[Prevention of embolism due to postoperative thrombosis by early deambulation].
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INTRODUCTION: Previous investigations have suggested a lower prevalence of the factor V Leiden mutation in patients with pulmonary embolism, as compared to patients with deep leg vein thrombosis. METHODS: We studied unselected patients with pulmonary embolism, in whom we also assessed the presence of deep vein thrombosis by ultrasonography. We assessed the prevalence of heterozygosity for the factor V Leiden mutation and compared the outcome of patients with a normal ultrasound (primary pulmonary embolism) to those with an abnormal ultrasound (combined form of venous thromboembolism). Furthermore, we performed a literature search to identify all articles regarding the prevalence of heterozygous factor V Leiden mutation in patients with primary deep vein thrombosis, primary pulmonary embolism and a combined form of venous thromboembolism. We calculated a (common) odds ratio for these 3 manifestations of venous thromboembolism, including the current findings. RESULTS: In 92 patients with proven pulmonary embolism, 25 (27%) had also an abnormal ultrasound. In these patients, the prevalence of the factor V Leiden mutation was 24% (95% CI 9%-45%), whereas the mutation was present in 5 of 67 patients with primary pulmonary embolism (7%; 95% CI 2%-16%). The literature analysis indicated the common odds ratio for the presence of heterozygous factor V Leiden mutation in patients with primary deep vein thrombosis, primary pulmonary embolism and the combined form of venous thromboembolism to be 7.9 (95% CI 5-12), 3.5 (95% CI 2-6) and 6.8 (95% CI 3-14), respectively. CONCLUSION: In patients with primary pulmonary embolism the prevalence of the factor V Leiden mutation appears to be half of that reported in patients with primary deep vein thrombosis. The mechanism remains unclear.
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Reduced fibrinolytic capacity due to increased plasminogen activator inhibitor-1 (PAI-1) activity in plasma is a common finding in patients with coronary heart disease or venous thromboembolism, although its clinical significance is debated. Recently, a dimorphism in the PAI-1 promoter (4G-5G) has been reported and homozygosity for the 4G allele is associated with increased transcription and higher PAI-1 levels. Homozygous 4G genotype has been suggested to be a risk factor for myocardial infarction. In the present study, the 4G-5G dimorphism was determined in 349 individuals from 21 thrombophilic families with hereditary protein S deficiency and in 140 unrelated healthy controls. Among the 143 protein S deficient individuals, there was no relationship between deep or superficial venous thrombosis and the PAI-1 dimorphism. However, 26% (12/46) of individuals having protein S deficiency combined with homozygosity for the 4G allele had suffered pulmonary embolism as compared to 7% (7/97) of protein S deficient individuals carrying at least one 5G allele (p = 0.0019). In protein S deficient individuals, arterial thrombosis was found to be associated with smoking and 4G homozygosity. No association was found between the PAI-1 dimorphism and arterial or venous thromboembolism in family members without protein S deficiency. In conclusion, the PAI-1 genotype affects the phenotypic expression of thrombophilia in protein S deficient individuals.
An association between venous thrombosis and cancer was first suggested by Trousseau, and has been confirmed by multiple postmortem studies. Clinical studies have shown that thrombophlebitis migrans may occur before malignancies become clinically evident, and therefore serves as a clue to occult cancer. A relation between occult cancer and the commoner deep venous thrombosis and pulmonary embolism has not been established. We ascertained the incidence of cancer before and after pulmonary embolism was diagnosed by pulmonary angiography in 128 patients. The incidence of cancer before pulmonary embolism (12%) was essentially the same as that in a comparison group of patients without pulmonary embolism (10%). In the 2 years after pulmonary angiography, however, cancer was diagnosed in 13 patients with pulmonary embolism in contrast to no patients in the comparison group (p less than 0.001). The most frequent cancers involved the lung, gastrointestinal tract, breast, and uterus. The malignancies were nearly always occult when pulmonary embolism occurred. These findings indicate that pulmonary embolism with or without overt deep venous thrombosis should alert the clinician to consider occult cancer.
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Patients with a first episode of symptomatic pulmonary embolism (PE) have a higher risk of recurrent venous thromboembolism (VTE) than patients with a first episode of proximal lower extremity deep vein thrombosis (DVT). Patients with symptomatic DVT and silent PE may have a different risk of VTE recurrence than patients that have symptomatic DVT without PE. Therefore, it was the aim of this prospective cohort study to compare the risk of recurrent symptomatic VTE in patients with proximal lower extremity DVT and silent PE to the risk in patients that only have proximal lower extremity DVT. Ninety-one consecutive outpatients presenting to the emergency department of a university hospital subsequently hospitalised with a first episode of unprovoked symptomatic proximal lower extremity DVT, and without new pulmonary symptoms were included. Standard initial treatment consisted of intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin for 5-7 days, overlapped with oral vitamin-K antagonist therapy, with long-term oral vitamin-K antagonist therapy (goal INR 2.5 [2.0-3.0]). Study endpoints were: symptomatic recurrent DVT, new PE, and recurrent PE, evaluated by standard objective testing. At enrollment, 28 of 91 (31%) patients with DVT had silent PE. In the patients with DVT and silent PE, there were 3 VTE recurrences during 20 person-years of follow-up, while there were no VTE recurrences during 61 person-years of follow- up in the patients with isolated DVT. The Kaplan-Meier estimated VTE recurrence rate at 1 year after the diagnosis of DVT was 11% (95% CI: 2-28%) for patients with symptomatic DVT and silent PE, compared to 0% in patients with isolated symptomatic DVT (p=0.0045). In patients with a first episode of unprovoked symptomatic acute proximal lower extremity DVT, the risk of recurrent VTE was significantly higher in those with silent PE compared to those without PE.
