Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PULMONARY EMBOLISM AND THROMBOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,315 records · Page 73Linked to original sources
PubMed1994

Surgical prophylaxis for pulmonary embolism.

The trauma patient population is at special risk for fatal pulmonary embolism. We experienced 11 fatalities in one 12-month period. Specific risk factors for both deep venous thrombosis and pulmonary embolism can be identified among trauma patients. The latter usually cannot be offered prophylactic anticoagulation, and the nature of their injuries (e.g., long bone fractures) makes not only bedside surveillance difficult but also precludes use of pneumatic compression, etc. We have developed a protocol for prophylactic inferior vena caval filtration for our trauma patients deemed at particular risk for pulmonary embolism. Since 1986 we have inserted 205 Greenfield filters in 201 patients. Two hundred were inserted prophylactically. There was no mortality, and morbidity was minimal. No patient with a Greenfield filter sustained a fatal pulmonary embolism during this period. Four patients died from pulmonary embolism before vena caval filters could be inserted. We believe that the trauma patient, at risk for pulmonary embolism, should be offered a Greenfield filter prophylactically as soon after hospitalization as logistically possible.

Adult↗
PubMed2005

No association between pulmonary embolism or deep vein thrombosis and the -455G/A beta-fibrinogen gene polymorphism.

Hyperfibrinogenaemia has been reported to be associated with deep vein thrombosis (DVT). However, whether or not the "fibrinogen-raising"-455G/A polymorphism of the beta-fibrinogen gene is associated with DVT is uncertain and there are no data on whether this polymorphism is associated with pulmonary embolism (PE). We have studied relationships between the -455G/A beta-fibrinogen gene polymorphism and the occurrence of PE and/or DVT (n = 339) (PE only, n = 76; DVT only, n = 216; PE and DVT, n = 47). There was no difference between the -455A allelic frequencies for the control (n = 190) and patient groups - PE, 0.187 and 0.171, respectively [P = 0.6087, chi test; odds ratio (OR), 1.12; 95% confidence interval (CI), 0.72-1.74]; DVT, 0.187 and 0.171, respectively (P = 0.5408, chi test; OR, 1.11; 95% CI, 0.78-1.59). This also applied when only Caucasian individuals were considered - PE allelic frequencies, 0.192 and 0.193, respectively (P = 0.9764, chi test; OR, 0.99; 95% CI, 0.62-1.60); DVT allelic frequencies, 0.192 and 0.186, respectively (P = 0.8404, chi test; OR, 1.04; 95% CI, 0.71-1.51). While the results should be interpreted with caution as the frequency of the -455A allele is rare, the -455A allele of the beta-fibrinogen gene does not appear to be associated with an increased risk of PE or DVT.

Adolescent↗
PubMed2002

New aspects of the blood coagulation cascade, anticoagulants and vein thrombosis in Asia.

PURPOSE: This review describes recent views on blood coagulation and abnormalities of its physiological control that predispose to thrombosis, suggests that venous thrombosis and pulmonary embolism are more prevalent in Asia than was previously thought, and examines recent trials of novel anticoagulants for thrombosis prevention. SOURCES: 'Medline' was used to search for publications in English or with English language abstracts. CONTENT AND CONCLUSIONS: The study of blood coagulation is basic to understanding clotting and bleeding disorders, their prevention and treatment. Tissue factor, factor Xa, and thrombin are pivotal; together with physiological controls (positive and negative feedback loops, and natural anticoagulants) that first enhance thrombin generation but then preserve vessel patency by limiting haemostatic plug formation to areas of injury. Abnormalities in these mechanisms can increase thrombosis risk (thrombophilia). The traditional impression that venous thromboembolism is rare in Asia has been reinforced by the rarity of thrombophilic genetic polymorphisms outside of European populations. Nevertheless, there is increasing evidence for an increasing prevalence of symptomatic vein thrombosis and pulmonary embolism in Asia, and that thrombosis rates in 'high risk' clinical settings among elderly patients (as after major joint surgery or a stroke) now approach levels reported from the West. This indicates the need for greater clinical awareness of these conditions. Drugs now used routinely for thrombosis prevention in the West (especially low molecular weight heparins) are effective and relatively safe. New anticoagulants were even more effective in recent trials. There is urgent need for studies in Asia that define the locally relevant benefits and hazards of the increasing range of agents now available.

