Recent advances in diagnosis of pulmonary embolism and deep venous thrombosis.
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Angiography↗
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Use of D-dimer assays in the diagnosis of venous thrombosis.
In the course of fibrin formation, the D-domains of adjacent fibrin molecules within the fibrin polymer are covalently linked by factor XIIIa, leading to the formation of a D-domain dimer. Proteolysis of this cross-linked fibrin generates fibrin fragments D-dimer and E as terminal products. Fragment D-dimer therefore is an indicator for the proteolysis of cross-linked fibrin, whereas the monomeric fragment D can stem from fibrinogen and non-cross-linked fibrin. Various monoclonal antibodies have been prepared that distinguish between fragments D-dimer and D and allow the detection of fibrin derivatives in the presence of fibrinogen. These anti-D-dimer-antibodies have been shown to react with fragment D-dimer, but also detect dimeric D-domains within larger fibrin compounds, including cross-linked fibrin complexes generated in an early phase of coagulation activation. Assay systems for D-dimer antigen therefore may uncover intravascular clot formation early, by detection of fibrin complexes, and after completion of clot formation, by the detection of proteolytic fragments released from the particulate clot. Various trials have shown that low concentrations of D-dimer antigen in the blood exclude recent venous thrombosis or pulmonary embolism. Elevated levels may be caused by venous thrombotic disease, but also by a variety of other conditions, leading to intra- or extravascular fibrin formation. Assay systems include manual immunoagglutination assays, immunofiltration assays, microtiter plate enzyme-linked immunosorbent assay (ELISA) systems, automated ELISA systems, and latex-enhanced photometric immunoassays. According to clinical studies, D-dimer assays may be the "first line" of technical screening in symptomatic outpatients with suspected venous thrombosis or pulmonary embolism, but further prospective management trials, and improved standardization of assay systems, are needed for the validation of this approach.
Antifibrinolytic Agents↗
Anticoagulation therapy in patients with venous thromboembolic disease.
OBJECTIVE: To determine, in a representative sample of patients drawn from a variety of hospitals, the degree of adherence to consensus recommendations for anticoagulation among patients with deep vein thrombosis or pulmonary embolism. DESIGN: Cross-sectional review of a population-based random sample. SETTING: Twenty-one randomly selected Pennsylvania hospitals. PATIENTS: Of 357 randomly selected Medicare beneficiaries discharged from study hospitals with a diagnosis of deep venous thrombosis or pulmonary embolism during 1992, 43 charts were not reviewed for administrative reasons, 31 were miscoded or not treated with intravenous administration of heparin, and 13 were excluded for other reasons, leaving 270 in the final sample. MEASUREMENTS AND MAIN RESULTS: Overall, 179 patients (66%, 95% confidence interval [CI] 59%, 72%) received therapeutic anticoagulation (two consecutive partial thromboplastin times more than 1.5 times control) within 24 hours of starting heparin. Platelet counts were checked at least once during the first week of heparin therapy in 66% (95% CI 58%, 74%). At least 5 days of heparin therapy was given to 84% (95% CI 79%, 87%). Among 266 (99%) of the patients receiving warfarin, 193 (72%; 95% CI 63%, 80%) received heparin until the prothrombin time ratio or International Normalized Ratio was therapeutic. Patients who were started on warfarin therapy within 2 days of heparin had decreased length of stay (geometric mean 8.2 vs 9.7 days, p = .003). Compliance varied among hospitals. CONCLUSIONS: In a wide variety of hospitals, we found fair, but variable, compliance with consensus recommendations for anticoagulation of patients with venous thromboembolic disease. Simple interventions to improve compliance with these recommendations might improve quality of care and reduce costs.
Aged↗
[Thromboembolism complication in multiple trauma patients: an underestimated problem? Results of a clinical observational study of 50 patients].
