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PubMed1990

Lower-extremity venous thrombosis in patients with acute hip fractures: determination of anatomic location and time of onset with compression sonography.

Patients with acute hip fractures are at increased risk for the development of lower-extremity deep venous thrombosis and its major complication, pulmonary embolism. It is furthermore recognized that the risk of clinically important pulmonary embolism depends to some degree on the anatomic location of the preexisting thrombosis. Because of the increased risk of thromboembolic disease, most patients with hip fracture are treated with one of several prophylactic regimens. The potential for effective prophylaxis may depend on the time of onset of the venous thrombosis. We used compression sonography to determine the anatomic location and time of onset of deep venous thrombosis in patients with hip fractures being treated with antithrombotic prophylaxis. Ninety-six patients had compression sonography of the injured extremity perioperatively and serially until discharge. Ninety-three also were examined with contrast venography when the sonogram suggested thrombus or at discharge if all sonograms were normal. Twenty areas of thrombus were identified in 18 patients, thereby yielding a prevalence of thrombosis of 19%. All patients were asymptomatic. Above-knee clot was diagnosed in 14 (78%) of these 18 patients. Nine (64%) of the 14 patients with significant clot had the abnormality on their first perioperative investigation (in eight of nine cases, the clot was adjacent to the fracture site), before any means of prophylaxis could have been initiated. Significant thrombosis developed in six patients later in their course (in only one case was the clot related to the fracture site), and the thrombus was an extension of below-knee clot in the minority of the patients. We conclude that although currently acceptable prophylaxis may decrease the frequency of thrombosis, it does little to prevent above-knee clot, which often antedates the initiation of therapy. Furthermore, as the clinical diagnosis of deep venous thrombosis is difficult in patients with acute hip fracture, serial compression sonograms are recommended so that patients with unsuspected clot may be treated with appropriate anticoagulation and/or caval interruption.

Acute Disease↗
PubMed1992

Thrombosis in antithrombin-III-deficient persons. Report of a large kindred and literature review.

PURPOSE: To estimate the prevalence of objectively proven thrombotic complications in antithrombin-III-deficient persons. STUDY DESIGN: Cross-sectional study and a critical review of the literature. DATA SOURCES AND EXTRACTION: The prevalence of thrombosis in antithrombin III-deficient and -nondeficient family members of a large kindred was estimated by history, review of diagnostic tests, and examination for venous reflux by Doppler ultrasonography, as an indicator of previous venous thrombosis. A MEDLINE search and literature review of the published English- and French-language literature from 1966 to 1990 that described antithrombin-III-deficient families was done, and the following information was obtained: the prevalence of thrombosis in deficient and nondeficient family members, the presence or absence of risk factors for thrombosis (surgery, pregnancy, the postpartum state, use of oral contraceptives, immobilization, metastatic cancer, major trauma) at the time of the thrombotic event, and age of onset of the first episode of thrombosis. The validity of the studies was assessed according to predetermined criteria. RESULTS: Sixty-seven research subjects were evaluated. Six of 31 (19.4%) antithrombin-III-deficient subjects compared with none of 36 (0%) nondeficient subjects had had one or more thrombotic events. The initial episode in five of six subjects had occurred in association with risk factors for thrombosis. The literature search indicated that the pooled prevalence of symptomatic venous thrombosis among the deficient subjects was 51%, but objective testing was done in only 17% of these subjects at the time of presentation. CONCLUSION: Based on the data from this antithrombin-III-deficient kindred, lifelong anticoagulant prophylaxis does not appear to be warranted in asymptomatic carriers, and prophylaxis could be limited to periods of high risk for thrombosis.

Adolescent↗
PubMed1997

Ultrasonographic screening before hospital discharge for deep venous thrombosis after arthroplasty: the post-arthroplasty screening study. A randomized, controlled trial.