Adult↗
PubMed1975

Pulmonary embolism after amputation of the lower extremity.

Patients requiring amputation of the lower extremity for arteriosclerosis are at high risk for the development of venous thrombosis and pulmonary embolism. Inapparent venous thrombosis was discovered in the amputated leg at operation in eight patients. Pulmonary embolism was documented by angiogram or at autopsy in ten patients. The majority of emboli discovered in this study was not suspected by the physician responsible for the care of the patient. The perfusion lung scan in this elderly group of patients had a false-positive rate of 60 per cent, while a normal lung scan was strong evidence against pulmonary embolsim. Although imperfectly randomized, the prophylactic use of low molecular weight dextran in this study did not decrease the incidence of pulmonary embolism. The pulmonary arteriogram proved a safe procedure in the elderly and should be used before therapy is initiated for suspected pulmonary embolism.

Adult↗
PubMedDate not supplied

[rt-PA in extracardiac thromboembolic vascular occlusions].

Recombinant tissue plasminogen activator (rt-PA) is a thrombolytic agent characterized by elevated but not absolute fibrin specificity. However, its therapeutic dose is high and associated with a variable degree of systemic activation of the fibrinolytic system. Thrombolytic drugs are widely used in acute myocardial infarction and have now begun to be considered for deep vein thrombosis (DVT), pulmonary embolism (PE), and peripheral artery thrombosis (PAT) as well. Although anticoagulant therapy is effective in reducing the immediate complications of venous thromboembolism, thrombolytic therapy has various advantages over anticoagulant therapy, including lysis of thrombi with recanalization of venous circulation, reduction of venous valve damage and prevention of post-phlebitic syndrome. The different dosage regimens of rt-PA recently evaluated (0.71 to 1.76 mg/kg/24 h for 2-4 days) in DVT have caused consistent thrombolysis but also excessive bleeding. The optimal therapeutic range for rt-PA in DVT remains to be determined. Thrombolytic therapy is superior to heparin treatment only in hemodynamically compromised patients with massive PE. The minor systemic fibrinolytic effect and the faster action on thrombi of rt-PA compared with the first generation thrombolytic agents, streptokinase (SK) and urokinase (UK), are very interesting and explain the positive results recently obtained in PE with this drug (50 mg over 2 h, followed, if necessary, by 40-50 mg over 4-5 h) by Goldhaber and Verstraete.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed2004

Embolization itself stimulates thrombus propagation in pulmonary embolism.

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.

Ancrod↗
PubMed2005

Molecular diversity and thrombotic risk in protein S deficiency: the PROSIT study.

The Protein S Italian Team (PROSIT) enrolled 79 protein S (PS) deficient families and found 38 PROS1 variations (19 novel) in 53 probands. Of these, 23 variants were selected for expression in'vitro, to evaluate their role as possible causative variants. Transient expression showed high secretion levels (>75%) for three variants, which were considered neutral. Seven missense and five nonsense variants showed low (<or=11%) expression levels and were classified as severe defects. Intermediate expression was observed for eight variants, which were evaluated by factor Va inactivation assay in order to be globally classified as severe or intermediate. Based on the cumulative data, the hazard ratio associated with causative variants was 4.9 (95% CI: 1.4-17.7) for deep vein thrombosis and/or pulmonary embolism, 5.1 (95% CI: 1.1-23.9) for superficial thrombophlebitis, and 4.8 (95% CI: 1.8-13.0) for any venous thrombosis. The hazard ratio for deep vein thrombosis and/or pulmonary embolism in carriers of severe defects only was 7.4 (95% CI: 1.6-24.1). PROSIT showed that dysfunctional variants causing PS deficiency are more common than expected and confirmed that PS deficiency is associated with increased thrombotic risk, although risk assessment is complicated by molecular heterogeneity.

Codon, Nonsense↗
PubMed2006

Hereditary thrombophilia in ethnic Omani patients.