INTRODUCTION: The incidence of thromboembolic complications in patients with severe polytrauma in the ICU is not well known. Only a few publications deal with this problem. Systematic investigations in this high-risk patient group are not routinely used. METHOD: From January 1996 to January 1998, 50 polytrauma patients with a mean ISS > 15 were included in a clinical study to evaluate the incidence of thromboembolism in this patient group. Further inclusion criteria were a minimum stay of 72 h in the ICU and mechanical ventilation for a minimum time of 72 h. All patients were examined with color-coded duplex sonography according to a standardized protocol. The duplex sonography was performed before the patients were first mobilized in the ICU (15 +/- 12.8 days). RESULTS: If not otherwise indicated all values are given as mean +/- SD. The age of the patients was 38 years (range 17-77 years), the severity of trauma was characterized by an ISS of 40 (range 16-70). Eight of the included patients died during their stay in the ICU after developing a multiple organ failure. According to autopsy data none of them had a deep venous thrombosis or pulmonary embolus. Eight patients (19%) developed deep venous thrombosis, and 4 patients with thrombosis developed pulmonary embolism. CONCLUSION: The incidence of deep venous thrombosis in polytrauma patients seems to be much higher than expected reviewing the results of other publications. The low detection rate of other authors results from using only clinical signs. The routine use of color-coded duplex sonography is effective in detecting unsuspected deep vein thrombosis.
Adolescent↗
Thrombosis during pregnancy: risk factors, diagnosis and treatment.
Venous thromboembolism occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium and remains a diagnostic and therapeutic challenge. In the general population the incidence of pregnancy associated VTE has been estimated to vary from 1 in 1000 to 1 in 2000 deliveries. The risk of VTE is five times higher in a pregnant woman than in a nonpregnant woman of similar age. Postpartum VTE is more common than antepartum VTE. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose deep-vein thrombosis clinically is generally poor and is further hampered during pregnancy since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury. Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant treatment of choice during pregnancy. In case of acute new onset of thrombosis during pregnancy, treatment is performed like in non-pregnant patients with acute deep vein thrombosis or pulmonary embolism. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.
Female↗
Venous thromboembolism after severe injury in children.
BACKGROUND: Deep vein thrombosis and pulmonary embolism are considered common complications after major trauma. Their incidence and the associated risk factors have rarely been identified in injured children. METHODS: Severely injured children (age <18 years; admitted in a pediatric intensive care unit or length of stay > or = 72 h) with a discharge diagnosis of venous thromboembolism (VTE; deep venous thrombosis and/or pulmonary embolism) were identified from the institutional trauma registry between January 1, 1999 and April 31, 2002. The study centers included a dedicated pediatric trauma center and an adult trauma center with pediatric patients. Risk factors for VTE were identified using multivariate analysis. RESULTS: VTE was found in 11 of the 3,291 admissions, for a rate of 3.3/1,000 admissions. Children with VTE were older and had higher Injury Severity Scores. Independent risk factors for VTE included thoracic injuries [odds ratio (OR): 6.9; 95% confidence interval (CI): 1.4-35.1] and spinal injuries (OR: 37.4; 95% CI: 3.5-396.7). The greatest risk of VTE was in children with central venous catheters (OR: 64.0; 95% CI: 16.8-243.9). CONCLUSION: Older children with high Injury Severity Scores, thoracic injuries, spinal injuries or venous catheters are at risk for VTE. Because VTE prophylaxis, screening and treatment are associated with complications and costs, it is essential to identify subgroups of pediatric patients in whom these strategies might be studied.
Adolescent↗
[Must we perform imaging in pulmonary embolism? Looking for deep venous thrombosis may be more efficient].
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Humans↗
Role of heparin and low-molecular-weight heparins in the management of acute ischemic stroke.