BACKGROUND: The clinical significance of asymptomatic deep venous thrombosis that develops after joint arthroplasty and the value of screening tests to detect thrombi are uncertain. OBJECTIVES: To determine 1) the rate of symptomatic deep venous thrombosis or pulmonary embolism occurring after hospitalization for joint arthroplasty and 2) the value of screening compression ultrasonography. DESIGN: Double-blind, randomized, controlled trial. SETTING: Tertiary care hospital. PATIENTS: 1024 patients undergoing elective total hip or knee arthroplasty who received warfarin prophylaxis. INTERVENTION: Patients were randomly assigned to undergo either bilateral compression ultrasonography or a sham procedure before hospital discharge. Patients with a diagnosis of asymptomatic deep venous thrombosis were treated after discharge with standard anticoagulant therapy; other patients had warfarin therapy discontinued at discharge. All patients were followed for 90 days. RESULTS: In the screening group, asymptomatic proximal deep venous thrombosis was detected in 13 of 518 patients (2.5%). Another 4 patients subsequently developed symptomatic proximal deep venous thrombosis, and 1 patient treated for asymptomatic deep venous thrombosis developed major bleeding, for a total outcome event rate of 1.0% (5 of 518 patients). In the placebo group, 3 patients developed symptomatic proximal deep venous thrombosis and 2 had nonfatal pulmonary embolism, for a total event rate of 1.0% (5 of 506 patients) (difference, 0 percentage points [95% CI, -1.2 to 1.2 percentage points]). CONCLUSIONS: In patients undergoing total hip or knee arthroplasty, the use of warfarin prophylaxis during hospitalization results in a very low rate of symptomatic deep venous thrombosis or pulmonary embolism after hospital discharge. The use of screening compression ultrasonography at hospital discharge does not seem to be justified in this setting.

Algorithms↗
PubMed1998

Clarification of the risk for venous thrombosis associated with hereditary protein S deficiency by investigation of a large kindred with a characterized gene defect.

BACKGROUND: Protein S is an important regulatory protein of the coagulation cascade. The risk for venous thrombosis associated with protein S deficiency has been uncertain because all previous risk estimates used phenotypic evaluation alone, which can be ambiguous. OBJECTIVE: To quantitate the risk for thrombosis associated with a characterized protein S gene mutation that causes a Gly295-->Val substitution and protein S deficiency. DESIGN: Retrospective study of a single extended family. SETTING: University hospital referral center. PARTICIPANTS: A 122-member protein S-deficient family, in which 44 members had a recently characterized gene defect. MEASUREMENTS: Comprehensive history of thrombosis, history of exposure to acquired risk factors for thrombosis, levels of total and free protein S antigen, and genotype for the mutation causing the Gly295-->Val substitution. RESULTS: Kaplan-Meier analysis of thrombosis-free survival showed that the probability of remaining free of thrombosis at 30 years of age is 0.5 (95% CI, 0.33 to 0.66) for carriers of the Gly295-->Val mutation compared with 0.97 (CI, 0.93 to 1.0) for normal family members (P < 0.001). In a multivariate Cox regression model that included smoking and obesity, the mutation was a strong independent risk factor for thrombosis (hazard ratio, 11.5 [CI, 4.33 to 30.6]; P < 0.001). For free (but not total) protein S antigen levels, the distributions of persons with and persons without the mutation did not overlap. CONCLUSIONS: Protein S deficiency, as defined by the presence of a causative gene mutation or a reduced level of free protein S antigen, is a strong independent risk factor for venous thrombosis in a clinical affected family.

Adolescent↗
PubMed1998

Relation of factor V Leiden genotype to risk for acute deep venous thrombosis after joint replacement surgery.

BACKGROUND: A point mutation in coagulation factor V (A1691G) is associated with increased risk for venous thrombosis. However, limited information is available about the prospective risk for deep venous thrombosis in specific high-risk clinical settings. OBJECTIVE: To determine whether the factor V Leiden mutation is associated with an increased occurrence of deep venous thrombosis in patients undergoing hip or knee replacement surgery. DESIGN: Retrospective analysis of plasma samples obtained during six prospective clinical trials that compared different antithrombotic prophylaxis regimens in patients undergoing hip or knee replacement surgery. SETTING: Inpatients at the University of Rochester Medical Center, McMaster University Medical Center, Hamilton Civic Hospitals, and the Genesee Hospital. PATIENTS: 825 patients hospitalized for hip or knee replacement surgery. MEASUREMENTS: Venographically diagnosed postoperative deep venous thrombosis was correlated with factor V genotype. RESULTS: The factor V Leiden mutation was not associated with a significantly increased risk for venographically detected deep venous thrombosis. The absolute incidence of deep venous thrombosis was 31% (95% CI, 15% to 47%) in patients with the mutation and 26% (CI, 22% to 29%) in patients without the mutation (relative risk, 1.2 [CI, 0.6 to 2.9]). The factor V Leiden mutation was not significantly associated with deep venous thrombosis in subgroups of patients receiving warfarin or heparin. The incidence of clinical hemorrhage was similar in patients with (10%) and without (8%) the mutation. CONCLUSIONS: The factor V Leiden mutation is not a significant risk factor for acute deep venous thrombosis in this group of patients. Current data do not justify routine preoperative screening for this mutation or intensified perioperative prophylaxis in patients with the factor V Leiden mutation who are undergoing hip or knee joint replacement surgery and are receiving effective antithrombotic prophylaxis.

