heparin sodium dosages administered by continuous i.v. infusion was evaluated by retrospective chart review in a California hospital. Charts of adult medical-surgical patients who received heparin infusions between June 1982 and December 1983 were reviewed for the following information: patient sex, age, and reason for receiving heparin; times, dates, numbers, and values of coagulation tests before and during heparin therapy; times, dates, and values of prothrombin time determinations during conversion to warfarin therapy; and times, number, and costs of heparin infusions. Charts were divided into two groups: those of patients for whom physicians prescribed heparin doses empirically and those of patients for whom physicians requested heparin dosing by the pharmacy department. Data were evaluated for 62 patients in the physician-dosed group and 26 patients in the pharmacy protocol group. Pulmonary embolism was the reason for heparin therapy in 34% of the physician-dosed patients and only 15% of the pharmacist-dosed patients. Pharmacists using the protocol ordered fewer anticoagulation tests and fewer heparin infusions per patient. Time from the start of heparin therapy to therapeutic anticoagulation was shorter in patients whose heparin dose was determined by the protocol, and values in the therapeutic range were achieved in a greater percentage of these patients than in the empirically dosed patients. Pharmacists using a standard dosing protocol effectively initiated and maintained heparin therapy that compared favorably with physician-dosed empiric therapy.
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PMID:Pharmacist-directed heparin therapy using a standard dosing and monitoring protocol. 405 Aug 13

Six patients are described in whom disseminated intravascular coagulation of uncertain cause was found to be due to occult pulmonary embolism. The peripheral blood smear showed thrombocytopenia in all patients and schistocytes in four. Coagulation studies revealed increased levels of fibrinogen/fibrin degradation products (six of six patients), positive results for fibrin monomer (five patients), prolonged thrombin times (four patients), hypofibrinogenemia (three patients), prolonged prothrombin times (two patients), and decreased plasma coagulation factors (two patients). Pulmonary embolism was confirmed by lung scanning or pulmonary angiography. Institution of full-dose heparin therapy was associated with hemostatic and clinical improvement in all patients. The association of disseminated intravascular coagulation with occult pulmonary embolism merits recognition since full-dose heparinization is required for successful therapy.
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PMID:Unrecognized pulmonary embolism presenting as disseminated intravascular coagulation. 672 Jul 24

One hundred thirty-four patients with venous thrombosis or pulmonary embolism, confirmed by radiological techniques, received continuous-pump heparin therapy while their responses were monitored by the activated coagulation time (ACT). The suggested protocol was as follows: (1) give an intravenous bolus of about 50 units/kg; (2) follow with 15 to 25 units/kg/hr; (3) modify infusion rate to maintain ACT of 150 to 190 s; (4) after two or three days with ACT in target range, start oral warfarin sodium therapy; (5) after three to five days of warfarin therapy, if prothrombin time is two to 2 1/2 times the control value, discontinue heparin administration. One hundred thirty-two patients responded, with no heparin failures. Dangerous bleeding occurred in two who received excessive amounts of heparin. Some patients, mostly with short ACTs, responded slowly; some, many with long ACTs, had minor bleeding. The protocol proved successful and safe when followed closely.
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PMID:Heparin therapy for thromboembolic disorders. A prospective evaluation of 134 cases monitored by the activated coagulation time. 688 62

Despite venous stasis and a hypercoagulable state during pregnancy, the reported incidences of deep venous thrombosis and pulmonary embolism are remarkably low, about 1 in 2,000 and 1 in 10,000 cases, respectively. Mortality from antepartum thromboembolism has been reported in about 15 percent of untreated patients and less than 1 percent of treated patients. Adequate anticoagulant therapy significantly reduces maternal mortality and decreases postpartum morbidity. The proper anticoagulant agent for use during pregnancy has been widely debated. Coumarin compounds pass through the placenta and into the fetus. Hemorrhagic complications in the fetus are uncommon if prothrombin times are carefully controlled and if the drug is discontinued before delivery. However, coumarin during the first trimester has the teratogenic hazard of producing chondrodysplasia punctata. Heparin, in contrast, does not cross the placental barrier and is considered more effective treatment for deep venous thrombosis; however, long-term intravenous administration during pregnancy has been considered both impractical and possibly hazardous due to the risk of osteoporosis after 6 months of therapy. In our study, a combined regimen of intravenous and subcutaneous heparin was used successfully in four women with deep venous thrombosis. One patient who had recurrent embolization while on adequate intravenous heparin underwent vena caval clipping and had an uneventful Cesarian section at term with a normal infant. Another patient also underwent Caesarian section with a normal infant, while the other two women had normal vaginal deliveries at term. Miniheparin therapy was continued for 3 months postpartum, followed by long-term aspirin and Ascriptin therapy. Carefully controlled heparin therapy in a pregnant woman with deep venous thrombosis both safe and beneficial for mother and fetus.
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PMID:Management of deep venous thrombosis and pulmonary embolism during pregnancy. 709 23

Despite significantly prolonged prothrombin time endogenously caused by factor VII deficiency, a 65-year-old woman suffered a fatal pulmonary embolism. This seemingly paradoxic phenomenon prompted our review of 14 other patients with various coagulation factor deficiencies who also had thromboembolic events. It is postulated that certain factor deficiencies may protect against venous and/or arterial thrombosis. A large-scale prospective study of this population may help define the relative importance of the various coagulation factors, platelets, and the vessel wall in thrombosis and atherogenesis and allow a rational evaluation of anticoagulant therapy.
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PMID:Thromboembolism in patients with hereditary deficiency of coagulation factors. 738 62

The activation of the clotting cascade leading to deep venous thrombosis begins during total hip arthroplasty, but few studies have assessed changes in coagulation during surgery. A better understanding of thrombogenesis during total hip arthroplasty may provide a more rational basis for treatment. In 3 separate studies, the following observations were made. Circulating indices of thrombosis and fibrinolysis: prothrombin F1.2, thrombin-antithrombin complexes, fibrinopeptide A, and D-dimer, did not increase during osteotomy of the neck of the femur or during insertion of the acetabular component, but rose significantly during insertion of the femoral component. Thrombin-antithrombin complexes, fibrinopeptide A, and D-dimer were higher after insertion of a cemented component than insertion of a noncemented femoral component. A significant decline in central venous oxygen tension was observed after relocation of the hip joint and after insertions of cemented and noncemented femoral components, providing evidence of femoral venous occlusion during insertion of the femoral component. In patients receiving a cemented femoral component, mean pulmonary artery pressure increased after relocation of the hip joint, indicating intraoperative pulmonary embolism. No changes in mean pulmonary artery pressure were noted with noncemented total hip arthroplasty. Administration of 1000 units of unfractionated heparin before insertion of a cemented femoral component blunted the rise of fibrinopeptide A. The results of these studies suggest that (1) the greatest risk of activation of the clotting cascade during total hip arthroplasty occurs during insertion of the femoral component; (2) femoral venous occlusion and use of cemented components are factors in thrombogenesis during total hip arthroplasty; and (3) measures to prevent deep venous thrombosis during total hip arthroplasty (such as intraoperative anticoagulation) should begin during surgery rather than during the postoperative period and be applied during insertion of the femoral component.
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PMID:The John Charnley Award. Thrombogenesis during total hip arthroplasty. 755 26


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