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

Spiral computed tomography is a new noninvasive diagnostic test for pulmonary embolism. The method provides tomographic images of the thorax in the axial plane, which depict the thoracic wall, the mediastinum, the lungs, and the pulmonary vessels. Thrombotic emboli in the vessels are seen as intraluminal filling defects in the contrast-enhanced pulmonary arteries. The physical principles of spiral computed tomography and several technical considerations concerning image quality will be briefly discussed. The accuracy of spiral computed tomography in the detection of pulmonary embolism is discussed by way of an overview of published validation and clinical outcome studies encompassing spiral computed tomography and the diagnosis of pulmonary embolism.
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PMID:Contrast-enhanced spiral computed tomography of the pulmonary arteries: an overview. 1128 46

Most deep vein thromboses (DVTs) start in the calf, and most probably resolve spontaneously. Thrombi that remain confined to the calf rarely cause leg symptoms or symptomatic pulmonary embolism (PE). The probability that calf DVT will extend to involve the proximal veins and subsequently cause PE increases with the severity of the initiating prothrombotic stimulus. Although acute venous thromboembolism (VTE) usually presents with either leg or pulmonary symptoms, most patients have thrombosis at both sites at the time of diagnosis. Proximal DVTs resolve slowly during treatment with anticoagulants, and thrombi remain detectable in half of the patients after a year. Resolution of DVT is less likely in patients with a large initial thrombus or cancer. About 10% of patients with symptomatic DVTs develop severe post-thrombotic syndrome within 5 years, and recurrent ipsilateral DVT increases this risk. About 10% of PEs are rapidly fatal, and an additional 5% cause death later, despite diagnosis and treatment. About 50% of diagnosed PEs are associated with right ventricular dysfunction, which is associated with a approximately 5-fold greater in-hospital mortality. There is approximately 50% resolution of PE after 1 month of treatment, and perfusion eventually returns to normal in two thirds of patients. About 5% of treated patients with PE develop pulmonary hypertension as a result of poor resolution. After a course of treatment, the risk of recurrent thrombosis is higher (ie, approximately 10% per patient-year) in patients without reversible risk factors, in those with cancer, and in those with prothrombotic biochemical abnormalities such as antiphospholipid antibodies and homozygous factor V Leiden.
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PMID:Natural history of venous thromboembolism. 1473 12

As blood clots it goes through predictable stages that reflect the oxygenation state of hemoglobin within the red cells. One of these stages results in the formation of methemoglobin. This substance acts an endogenous contrast agent when imaged using a T1-weighted magnetic resonance sequence (Magnetic Resonance Direct Thrombus Imaging, MRDTI) - appearing as high signal. MRDTI can therefore be used to detect subacute thrombosis. This technique has been applied in a number of clinical settings arising as a result of thrombosis. Deep vein thrombosis and pulmonary embolism are both readily detected using MRDTI, providing a single imaging modality for the detection of venous thromboembolic disease. The technique is also effective in the peripheral arterial tree. Furthermore, thrombosis within vessel wall atherosclerosis is a marker of vulnerable plaque likely to produce symptoms. The MRDTI technique has thus proved useful in identifying complicated plaque in the carotid arteries in the setting of transient and permanent cerebral ischemia. MRDTI therefore holds promise as a technique that is capable of detecting high risk vessel wall disease prior to significant or permanent end organ damage. Because of the non-invasive nature of magnetic resonance imaging (MRI), application of MRDTI in the research setting for the monitoring of therapeutic interventions in a wide number of settings within vascular disease is very appealing.
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PMID:Magnetic resonance direct thrombus imaging. 1287 Dec 74