Aged↗
PubMed2001

[Prevalence of duplex ultrasonography detectable venous thrombosis in patients with suspected or acute pulmonary embolism].

OBJECTIVES: Duplex ultrasonography performance in detecting embolic foci has not been proven satisfactory compared with phlebography or autopsic findings. In case of suspected pulmonary embolism, the embolic focus is only discovered in 11 to 18% of the cases compared with more than 30% with phlebography. For overt acute pulmonary embolism, the discovery rate is in the 30 to 45% range versus 70 to 80% with phlebography or autopsy findings. This discrepancy might result from the fact that duplex ultrasonographic explorations are generally limited to the deep collectors at the cruropopliteal level. The purpose of this study was to assess the prevalence of duplex ultrasonography detected venous thrombosis in patients with suspected or acute pulmonary embolism when the exploration includes the entire venous system from the inferior vena cava to the ankles and examines not only the deep collectors but also the muscle and superficial networks. MATERIAL AND METHODS: This study included all patients with suspected pulmonary embolism referred to the emergency unit from January 1, 1995 through December 31, 1998. The patients' hospital files were used to determine the suspected pulmonary embolism population. The acute pulmonary embolism population was defined as the patients whose files contained documented proof of pulmonary embolism (highly probable ventilation/perfusion pulmonary scintigraphy, positive pulmonary angiography, positive proximal angioscan). Thrombosis of the deep venous collectors with or without associated superficial or muscular localization was classed as "deep venous thrombi" and superficial or muscular thrombosis without involvement of the deep collectors was classed as "other venous thrombi". Subpopliteal thrombosis was classed as distal and popliteal or suprapopliteal thrombosis as proximal. RESULTS: The suspected pulmonary embolism group included 352 patients, 118 men and 234 women aged 67.6 +/- 15.4 and 70.8 +/- 20.0 years respectively (m +/- SD). The acute pulmonary embolism group included 60 patients, 17 men and 43 women aged 66.2 +/- 12.5 and 69.7 +/- 16.6 years respectively. Overall prevalence of duplex-ultrasound detected venous thrombosis was 30.4% (107/352) (95%CI: 25.6-35.2) in the suspected pulmonary embolism group and 80% (48/60) (95%CI: 69.9-90.1) in the acute pulmonary embolism group. Deep venous thrombi reaching the collectors and proximal thrombi predominated. Prevalence of "other venous thrombi" and distal venous thrombi were 6.5% (23/352) and 11.4% (40/352) respectively in the suspected pulmonary embolism group and 15.0% (9/60) and 26.7% (16/60) in the acute pulmonary embolism group. The frequency of asymptomatic venous thrombosis of the lower limbs, irrespective of the localization, was 42.1% (45/107) in the suspected pulmonary embolism group and 52.1% (25/48) in the acute pulmonary embolism group. CONCLUSIONS: The prevalence of duplex-ultrasonography detected venous thrombosis in patients with suspected or proven pulmonary embolism found in this series was equivalent to the rates reported in phlebography and autopsy series. The prevalence was higher than usually reported for duplex-ultrasonography studies limited to the cruro-popliteal level. The difference came from the "other venous thrombi" and "distal deep venous thrombi" discovered by exploring the superficial and muscular networks and the calves. This study demonstrates the contribution of duplex-ultrasonography to the diagnostic strategy for pulmonary embolism.

Acute Disease↗
PubMed1991

Heparin cofactor II: an acute phase reactant in patients with deep vein thrombosis.