Hereditary thrombophilias are a group of inherited conditions that predispose to thrombosis. Mutations like factor V Leiden, prothrombin gene variant 20210A, and hereditary hyperhomocysteinemia are associated with an increased risk for thromboembolism as compared to mutations in natural inhibitors of coagulation. There is also evidence that multiple defects co-exists in persons with a tendency for thrombosis. We studied prothrombotic determinants, namely protein C, protein S, and AT along with factor V Leiden (1691G-->A), prothrombin gene mutation (20210G-->A), CBS 844ins68 mutation, and MTHFR mutation (677C-->T) in consecutive ethnic Omani patients with first episode of a thrombophilic event, namely, deep vein thrombosis (DVT), and/or pulmonary embolism (PE) or thrombosis at an unusual site. Fasting plasma homocysteine was also analyzed. Factor V Leiden and the prothrombin gene mutation were not seen in any patient nor in any control subject studied. The thermolabile MTHFR mutation (677C-->T) was present in 14 patients (35.89%) whereas the CBS 844ins68 mutation was documented in 6 patients (15.38%); 3 patients were common in both groups. Six patients had low protein C (15.38%), two patients had low protein S (5.12%), but none had low AT levels. Interestingly, one patient had triple abnormality, namely, PC deficiency with both CBS 844ins68 mutation as well as the MTHFR mutation (677C-->T) whereas another two patients had the latter two mutations together. This data set, although small, reflects the importance of multiple screening strategies. The yield appears high, emphasizing the referral pattern to a tertiary health center. Of these patients, 43.58% had either or both the hyperhomocysteinemic mutations studied, whereas in 38.46% of these patients, no underlying cause for thrombophilia could be documented.

Adolescent↗
PubMed1993

Pulmonary thromboendarterectomy for pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension is a term that has been proposed by Dr. Kenneth Moser to describe a progressively debilitating process that occasionally follows venous thrombosis and pulmonary embolism. In the past, the disease was dramatically underdiagnosed for several reasons: 1) the initial event--deep vein thrombosis or pulmonary embolism--is usually clinically silent; 2) there is a subsequent asymptomatic "honeymoon period" in most patients; 3) there is no clinical description of chronic thromboembolic pulmonary hypertension in most textbooks of medicine and surgery; and 4) until recently, surgical therapy could be performed by only a few surgeons, and with a prohibitive operative mortality. Intensive efforts by physicians at the University of California, San Diego have led to increased recognition of the disease, a better understanding of its pathophysiology, and development of a curative procedure with an acceptable operative mortality. Chronic thromboembolic pulmonary hypertension is truly the "aortic stenosis" of the pulmonary circulation, and the clinical improvement after pulmonary thromboendarterectomy is even more dramatic than that seen after aortic valve replacement.

Endarterectomy↗
PubMed1998

Diagnostic management of venous thromboembolism.

The accuracy of diagnostic methods for the diagnosis of deep vein thrombosis and pulmonary embolism in symptomatic patients is critically reviewed. In addition, the safety of withholding anticoagulant therapy from patients with suspected deep vein thrombosis or pulmonary embolism in whom the qualified diagnostic strategy was normal is evaluated by determining the frequency of venous thromboembolic complications during 3 months of follow-up. It is shown that the currently used available diagnostic techniques for deep vein thrombosis are all able to identify the majority of patients who indeed have venous thrombosis. However, as result of its accuracy and practical advantages, compression ultrasound is the test of choice in the evaluation of symptomatic patients. Patients with a normal test outcome should be re-tested to detect the small proportion of patients with proximally extending calf vein thrombosis. In the strategy of repeated diagnostic testing, impedance plethysmography could be used as an alternative to ultrasonography. To obtain a reduction in repeat tests various diagnostic strategies have been evaluated and it was shown that these strategies, using non-invasive tests, can be as accurate and safe as the invasive reference strategy. The safeties of the various strategies were very similar; however, important differences were observed with respect to the practical implementation of the various diagnostic strategies. Simplification of the repeated testing strategy by using a D-dimer assay and/or a clinical decision rule seems to be promising. The reference standard for the diagnosis of pulmonary embolism remains pulmonary angiography. Several strategies based on non-invasive diagnostic methods have been evaluated for their safety and complexability. Perfusion-ventilation lung scanning is the most thoroughly evaluated non-invasive technique so far. It seems safe to withhold anticoagulant therapy in patients suspected of pulmonary embolism with a normal perfusion lung scan result; however, further testing is needed in the case of a non-diagnostic perfusion-ventilation lung scan result. At this moment angiography is the method of choice in this category of patients. D-dimer assays, clinical decision rules and ultrasound examinations of the legs seem to have a high potential to limit the need for angiography. Also, spiral computerized tomography and magnetic resonance imaging are promising techniques, but their role in the diagnostic management of pulmonary embolism is still uncertain.