Thrombosis is a major cause of mortality and morbidity in polycythemia vera (PV). The wide range of thrombotic events reflects the complex picture in PV. There are multiple factors involved in thrombogenesis in this disease, including increased hematocrit, thrombocytosis, impaired fibrinolytic activity, platelet activation, leukocyte activation, endothelial damage, interactions between platelets and endothelium, various modalities of therapy, and increased in whole-blood viscosity. Among them, the increase in blood viscosity, and hence the impairment of blood flow, is the major factor. In this article, the role of hyperviscosity in PV is reviewed. A high hematocrit occurs under PV and many other conditions with abnormal red blood cell aggregation. The impaired capillary blood flow results in neurological manifestations and increased bleeding risk in PV. Thrombotic complications can also occur in both arteries and veins and manifest as stroke, myocardial infarction, deep vein thrombosis, or pulmonary embolism. The hemodynamic principle is aptly applied in the management of PV. The most important objective is the reduction of the patient's hematocrit.
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PMID:Hyperviscosity in polycythemia vera and other red cell abnormalities. 1463 44

The role of active thrombosis in the pathophysiology of pulmonary embolism is unclear. We tested the hypothesis that venous thrombi significantly increase their thrombotic activity once they embolize into the high-flow circulation of the pulmonary arteries. Thrombotic activity was measured using an immunoassay that measures both fibrinopeptide B (FPB) as well as its most abundant metabolite des-arginine FPB. Thrombi were formed in the femoral veins of adult dogs. In one group, the thrombi were embolized without anticoagulation. In the second group, heparin (300 U/kg bolus, then 90 U x kg(-1) x h(-1) infusion) was administered before embolization to prevent subsequent thrombotic activity. Plasma FPB concentrations were significantly suppressed in the heparinized group relative to the nonheparinized group for 1 h postembolization (P = 0.038). We conclude that pulmonary embolization itself causes preexisting venous thrombi to greatly intensify their thrombotic activity and that embolization-associated thrombus propagation can be prevented by heparin.
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PMID:Embolization itself stimulates thrombus propagation in pulmonary embolism. 1504

Pulmonary embolism is a common postoperative complication in gynecological oncology patients and is often fatal. A substantial proportion of venous thrombi responsible for pulmonary emboli originate in the pelvic veins. The significance of thrombi in the veins of the broad ligament identified in surgical specimens is unknown. In a case-control study, women with postoperative pulmonary embolism (cases) were identified from the Gynecological Oncology service at the Washington Hospital Center and compared with consecutive surgical pathology accessions (controls). Only the broad ligament veins were evaluated for the presence of organizing thrombi. Eight patients, all of whom had a gynecological malignancy, were diagnosed postoperatively with pulmonary embolism. Six were diagnosed clinically by spiral CT from 4 to 115 days after surgery, and two were diagnosed by open lung biopsy of a new pulmonary lesion approximately 1 year postoperatively. None of the cases was shown to have thrombi in the broad ligament veins. Thrombi in the broad ligament veins were present in three of 30 control patients with malignancies. Among 56 controls without malignancies, 3 had broad ligament thrombi. These findings suggest that the presence of organizing thrombi in the broad ligament veins does not predict postoperative pulmonary embolism.
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PMID:Venous thrombosis in the broad ligament: is it a predictor of postoperative pulmonary embolism in gynecological cancer patients? A case-control study. 1508 47

The clinical picture of cerebral venous thrombosis (CVT) depends on the site of thrombosis in the venous system including superficial veins, deep veins and venous sinuses. Thrombotic changes may occur simultaneously in various parts of the venous system. Since CVT may have various causes, the knowledge of its etiology helps to make the diagnosis. In systemic diseases multiple intravascular clots may result, while in localized pathological conditions thrombosis maybe restricted to the lesion site. The clinical picture is often serious, leading to death, or to severe complications such as pulmonary embolism, and to distant complications--like epilepsy or intracranial hypertension being the cause of chronic headaches (lumbar puncture and CSF pressure measurement are helpful in the diagnosis of intracranial hypertension). In order to prevent complications of crucial importance is not only the proper diagnosis (with MRI and venography as the diagnostic techniques of choice), but also an early and prolonged treatment with anticoagulants. Heparin or fractionated heparin is recommended even though there is a possibility of cerebral haemorrhagic lesions.
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PMID:[Cerebral venous thrombosis--clinical aspects and consequences]. 1517 53

