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

Pulmonary embolus (PE) is not an uncommon cause of sudden death, and forensic pathologists are not unaccustomed to being the first to diagnose a PE in a patient, since they are often fatal. Forensic pathologists are also familiar with the known risk factors for development of PEs, including advanced age, use of oral contraceptives, smoking, obesity, a sedimentary lifestyle, postsurgery or postinjury, pregnancy, certain malignancies, factor V Leiden and prothrombin mutations, and anticardiolipin antibodies. It has recently been shown in the clinical literature that antipsychotic medications are associated with an increased risk of thromboembolic events. Clozapine, a close relative of olanzapine, has been implicated as an independent risk factor for developing a PE. Four cases have been published within the last 2 years questioning whether olanzapine may also be associated with an increased risk for PE. We report 6 cases from the Bexar County Medical Examiner's Office, occurring between 1998 and 2005 where olanzapine may have been a risk factor in the development of, and death from, PE.
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PMID:Olanzapine: a new risk factor for pulmonary embolus? 2151 77

Genetic mutations of the coagulation factors II and V (G20210A and G1691A - factor V Leiden)--as well as the one for methylene tetrahydrofolat reductase's (MTHFT) gene C677T are diseases with dominant autosomal transmission characterized by thromboembolic events leading to deep vein thrombosis and/or pulmonary embolism. The authors show the clinical observation of 2 cases of recurrent deep venous thrombosis evolving with pulmonary embolism in patients with genetic defects of the coagulating factors. The positive diagnostic was put on the paraclinical findings and the etiology was established from the homocysteine genetic modification of the G20210A prothrombin and factor V Leiden and MTHFT mutation. Publishing these cases will allow us to emphasize the importance of the genetic factors for thromboembolic episodes and especially for the consequences of the long-term anticoagulant therapy.
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PMID:Recurrent thrombembolic risk in patients with multiple thrombophilic disorders. 1936 87

Venous thrombosis (deep vein thrombosis, pulmonary embolism) is a common and serious disorder, with genetic and acquired risk factors. The genetic risk factors can be subdivided in to those that are strong, moderate and weak. Strong risk factors are deficiencies of antithrombin, protein C and protein S. Moderately strong are factor V Leiden, prothrombin 20210A, non-O blood group and fibrinogen 10034T. There are many weak genetic risk factors, including fibrinogen, factor XIII and factor XI variants. Even for moderately strong risk factors (relative risks 2-5), the majority of carriers will never develop thrombosis.
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PMID:Genetics of venous thrombosis. 1963 Aug 21

Bleeding and thrombosis are serious complications of living donor liver transplantation (LDLT). The aim of this paper was to describe the results of a screening for coagulation disorders, including for thrombophilic factors, in potential living liver graft donors and to evaluate thrombotic and bleeding events in donors and recipients, during and after the procedure. From January 2001 to January 2007, 41 LDLTs were performed at our institution. We performed systematic screening for bleeding or prothrombotic states among 188 potential donors, 38 (20.2%) of whom showed at least one abnormality. We rejected potential donors with factor V Leiden, prothrombin mutation G20210A, and deficiencies in anticoagulant proteins (protein C, protein S, and antithrombin) or coagulation factors. Bleeding and thrombotic events in donors and recipients of the 41 LDLTs were evaluated during 7 days to 70 months follow-up. No major bleeding events were detected in the donors. Neither donor nor recipient experienced venous thrombosis or pulmonary embolism. Among all recipients, six suffered hepatic artery thrombosis including five in the first month probably related to surgery. Deep venous thrombosis and pulmonary embolism are well-known complications of hepatic surgery; Prothrombotic abnormalities in the donor can be transmitted to the recipient, leading to increased risk of serious postoperative events. Although the cost-effectiveness is not definitely established, we recommend systematic screening for hemostatic and prothrombotic disorders to prevent more morbidity of a procedure that already has high risks of bleeding and thrombosis.
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PMID:Living donor liver transplantation: usefulness of hemostatic and prothrombotic screening in potential donors. 1991 89