Diagnostic Techniques and Procedures↗
PubMed2000

A population-based study of the effectiveness of inferior vena cava filter use among patients with venous thromboembolism.

BACKGROUND: There are few population-based data regarding the effectiveness of inferior vena cava filter use in the prevention of symptomatic pulmonary embolism. OBJECTIVE: To determine the 1-year cumulative incidence of rehospitalization for venous thrombosis or pulmonary embolism among patients with thromboembolism treated with a vena cava filter compared with the incidence in a control population with thromboembolism. PATIENTS AND METHODS: Population-based retrospective analysis of linked hospital discharge abstracts in California. From January 1, 1991, through December 30, 1995, 3632 patients were treated with a filter and 64,333 controls were admitted with a principal diagnosis of venous thromboembolism. RESULTS: Filter-treated patients had significantly greater comorbidity, with a higher frequency of previous pulmonary embolism, recent major bleeding, malignant neoplasm, and stroke. Patients who initially manifested pulmonary embolism were significantly more likely to be rehospitalized for pulmonary embolism than patients with an initial diagnosis of venous thrombosis alone, among filter-treated patients (relative risk, 6.72; 95% confidence interval, 3.61-12.49) and controls (relative risk, 5.30; 95% confidence interval, 4.61-6.10). Risk-adjusted proportional hazards modeling showed no significant difference between filter-treated patients and controls in the relative hazard of rehospitalization for pulmonary embolism. However, filter placement was associated with a significantly higher relative hazard of rehospitalization for venous thrombosis among patients who initially manifested pulmonary embolism (relative hazard, 2.62; 95% confidence interval, 2.09-3.29), but not among those who presented with venous thrombosis (relative hazard, 1.14; 95% confidence interval, 0.92-1.43). CONCLUSIONS: Insertion of a vena cava filter was not associated with a significant reduction in the 1-year incidence of rehospitalization for pulmonary embolism. Use of a filter was associated with a higher incidence of rehospitalization for venous thrombosis, but only among patients who initially manifested pulmonary embolism. A prospective clinical study is needed to determine the efficacy of filter use among patients with pulmonary embolism who do not meet strict guidelines for insertion of a vena cava filter.

Adult↗
PubMed1990

Aspirin prophylaxis and surveillance of pulmonary embolism and deep vein thrombosis in total hip arthroplasty.

This is a prospective study of aspirin prophylaxis and thromboembolism surveillance in 159 patients having total hip arthroplasty by one surgeon at one institution. All patients had preoperative venous Doppler examination of the lower extremities and a ventilation-perfusion lung scan. Aspirin (650 mg) was given the night prior to surgery and continued at that dose twice per day. Venous Doppler examination was performed 10-14 days after operation. Asymptomatic pulmonary embolism was treated with oral anticoagulation only. There was a 12.6% incidence of pulmonary embolism, but only 1.9% of all patients developed a symptomatic pulmonary embolus. No patient had a fatal pulmonary embolus. No patient had a clinically evident deep vein thrombosis, and venous Doppler examination detected only nine patients with deep vein thrombosis (5.7%). The venous Doppler examination could not predict which patients would develop a pulmonary embolism. The authors could not determine a group of patients at high risk for the development of pulmonary embolism. There was no correlation between well-established "risk factors" and the development of pulmonary embolism. There was no correlation between the use of cemented or uncemented components and the development of pulmonary embolism. There were few complications of this prophylactic regimen of aspirin and surveillance. The authors believe this may be an acceptable prophylactic regimen for patients having total hip arthroplasty. However, the value of venous Doppler examination in the detection of deep vein thrombosis following total hip arthroplasty is uncertain.

Aspirin↗