The numerous large-scale randomized clinical trials performed during the last decade on either unfractionated heparin, or low molecular weight heparin have not been able to demonstrate undisputed benefits in patients with acute ischemic stroke, compared with no treatment or aspirin. However, a large number of these trials, including the International Stroke Trial and Chinese Acute Stroke Trial, exhibit severe methodological limitations and need to be interpreted with caution. Knowledge of thromboembolism pathophysiology and clinical experience leads to the theory that heparins will prevent red thrombus formation, propagation and embolism. Heparins effectively prevent venous thrombosis and pulmonary embolism. More trials are needed to test heparins in patients whose cardiocerebrovascular lesions are better defined by newer neuroimaging techniques. The efficacy of heparins has not been adequately tested in patients with defined stroke subtypes and occlusive vascular lesions. Heparins should not be indiscriminately given to all patients with acute ischemic stroke. High-quality, randomized trials that adequately study heparin use in patients using modern technology for vascular lesions and stroke subtypes are lacking, and need to be performed.
Acute Disease↗
Comparison of enoxaparin and warfarin for the prevention of venous thromboembolic disease after total hip arthroplasty. Evaluation during hospitalization and three months after discharge.
BACKGROUND: Venous thromboembolic disease in the form of deep venous thrombosis and pulmonary embolism is a major risk after a total hip arthroplasty. Enoxaparin, a low-molecular-weight heparin, has been shown to reduce the prevalence of deep venous thrombosis after total hip arthroplasty. Warfarin, an orally administered anticoagulant, has been used historically to reduce the risk of deep venous thrombosis after total hip arthroplasty. METHODS: We compared enoxaparin and adjusted-dose warfarin with respect to their safety and their efficacy in the prevention of clinically important venous thromboembolic disease, defined as distal or proximal deep venous thrombosis or pulmonary embolism, or both, during hospitalization after total hip arthroplasty. We also evaluated the prevalence of complications and mortality from venous thromboembolic disease within three months after discharge. RESULTS: Three thousand and eleven patients at 156 centers were randomly assigned to prophylactic treatment with injection of enoxaparin or oral administration of adjusted-dose warfarin during hospitalization. During the study, fifty-five (3.6 percent) of the 1516 patients who were managed with enoxaparin and fifty-six (3.7 percent) of the 1495 patients who were managed with warfarin had venous thromboembolic disease. Twenty-one patients (0.7 percent), which included four (0.3 percent) of those managed with enoxaparin and seventeen (1.1 percent) of those managed with warfarin (p = 0.0083), had venous thromboembolic disease during hospitalization. After discharge from the hospital, venous thromboembolic disease developed in ninety patients (3.0 percent): fifty-one (3.4 percent) of those managed with enoxaparin and thirty-nine (2.6 percent) of those managed with warfarin. One patient who had been managed with enoxaparin died because of a pulmonary embolism, which was confirmed at autopsy. Three additional patients (one who had been managed with enoxaparin and two who had been managed with warfarin) died, and the deaths were attributed to venous thromboembolic disease; however, no autopsies were performed. Twenty-six patients (0.9 percent) (eighteen managed with enoxaparin and eight managed with warfarin) had clinically important bleeding. CONCLUSIONS: Inpatient programs providing treatment with either enoxaparin (thirty milligrams every twelve hours) or adjusted-dose warfarin for a mean of 7.3 days afforded protection against venous thromboembolic disease, with overall rates of morbidity and mortality of 3.7 and 0.6 percent, respectively, and a very low rate of major bleeding complications (0.9 percent) for three months after total hip arthroplasty. During hospitalization, the patients managed with enoxaparin had a lower rate of venous thromboembolic disease than those managed with adjusted-dose warfarin (p = 0.0083). This benefit was lost after the medication was discontinued, with no difference in the prevalences of venous thromboembolic disease between the two groups at three months after discharge from the hospital.
Adolescent↗
One novel and one recurrent mutation in the PROS1 gene cause type I protein S deficiency in patients with pulmonary embolism associated with deep vein thrombosis.