The term factor V Leiden (FVL) paradox is used to describe the different risk of deep vein thrombosis and pulmonary embolism that has been found in carriers of FVL. In a thrombophilic family-cohort, we estimated differences in absolute risks of deep vein thrombosis and pulmonary embolism for various thrombophilic defects. Of 2,054 relatives, 1,131 were female, 41 had pulmonary embolism and 126 deep vein thrombosis. Annual incidence for deep vein thrombosis in non-carriers of FVL was 0.19% (95%CI, 0.16-0.23), and 0.41% (95%CI, 0.28-0.58) in carriers; relative risk (RR) 2.1 (95%CI, 1.4-3.2). For pulmonary embolism these incidences were similar in carriers and non-carriers 0.07%, respectively; RR 1.0 (95% CI, 0.4-2.5). When co-inheritance of other thrombophilic defects was excluded the RR for deep vein thrombosis in FVL carriers was 7.0 (95%CI, 2.3-21.7) compared to non-carriers and 2.8 (95%CI, 0.5-14.4) for pulmonary embolism. For other thrombophilic defects no such effect was observed. Thus the FVL paradox was confirmed in our study. However, a similar paradox in carriers of other thrombophilic defects was not observed.
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PMID:Different risk of deep vein thrombosis and pulmonary embolism in carriers with factor V Leiden compared with non-carriers, but not in other thrombophilic defects. Results from a large retrospective family cohort study. 2000 42

The aim of this paper is to present the latest developments in therapy and prophylaxis of deep vein thrombosis and other pregnancy complications in women with inherited or acquired thrombophilia and in women with mechanical heart valves. The data presented in the paper have been extracted from the Current Contents database. It is well known that the hypercoagulable state in pregnant women, caused either by the physiological changes of pregnancy or by inherited thrombophilia, increases the risk of venous thromboembolism (VTE), pulmonary embolism (PE), preeclampsia, recurrent early and late fetal loss, intrauterine growth retardation (IUGR), placental abruption, and other less probable complications of pregnancy and its outcome. In women with mechanical heart valves, the risk of systemic embolism is also seen to increase during pregnancy. According to data analyzed, positive antiphospholipid antibodies (APLA) as well as anticardiolipin antibody and lupus anticoagulant (nonspecific inhibitor) positivity, homozygosity and heterozygosity for factor V Leiden mutation and heterozygosity for the prothrombin G20210A variant, MTHFR C677T variant homozygosity and hyperhomocysteinemia are in strong association with pregnancy complications and severe pregnancy outcome. The strongest association for late fetal loss was seen in women with protein S deficiency. In order to reduce such risks, anticoagulation therapy is administered throughout pregnancy. The antithrombotic agents available for the prevention and treatment of VTE during pregnancy and pregnancy complications include unfractionated heparin (UFH), low-molecular-weight heparin (LMWH) and aspirin. Vitamin K antagonists are contraindicated in pregnancy. Low-dose aspirin may have a role in the prevention of some pregnancy complications, although its safety in early pregnancy is uncertain. LMWH and UFH are quite safe and efficacious when properly selected, dosed and monitored. The efficacy and safety of LMWH have been demonstrated in the prevention and treatment of VTE in pregnancy. LMWH in association with aspirin administered throughout pregnancy have been shown to be associated with a lower risk of complications in women with APLA syndrome. Women at a high risk of preeclampsia are recommended to use low-dose aspirin throughout pregnancy. When there is a history of preeclampsia, the administration of anticoagulation therapy is not recommended as a prophylaxis in subsequent pregnancies, as the risk appears to be already decreased as compared with previous pregnancy. LMWH has probable advantages over UFH for the incidence of side effects. In pregnant women with mechanical heart valves, anticoagulant therapy during pregnancy should include assessment of additional risk factors for thromboembolism including valve type, position, and history of thromboembolism, and decision should also be strongly influenced by the patient's preferences. If the risk of thromboembolism in patients with mechanical heart valves is considered very high, and efficacy or safety of prophylaxis with UFH or LMWH is not satisfactory (older-generation prosthesis in the mitral position or history of thromboembolism), administration of vitamin K antagonists throughout pregnancy is recommended with replacement by UFH or LMWH close to delivery. It should be considered that limited effectiveness of UFH or LMWH in patients with mechanical heart valves might be due to inadequate dosing. The necessity of anticoagulation therapy in women with inherited or acquired thrombophilia is biologically plausible; nevertheless, optimum management in such cases remains unknown.
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PMID:[Thrombophilia, preeclampsia and other pregnancy complications]. 2003 30

