Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin is indicated in pulmonary embolism suspicion, in minor and a part of submassive embolism. The dose is 15,000-20,000 U (acute) and 40,000 U/day subsequently. Fibrinolytic therapy with streptokinase or urokinase is indicated in massive embolism. Submassive embolism is treated by fibrinolysis if no contraindications against fibrinolysis are to be registered.
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PMID:[Drug therapy of pulmonary embolism]. 380 72

Hereditary protein C deficiency, which is inherited as an autosomal-dominant trait, predisposes to venous thrombotic disease. Heterozygotes are at risk for superficial thrombophlebitis, deep venous thrombosis and/or pulmonary embolism, which may occur without apparent cause at a young age. Other manifestations are cerebral venous thrombosis and mesenteric vein thrombosis. In severe, often homozygous, protein C deficiency, a purpura fulminans syndrome may occur shortly after birth, resulting in death due to extensive thrombosis, if it is not adequately treated. The thrombotic manifestations in heterozygotes are effectively prevented by coumarin therapy. However, in the initial phase of oral anticoagulant therapy, the patients have an increased risk for the development of coumarin-induced haemorrhagic skin necrosis. The purpura fulminans syndrome can be treated with either replacement therapy or with coumarin therapy. Heparin appears to be ineffective in the prevention of both the purpura fulminans syndrome and the coumarin-induced skin necrosis.
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PMID:Hereditary protein C deficiency. 384 Jan 12

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

It has been suggested that early heparin requirements are greater in patients with acute deep venous thrombosis (DVT) and pulmonary embolism (PE). Heparin requirements were recorded for 73 patients with suspected DVT and PE. The maintenance dosage (days 1 through 4) of heparin sodium required to achieve therapeutic partial thromboplastin times (PTTs) was significantly higher in patients with DVT (n = 54; mean +/- SD dosage, 1,151 +/- 246 units/hr) compared with patients with no DVT (n = 19; mean +/- SD dosage, 952 +/- 190 units/hr). The first posttreatment PTT was significantly lower in patients with DVT (mean +/- SD PTT, 68.74 +/- 27.96 s) compared with control patients (mean +/- SD PTT, 89.41 +/- 23.25 s). This study supports the clinical impression that initial heparin requirements are greater and heparin clearance is more rapid in patients with acute DVT and PE.
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PMID:Prediction of heparin requirements in acute thromboplastic venous disease. 398 88

Since thrombin cleaves fibrinopeptides A (FPA) and B from the NH(2)-terminal end of the fibrinogen molecule, measurement of fibrinopeptide levels in plasma may provide a direct index of thrombin action. Recently a radioimmunoassay for FPA has been developed, and in the present paper, we describe the application of this assay to the measurement of FPA levels in clinical blood samples. Since fibrinogen cross-reacts with antibodies to FPA, dialysis was used to extract the peptide from plasma. In vitro generation of FPA was prevented by removing the fibrinogen from the plasma by precipitation with ethanol before dialysis. The processing technique permitted recovery of 75% of FPA added to blood in vitro. Evidence that the immunoreactivity measured in plasma is due to FPA was provided by the results of experiments in which two antisera to FPA with different specificities showed comparable results and addition of thrombin caused no change in immunoreactivity. In contrast, extracts of streptokinasetreated plasma showed a five-fold increase in activity when treated with thrombin and markedly different immunoreactivity with the two antisera. Plasma FPA levels in 30 normal men were below 2 ng/ml, with a mean of 0.5 ng/ml. FPA levels in 12 patients with reduced fibrinogen levels or reduced platelet counts or both ranged between 4 and 289 ng/ml. FPA levels in 13 patients with normal or elevated fibrinogen levels, including 6 patients with clinical evidence of venous thrombosis or pulmonary embolism or both, ranged between 5 and 23 ng/ml. FPA and fibrinogen degradation product levels did not correlate, and in several patients, elevated FPA levels were found in the presence of normal fibrinogen degradation product levels. After infusion of FPA-containing solutions in four normal individuals, FPA showed a disappearance rate from the plasma consistent with a t((1/2)) of 3-5 min. Heparin infusions in six patients with venous thrombosis or pulmonary embolism or both and elevated FPA levels were followed by a prompt decline in FPA level at a mean rate equivalent to a 3-5 min t((1/2)).
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PMID:Measurement of fibrinopeptide A in human blood. 460 45