We investigated the molecular basis of type I protein S (PS) deficiency in two unrelated Japanese families, in which both probands developed pulmonary embolism associated with deep vein thrombosis. Nucleotide sequencing of amplified DNA revealed distinct point mutations in the PROS1 gene of the probands, which were designated protein S Sapporo 1 and protein S Sapporo 2. Additional mutations in the PROS1 gene were excluded by DNA sequencing of all exons and intron/exon boundaries. In the 25-year-old Japanese male patient who carried protein S Sapporo 1, we identified a heterozygous A-to-T change in the invariant ag dinucleotide of the acceptor splice site of intron f of the PROS1 gene. This mutation is a novel splice site mutation that impairs normal mRNA splicing, leading to exon 7 skipping, which was confirmed by platelet mRNA analysis. Translation of this mutant transcript would result in a truncated protein that lacks the entire epidermal growth factor-like domain 3 of the PS molecule. In a 31-year-old Japanese male and his younger brother who each carried protein S Sapporo 2, we detected a previously described heterozygous T-to-C transition at nucleotide position 1147 in exon 10 of the PROS1 gene, which predicts an amino acid substitution of tryptophan by arginine at residue 342 in the laminin G1 domain of the PS molecule. Both mutations would cause misfolding of the PS protein, resulting in the impairment of secretion, which is consistent with the type I PS deficiency phenotype.
Adult↗
Travel, venous thromboembolism, and thrombophilia.
Current evidence indicates that prolonged air travel predisposes to venous thrombosis and pulmonary embolism. An effect is seen once travel duration exceeds 6 to 9 hours and becomes obvious in long-haul passengers traveling for 12 or more hours. A recent records linkage study found that increase in thrombosis rate among arriving passengers peaked during the first week and was no longer apparent after 2 weeks. Medium- to long-distance travelers have a 2- to 4-fold increase in relative thrombosis risk compared with nontravelers, but the averaged absolute risk is small (approximately one symptomatic event per 2 million arrivals, with a case-fatality rate of approximately 2%) and there is no evidence that thrombosis is more likely in economy class than in business- or first-class passengers. It remains uncertain whether and to what extent thrombosis risk is increased by short-distance air travel or prolonged travel by motorcar, train, or other means. Most travelers who develop venous thrombosis or pulmonary embolism also have one or more other predisposing risk factors that may include older age, obesity, recent injury or surgery, previous thrombosis, venous insufficiency, malignancy, hormonal therapies, or pregnancy. Limited (though theoretically plausible) evidence suggests that factor V Leiden and the prothrombin gene mutation predispose to thrombosis in otherwise healthy travelers. Given that very many passengers with such predispositions do not develop thrombosis, and a lack of prospective studies to link predisposition with disease, it is not now possible to allocate absolute thrombosis risk among intending passengers or to estimate benefit-to-risk ratios or benefit-to-cost ratios for prophylaxis. Randomized comparisons using ultrasound imaging indicate a measurable incidence of subclinical leg vein thrombosis after prolonged air travel, which appears to increase with travel duration and is reduced by graded pressure elastic support stockings. Whether this surrogate outcome measure translates into clinical benefit remains unknown, but support stockings are likely to be more effective and have less adverse effects than the use of aspirin.
Aerospace Medicine↗
Peripheral venous aneurysms with recurrent pulmonary embolism: report of a case and review of the literature.
This clinical report deals with a femoral venous aneurysm as a source of recurrent pulmonary embolism. The literature concerning venous aneurysms is reviewed with emphasis on those cases which were complicated by venous thrombosis and pulmonary embolism. This case demonstrates that lower leg venous aneurysms can occur in either sex and in different age groups. Venography was shown to be important in diagnosing these lesions. Surgical resection may be necessary to prevent potential thrombosis and life-threatening pulmonary embolism.
Adult↗
[Pulmonary embolism and unusual deep venous thrombosis. Report of two cases].