In human plasma, heparin cofactor II (HCII) is a thrombin inhibitor which displays similarities with antithrombin III (ATIII). As previously reported for hereditary ATIII deficiency, cases of recurrent thrombosis were reported in patients with hereditary HCII deficiency. Here, plasma HCII activity was studied in 372 patients with a history of thrombosis, classified according to their anticoagulant therapy. The mean plasma HCII level was significantly higher in patients with acute deep vein thrombosis (DVT) under heparin therapy than in patients with a history of thrombosis, who were studied more than 3 months after the acute event, and were either on, or had been on, oral anticoagulant therapy. HCII and fibrinogen were significantly correlated in all three groups of patients. These results were strengthened by those of a follow-up study in 23 patients with acute DVT. Changes in plasma HCII activity paralleled those of fibrinogen. This suggests that HCII might behave like an acute phase reactant in patients with thrombosis and that the measurement of its plasma level as a risk factor for thrombosis should be performed some time after the acute episode. In conclusion, the prevalence of HCII deficiency in patients with a history of thrombosis might have been underestimated in series which included patients with acute thrombosis.

Acute-Phase Proteins↗
PubMed1987

Variables associated with postoperative deep venous thrombosis: a prospective study of 411 gynecology patients and creation of a prognostic model.

Deep venous thrombosis is a major complication following gynecologic surgery. Assessing a patient's risk of developing deep venous thrombosis is important for patient selection and in choosing appropriate prophylactic methods. Four hundred eleven patients undergoing major gynecologic surgery were evaluated prospectively. All known variables associated with deep venous thrombosis were recorded. Deep venous thrombosis was diagnosed by 125I fibrinogen leg counting of all patients. Univariate analysis of all variables identified the following to be significantly related (P less than .05) to postoperative deep venous thrombosis: a prior history of deep venous thrombosis, leg edema or venous stasis changes, venous varicosities, degree of preoperative ambulation, type of surgery, nonwhite race, recurrent malignancy, prior pelvic radiation therapy, age above 45 years, excessive body weight, intraoperative blood loss, and duration of anesthesia. A stepwise logistic regression analysis of these variables was performed. The following preoperative prognostic factors remained significant: type of surgery, age, leg edema, nonwhite patients, severity of venous varicosities, prior radiation therapy, and prior history of deep venous thrombosis. Duration of anesthesia was also important when intraoperative factors were considered in the analysis. Using these factors, a prognostic model was created and tested. The model resulted in a degree of concordance of 0.82 and allows one to evaluate the risks of postoperative deep venous thrombosis for an individual patient.

Analysis of Variance↗
PubMed1976

Interrelationships between platelets and coagulation in the pathogenesis of venous thrombosis.

The relationship between platelets and coagulation in the pathogenesis of venous thrombosis is reviewed. Platelet coagulant activities, coagulation factors and platelet numbers were measured pre- and postoperatively in patients who underwent hip surgery. About 50% of patients developed venous thrombosis. No significant pre-operative differences were observed in platelet coagulant activities between the group of patients who developed thrombosis and the group who did not. However, platelet counts and coagulation activities were significantly higher postoperatively in patients with thrombosis. The postoperative increase in platelet activity preceded venographically observable thrombosis. The author concludes that in patients with thrombosis there may be an increase of young platelets which are 'hyperactive' and which may trigger thrombosis in areas of stasis. It is not impossible that the increased platelet coagulation activity was the result rather than the cause of thrombosis. However, the temporal sequence of effects observed militate against this possibility.

Blood Cell Count↗
PubMed1995

Protein C deficiency in a controlled series of unselected outpatients: an infrequent but clear risk factor for venous thrombosis (Leiden Thrombophilia Study)

A deficiency of protein C (PC), antithrombin, or protein S is strongly associated with deep-vein thrombosis in selected patients and their families. However, the strength of the association with venous thrombosis in the general population is unknown. This study was a population-based, patient-control study of 474 consecutive outpatients, aged less than 70 years, with a first, objectively diagnosed, episode of venous thrombosis and without an underlying malignant disease, and 474 healthy controls who matched for age and sex. Relative risks were estimated as matched odds ratios. Based on a single measurement, there were 22 (4.6%) patients with a PC deficiency (PC activity, less than 0.67 U/mL or PC antigen, less than 0.33 U/mL when using coumarins). Among the controls, the frequency was 1.5% (seven subjects). Thus, there is a threefold increase in risk of thrombosis in subjects with PC levels below 0.67 or 0.33 U/mL [matched odds ratio, 3.1; 95% confidence interval (CI), 1.4 to 7.0]. When a PC deficiency was based on two repeated measurements, the relative risk for thrombosis increased to 3.8 (95% CI, 1.3 to 10); when it was based on DNA-confirmation, the relative risk increased further to 6.5 (95% CI, 1.8 to 24). In addition, there was a gradient in thrombosis risk, according to PC levels. The results for antithrombin are similar to those for PC, although less pronounced (relative risk, 2.2; 95% CI, 1.0 to 4.7). We could not find an association between reduced total protein S (relative risk, 0.7; 95% CI, 0.3 to 1.8) or free protein S levels (relative risk, 1.6; 95% CI, 0.6 to 4.0) and thrombosis risk. Although not very frequent, PC and antithrombin deficiency are clearly associated with an increase in thrombosis risk.