Pulmonary embolism (PE) is an important cause of morbidity and mortality during pregnancy. A 21-year-old pregnant woman presented with chest pain and progressive shortness of breath at 35 weeks of gestation. Her respiratory rate was 26 breaths/min. Electrocardiography showed sinus tachycardia and nonspecific ST-T changes. Her plasma D-dimer level was elevated (1,325 ng/ml). Transthoracic echocardiography revealed enlargement of the right ventricle and a large, highly mobile thrombus in the right atrium moving during diastole into the right ventricle. Doppler ultrasonography of the lower extremities showed bilateral acute deep femoral vein thrombosis. Following the diagnosis of right heart thrombosis with massive PE, low-dose and prolonged infusion of tissue-type plasminogen activator (25 mg in three hours) was administered. Echocardiography performed six hours after thrombolysis showed a significant decrease in the right ventricular size and complete lysis of the thrombus in the right heart. Thrombosis risk panel studies showed factor V Leiden homozygote mutation. A live newborn was delivered by cesarean section at 37 weeks of gestation. No complications were seen during a 6-month follow-up.
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PMID:Successful treatment of massive pulmonary embolism in a pregnant woman, with low-dose, slow infusion of tissue plasminogen activator. 2021 40

A 70 year-old diabetic man receiving anti-coagulant therapy (Warfarin) for pulmonary embolism secondary to factor V Leiden deficiency, presented to the hospital for chest pain. After initial evaluation, he was started on aspirin (300 mg) and clopidogrel (300 mg). Three days after he was discharged, he presented with preseptal cellulitis complicating left upper eyelid chalazion. Initially, he was treated with several anti-microbial agents used sequentially. Although, the cellulitis resolved, he developed total hyphema of the left eye. The complication seems to have resulted from a complex interaction amongst anti-microbial agents, Warfarin and anti-platelet agents.
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PMID:A serious drug interaction leading to spontaneous total hyphema. 2039 56

When compared with Whites, Black-Americans may have a 40% higher incidence venous thromboembolism (VTE) incidence. However, whether other VTE characteristics and risk factors vary by race is uncertain. To compare demographic and baseline characteristics among White- and Black-Americans with VTE, we used data prospectively collected from consecutive consenting adults enrolled in seven Centers for Disease Control (CDC) Thrombosis and Hemostasis Centers from August 2003 to March 2009. These characteristics were compared among Whites (n = 2002) and Blacks (n = 395) with objectively diagnosed VTE, both overall, and by age and gender. When compared with Whites, Blacks had a significantly higher proportion with pulmonary embolism (PE), including idiopathic PE among Black women, and a significantly higher proportion of Blacks were women. Blacks had a significantly higher mean BMI and a significantly lower proportion with recent surgery, trauma or infection, family history of VTE, and documented thrombophilia (solely from reduced factor V Leiden and prothrombin G20210A prevalence). Conversely, Blacks had a significantly higher proportion with hypertension, diabetes mellitus, chronic renal disease and dialysis, HIV, and sickle cell disease. When compared with White women, Black women had a significantly lower proportion with recent oral contraceptive use or hormone therapy. We conclude that Whites and Blacks differ significantly regarding demographic and baseline characteristics that may be risk factors for VTE. The prevalence of transient VTE risk factors and idiopathic VTE among Blacks appears to be lower and higher, respectively, suggesting that heritability may be important in the etiology of VTE among Black-Americans.
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PMID:Comparison of characteristics from White- and Black-Americans with venous thromboembolism: a cross-sectional study. 2088 15

We report an unusual case of impending paradoxical embolization in a 69-year-old woman heterozygote carrier of factor V Leiden mutation. The patient presented to the emergency room with the clinical scenario of massive pulmonary embolism. Serial echocardiographic examinations revealed a large thrombus in the right atrium floating via a patent foramen ovale into the left atrium. Anticoagulation therapy was started. After 72 h, due to the unresolved thrombus, the patient underwent surgical treatment consisting of complete excision of the thrombus, closure of the foramen ovale, and pulmonary embolectomy. No in-hospital complications were noted. At 1-year follow-up, the patient is doing well on long-term anticoagulation treatment free of thromboembolic events.
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PMID:Surgical treatment of impending paradoxical embolization associated with pulmonary embolism in a patient with heterozygosis of factor V Leiden. 2063 67


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