Contrast venography is the gold standard for the diagnosis of deep vein thrombosis in the lower limb extremities, but it fails to visualize deep veins like deep femoral vein and internal iliac vein. The internal iliac can be examined with duplex scanning if the technique and the examination conditions are correct. As reported in these two cases, thrombosis of these deep veins may lead to pulmonary embolism. The first case is a young female with venous thromboembolic disease in whom internal iliac vein thrombosis was documented only at the second examination. In the second case, deep femoral vein thrombosis appeared early in a comatose young male. This thrombosis may be classified as proximal muscular vein thrombosis. These two cases emphasize the importance of a duplex scanning examination performed with rigorous technique, whose the main limitation being examination conditions.
Adult↗
Paradoxical coronary embolism, extensive pulmonary embolism and deep venous thrombosis.
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Coronary Angiography↗
[The surgical treatment of deep venous thrombosis].
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Humans↗
Prophylactic vena caval filters in trauma: the rest of the story.
OBJECTIVE: The purpose of this study was to describe outcomes for patients with trauma who had vena caval filters placed in the absence of venous thromboembolic disease (group P) and compare them with outcomes for patients with trauma who had filters placed after either deep venous thrombosis or pulmonary embolism (group T). DESIGN: The study is a case series of consecutive patients who received vena caval filters after traumatic injury. Data were collected prospectively at the time of filter placement from reports of diagnostic studies obtained for clinical indications and during the annual follow-up examinations. Event rate findings are based on objective tests. Data were obtained from the Michigan Vena Cava Filter Registry. RESULTS: Filters were placed in 385 patients with trauma; 249 of these filters were prophylactic (group P). Event rates were similar in the two groups. New pulmonary embolism was diagnosed in 1.5% of the patients in group P and 2% of the patients in group T. Caval occlusion rates were 3.5% for group P and 2.3% for group T. In all, 15.6% of the patients in group P had deep venous thrombosis or pulmonary embolism after placement. The frequencies of lower extremity swelling and use of support hose were higher in group T than in group P (43% vs 25% and 25% vs 3.5%, respectively; P <.005). Outcomes were comparable in the two groups with respect to mechanical stability of the filter. CONCLUSIONS: The prophylactic indication for vena caval filter placement in patients with trauma is associated with a low incidence of adverse outcomes while providing protection from fatal pulmonary embolism. The current challenge is to limit the number of unnecessary placements through improved methods of risk stratification.
Adolescent↗
Fibrin-specific thrombolytic agents.
The mammalian fibrinolytic system comprises a proenzyme, plasminogen, which can be converted to the active enzyme plasmin, which will degrade fibrin. Plasminogen activation is mediated by plasminogen activators which are classified as either tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA). t-PA and single-chain u-PA (scu-PA) induce clot-specific thrombolysis, however via entirely different mechanisms. t-PA is relatively inactive in the absence of fibrin, but fibrin strikingly enhances the activation rate of plasminogen by t-PA. This is explained by an increased activity of fibrin-bound t-PA for plasminogen and not by alteration of the catalytic efficiency of the enzyme. scu-PA has a high affinity for plasminogen but, however, does not activate plasminogen in plasma in the absence of a fibrin clot, due to competitive inhibition. Fibrin-specific thrombolysis appears to be due to the fact that fibrin reverses the competitive inhibition, but this does not seem to occur via specific binding of scu-PA to fibrin. The thrombolytic efficacy and fibrin-specificity of natural and recombinant t-PA has been demonstrated in animal models of pulmonary embolism, venous thrombosis and coronary artery thrombosis. In all these studies thrombolysis and relative fibrinogen sparing effect of t-PA was recently confirmed in several multicenter clinical trials in patients with acute myocardial infarction. Specific thrombolysis by scu-PA has also been demonstrated in animal models of pulmonary embolism, venous thrombosis and coronary artery thrombosis.
Humans↗