OBJECTIVE: Because deep venous thrombosis is clinically linked with pulmonary embolism and often treated similarly, we sought to assess the usefulness of obtaining bilateral lower extremity compression sonograms when findings on ventilation-perfusion lung scans indicate a low or indeterminate probability of pulmonary embolism. Demonstration of deep venous thrombosis would provide a rationale for treating both pulmonary embolism and deep venous thrombosis. MATERIALS AND METHODS: Two hundred twenty-three consecutive patients with suspected pulmonary embolism had ventilation-perfusion lung scans and concurrent bilateral lower extremity compression sonograms; 34 also had pulmonary arteriography. RESULTS: In 75 cases, the results of ventilation-perfusion lung scanning indicated an indeterminate probability of pulmonary embolism. Evidence of thrombosis was seen on sonograms in 11 of these 75. In the remaining 64, 17 underwent pulmonary arteriography and four (24%) had pulmonary embolism. Findings on lung scans indicated a low probability of pulmonary embolism in 70 of 223 patients. Evidence of thrombosis was seen on sonograms in 11 of these 70. Five of the remaining 59 underwent pulmonary arteriography and one (20%) had pulmonary embolism. According to the 1993 Medicare Fee Schedule, if all 145 patients whose lung scans were nondiagnostic had sonography and only those with normal sonograms had pulmonary arteriography, the professional and hospital charges would be $359,552. If all 145 had pulmonary arteriography without sonography, the charges would be $395,031. CONCLUSION: If ventilation-perfusion lung scans indicate a low or an indeterminate probability of pulmonary embolism and bilateral lower extremity compression sonography is performed, only those patients with normal sonographic findings would need further study. Thus, 15% (22/145) of patients could be spared pulmonary arteriography, and the estimated savings in cost would be 9%.
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Previous publications have highlighted seasonal variations in the incidence of thrombosis and pulmonary embolism, and that weather patterns can influence these. While medical risk factors for pulmonary thrombo-embolism such as age, obesity, hypercoagulable states, cancer, previous thrombo-embolism, immobility, limb paralysis, surgery, major illness, trauma, hypotension, tachypnoea and right ventricular hypokinesis are not directly implicated regarding environmental factors such as weather, they could be influenced indirectly by these. This would be especially relevant in polluted areas that are associated with a higher pulmonary embolism risk. Routine nuclear medicine lung ventilation/perfusion studies (V/Q scans) of 2071 adult patients referred to the nuclear medicine department of the Royal Surrey County Hospital in Guildford, UK, between January 1998 and October 2002 were reviewed and 316 of these patients were classified as positive for pulmonary embolism with high probability scan on PIOPED criteria. The occurrence of positive scans was compared to environmental factors such as temperature, humidity, vapour pressure, air pressure and rainfall. Multiple linear regression was used to establish the significance of these relations. The incidence of pulmonary embolism was positively related to vapour pressure and rainfall. The most significant relation was to vapour pressure (p=0.010) while rainfall was less significant (p=0.017). There was no significant relation between pulmonary embolism and air pressure, humidity or temperature. It is postulated that rainfall and water vapour may be contributary factors in thrombosis and pulmonary embolism by way of pollutants that are carried as condensation nuclei in micro-droplets of water. In particular, fossil fuel pollutants are implicated as these condensation nuclei. Pollutants may be inhaled by populations exposed to windborne vapour droplets in cities or airports. Polluted vapour droplets may be absorbed by the lung to hasten coagulation cascades in the blood. This may lead to thrombosis and increased pulmonary embolism under high vapour pressure conditions. With combined factors such as pre-existing ill health or immobility on long flights, the risk of thrombosis and consequent embolism might increase substantially.
Pulmonary embolism (PE) and deep venous thrombosis (DVT) are major causes of morbidity and mortality, which can be reduced with accurate diagnosis and proper treatment. More than 90% of PEs originate in lower-extremity DVT. Currently, evaluation of PEs and lower-extremity DVT requires 2 separate tests (ventilation-perfusion scan, computed tomographic pulmonary angiography (CTPA), or pulmonary angiography for PE and sonography, computed tomographic venography (CTV), conventional venography, or magnetic resonance venography for DVT). Combined computed tomographic pulmonary angiography and venography (CTPAV) is a new diagnostic technique that combines CTPA and CTV into a single study for the screening of PE and subdiaphragmatic DVT. CTPAV is a modified CTPA study that evaluates the subdiaphragmatic deep vein system at the time of CTPA, without additional venipuncture or contrast medium. It is easy to perform, fairly easy to interpret, readily available, and requires no invasive procedure. We present 2 cases of multiple PE and lower-extremity DVT in which CTPAV was used.
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