Heparin (1 IU kg-1 h-1) given intravenously for 3-5 days during and after operation in a double-blind randomised study, significantly reduced the frequency of deep-vein thrombosis detected by 125I-fibrinogen uptake, and pulmonary embolism. 22% (11/50) control patients and 4% (2/45) patients receiving heparin had deep-vein thrombosis or pulmonary embolism. Heparin administration was not associated with any increase in preoperative or postoperative bleeding.
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PMID:Ultra-low dose intravenous heparin in the prevention of postoperative deep-vein thrombosis. 610 55

The efficacy of intravenous infusion of dextran 70 or subcutaneous administration of low-dose heparin in preventing postoperative thromboembolic complications has been investigated in a prospective randomized trial. During part 1 of the study, 232 patients over the age of 40 years who were undergoing major gynecologic surgery underwent a complete test protocol. The 125I fibrinogen uptake test (FUT) was used for the diagnosis of deep vein thrombosis (DVT) in 117 patients in the dextran and 115 patients in the heparin group. Heparin was significantly more effective than dextran for reducing DVT (P less than .001). During part 2 of the study no FUT was done but the incidence of clinical and fatal pulmonary embolism (PE) and the number of complications were studied. Of 444 patients (parts 1 and 2) 1 fatal and 2 nonfatal pulmonary emboli were diagnosed. All the emboli occurred in the dextran group. The benefit: hazard ratio appeared to favor heparin for the prophylaxis of DVT.
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PMID:Prevention of postoperative thromboembolism by dextran 70 or low-dose heparin. 615 72

In a prospective study, 280 patients with phlebographically proven deep venous thrombosis received intravenous heparin infusion; 224 of the patients were subjected to control phlebography after 5-8 days of treatment. Females above 70 years showed least phlebographic improvement despite similar heparin dosage and heparin activity. Heparin activity in daily drawn blood samples was determined by four different assays. Chromogenic substrate (CS) assay (Coatest heparin), activated partial thromboplastin time (Cephotest), and thrombin time with recalcified plasma (CaTT) showed weak but significant correlations with thrombus resolution judged by phlebography (p = 0.004, 0.003 and 0.018, respectively). A linear prediction equation showed that the phlebographic result was about equally influenced by the mean dose and by the result of any of the three heparin assays. Thrombin time with citrated plasma showed no correlation. CS assay and CaTT showed significantly lower mean heparin activity in patients with (n = 13) than without clinically diagnosed pulmonary embolism (p = 0.012 and 0.001, respectively).
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PMID:The antithrombotic effect of heparin in deep venous thrombosis: relation to four heparin assays. 649 86

Pulmonary embolism was suspected in 45 neurosurgical patients who were treated between January, 1980, and December, 1981. Hypoxemia with respiratory alkalosis and sudden tachycardia gave rise to this suspicion more often than any other sign or symptom. Perfusion lung scanning confirmed the presence of pulmonary embolism in 23 of these cases. A retrospective analysis of the clinical course of these 23 patients suggested that one or more previous episodes of pulmonary embolism had occurred in 16 cases (69.6%), and had been either overlooked or misdiagnosed. Treatment was started immediately after diagnosis. Twenty-one patients were given heparin; however, two could not be treated because of contraindication to using anticoagulant drugs. Two patients died during treatment. The 21 surviving patients were assessed and 11 of them submitted again to perfusion lung scanning 1 week after diagnosis: 14 had improved, but seven did not show significant changes either clinically or on perfusion lung scanning. Nine treated patients developed hemorrhage, but it was readily controlled. In two of the nine patients, hemorrhage involved the surgical area. It is stressed that pulmonary embolism may be suspected and diagnosed in neurosurgical patients at an early stage. Heparin may be given and the survival rate appears to be better than previously reported figures.
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PMID:Pulmonary embolism in neurosurgical patients: diagnosis and treatment. 671 66

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12


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