Deep vein thrombosis and its sequelae pulmonary embolism and post-thrombotic syndrome are some of the most common disorders. A thrombus either arises spontaneously or is caused by clinical conditions including surgery, trauma, or prolonged bed rest. In these instances, prophylaxis with low-dose anticoagulation is effective. Diagnosis of deep vein thrombosis relies on imaging techniques such as ultrasonography or venography. Only about 25% of symptomatic patients have a thrombus. Thus, clinical risk assessment and D-dimer measurement are used to rule out deep vein thrombosis. Thrombus progression and embolisation can be prevented by low-molecular-weight heparin followed by vitamin K antagonists. Use of these antagonists for 3-6 months is sufficient for many patients. Those with antithrombin deficiency, the lupus anticoagulant, homozygous or combined defects, or with previous deep vein thrombosis can benefit from indefinite anticoagulation. In cancer patients, low-molecular-weight heparin is more effective than and is at least as safe as vitamin K antagonists. Women seem to have a lower thrombosis risk than men, but pregnancy or use of oral contraceptives or hormone replacement therapy represent important risk factors.
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PMID:Deep vein thrombosis. 1600 25

Thrombotic occlusive diseases are manifested in several disorders that have significant morbidity and mortality, including acute myocardial infarction, pulmonary embolism, deep venous thrombosis, and cerebrovascular accidents. This review summarizes the recently published literature covering thrombolytic therapies in these diseases, with particular attention to comparisons between the fibrin-specific tissue plasminogen activators (alteplase, reteplase, and tenecteplase) and the nonfibrin-specific activators (streptokinase or urokinase plasminogen activator). These agents act to convert plasminogen to plasmin, which in turn cleaves fibrin as part of the lysis process. Fibrin-specific activators were anticipated to be more efficacious and safer than nonspecific agents in thrombolytic occlusive diseases because of their pathophysiologically restricted mechanism of action. However, the fibrin-specific activators also lyse physiological hemostatic plugs, which can result in costly adverse events. Efficacy of fibrin-specific tissue plasminogen activators has been shown to be generally equivalent, with similar mortality rates compared with nonspecific agents; however, fibrin-specific agents may be associated with an increased incidence of intracerebral hemorrhage and with increased costs. Therefore, it appears that given equivalent efficacy, nonfibrin-specific activators, such as streptokinase or urokinase, may be a safer choice in many thrombotic situations.
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PMID:Thrombolytic therapies: the current state of affairs. 1582 70

Thrombotic events are an increasingly recognized complication of treatment with intravenous immunoglobulins (IVIg). We aimed to define clinical characteristics, risk factors and outcome for venous thrombosis as opposed to arterial thrombosis following administration of IVIg. Six patients with post-IVIg venous thrombosis were identified at our institution. In addition, a review of the literature revealed 65 reported cases. Arterial thrombosis (stroke and myocardial infarction) was four times more common than venous thrombosis (deep vein thrombosis and pulmonary embolism). The incidence rate was estimated at 0.15-1.2% per treatment course, but the large increase in reported cases in 2003 suggests that the true incidence may be significantly greater. The following differences were found between arterial and venous events: arterial thrombosis occurred early after IVIg administration (49% within 4 h, 77% within 24 h) and was associated with advanced age and atherosclerotic vascular disease; venous thrombosis occurred later (54% more than 24 h after IVIg administration) and was associated with factors contributing to venous stasis (obesity and immobility). Thirteen patients died (mortality 20%), 11 of whom had arterial thrombosis. In conclusion, IVIg-associated thrombosis is more common than previously recognized, and is associated with significant mortality. The different characteristics of arterial and venous events may reflect different pathophysiological mechanisms. A better understanding of these mechanisms should aid in defining a risk-benefit ratio for the individual patient.
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PMID:Venous and arterial thrombosis following administration of intravenous immunoglobulins. 1660 87


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