Adolescent↗
PubMed1994

Factor VII and fibrinogen levels as risk factors for venous thrombosis. A case-control study of plasma levels and DNA polymorphisms--the Leiden Thrombophilia Study (LETS).

The plasma levels of coagulation factor VII and fibrinogen are well known risk factors for arterial thrombosis. We tested the hypothesis that this association also exists for venous thrombosis. Additionally, MspI and HaeIII polymorphisms in the factor VII and fibrinogen genes have recently been reported to be associated with the concentration of both proteins in the plasma. However, no conclusion could be drawn with respect to an increase or decrease in thrombosis risk. We undertook a population-based case-control study, in which 199 patients with a population-based case-control study, in which 199 patients with a first, objectively confirmed episode of deep vein thrombosis, aged less than 70, and without a known malignant disorder were compared to 199 age- and sex-matched healthy controls, to evaluate the clinical importance of these reported findings. For fibrinogen we found a positive level-related association between the plasma fibrinogen level and thrombotic risk. Subjects with a plasma fibrinogen greater than 5 g/l had an almost 4-fold increase of thrombosis risk. The frequencies of the different HaeIII genotypes were out of balance only for the thrombosis patients, with a deficit of the H1H2 genotype. Possession of an H1H2 genotype was associated with a 40% reduction in thrombosis risk. For factor VII, neither the plasma level nor the MspI genotypes were related to deep vein thrombosis, although possession of a M2 allele was clearly associated with significantly lower factor VII levels. The frequencies of the MspI-genotypes were the same for patients and control subjects and exhibited Hardy-Weinberg equilibrium. (ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Frequent asymptomatic pulmonary embolism in patients with deep venous thrombosis.

OBJECTIVE: To determine the frequency of pulmonary embolism in patients admitted for treatment of deep venous thrombosis. DESIGN: An open, multicenter, dose-ranging study to assess the safety and pharmacokinetic characteristics of tissue-type plasminogen activator in deep venous thrombosis and pulmonary embolism. Perfusion and ventilation lung scans, chest roentgenograms, and venograms (in deep venous thrombosis) or pulmonary angiograms (in pulmonary embolism) were obtained before and 24 hours after inception of therapy. Heparin therapy was then administered. SETTINGS: Five tertiary-care hospitals. PATIENTS: All patients with suspected deep venous thrombosis or pulmonary embolism seen from August 1987 through November 1988 entered the study if they met inclusion criteria and if the diagnosis was confirmed by venogram (deep venous thrombosis) or pulmonary angiogram (pulmonary embolism). INTERVENTIONS: All patients received tissue-type plasminogen activator followed by intravenous heparin therapy. MAIN OUTCOME MEASURES: The primary measure was the frequency of pulmonary embolism in patients with deep venous thrombosis who had no symptoms of pulmonary embolism. This was not the original purpose of the study but emerged as an important finding as the data were analyzed. RESULTS: Nearly 40% of patients with deep venous thrombosis who had no symptoms of pulmonary embolism had evidence of pulmonary embolism based on ventilation-perfusion scan and chest roentgenogram findings. CONCLUSIONS: Because all of those considered to have embolism had so-called high-probability scan results, the frequency of embolism reported likely represents the minimum incidence of pulmonary embolism in patients with deep venous thrombosis who have no embolic symptoms. These data emphasize that venous thromboembolism is one disorder.

Angiography↗
PubMed1996

[Value of abdominal ultrasonography in deep venous thrombosis. Retrospective study of 104 patients].

An association between venous thrombosis and cancer was first suggested by Armand Trousseau in 1865 and subsequently confirmed by a number of studies. It was therefore concluded that laboratory tests, chest radiograph and abdominal ultrasonography should be routinely performed on all patients with deep venous thrombosis. The aim of our retrospective study was to detect the clinical relevance of abdominal ultrasonography findings, especially tumors, in patients with deep venous thrombosis of the lower extremities. All patients with deep venous thrombosis hospitalized between 1990 and 1994 in the department of internal medicine of our hospital were registered. Only patients were included in the study who (1) underwent abdominal ultrasonography in our department; (2) had confirmed acute deep venous thrombosis; (3) had no known malignancy. Malignancies which appeared after hospital stay were detected by telephone inquiry among patients and general practitioners in February 1995. Of the 371 patients with deep venous thrombosis 104 were included in the study. We found abnormal ultrasound findings in 68 patients (65%), but only in 23 patients were the findings of clinical relevance, in 12 of whom (12%) there was a connection with deep venous thrombosis. Ultrasound detected 3 malignancies (3%). The overall rate of newly detected malignancies was 10 (10%), of which 6 were detected during hospitalization and 4 afterwards. Based on these results we can recommend routine performance of abdominal ultrasonography on patients with deep venous thrombosis. A literature overview is given.

Abdomen↗
PubMed1996

[Significance of hereditary thrombophilia for risk of thrombosis with oral contraceptives].

Oral contraceptives increase the natural incidence of venous thromboses of 1-2/10,000 women per year 3-to 4fold. Recent investigations have shown that during intake of desogestrel or gestodene containing formulations the risk is twice that with older low-dose ovulation inhibitors. This difference is larger in first time users than in women who had previously used an oral contraceptive. During pregnancy, the incidence of thromboses rises up to 10/10,000 women-years and post partum up to 40/10,000 women-years. In about 60 % of thromboses no causal explanation can be found. It is suggested that in 40 % of all cases an inherited thrombophilia is present. Among the hereditary types of thrombophilia, the resistance against activated protein C (APC-resistance) represents nearly 50 %, while altogether 15 to 20 % is based on a deficiency of antithrombin III, protein C or protein S. APC-resistance the prevalence of which is 3-5 % in the general population, increases the risk of thrombosis 8fold and in users of oral contraceptives 35fold. Protein C-deficiency (prevalence 0.1-0.5 %) increases the risk of thrombosis 9fold and in users of oral contraceptives 15fold, while antithrombin III-deficiency (prevalence 0.02-0.05 %) enhances the risk in pill-users 8fold. Ovulation inhibitors do not influence risk of thrombosis in women with protein S-deficiency. Antiphospholipid-antibodies the concentration of which may increase during treatment with oral contraceptives, represent a considerably enhanced risk of thrombosis, too. A positive family history (before age of 40 years) indicates an inherent thrombophilia. In these risk groups, the cost/benefit ratio of a selective screening is unfavorable, as at most 70 % of the hereditary thrombophilias can be diagnosed by laboratory analysis, and only very few patients will actually experience a thrombotic event: only 3 of 1000 carriers of APC-resistance will suffer from thrombosis during oral contraception per year. On the other hand, a negative result of laboratory tests does not exclude a hereditary thrombophilic disorder which as yet cannot be substantiated. It is not yet clarified whether a selective screening is superior to a careful assessment of individual and family history. A general screening cannot be justified because of the unfavorable cost/benefit ratio. If the individual or family history or pathological laboratory parameters indicate an enhanced risk of thrombosis, this risk has to be carefully weighed against the consequences of discontinuation of pill use. Those few individuals with risk factors who will experience a thrombosis, cannot be identified in advance. If in patients with thrombophilic disorders and/or other risk factors the use of oral contraceptives represents a particularly high risk, other contraceptive methods should be taken into consideration. If a patient with risk factors decides for the use of oral contraceptives, she has to be informed that in the case of symptoms indicating a thrombosis, the physician has to be consulted immediately. The earlier an appropriate therapy is initiated, the more effectively an acute pulmonary emboli or permanent damages, e.g. the post-thrombotic syndrome, can be prevented.

Adult↗
PubMed1997

[Clinical diagnosis of deep venous thrombosis after hip replacement surgery].

Hip replacement surgery is associated with a high frequency of postoperative deep vein thrombosis. This prospective study was performed in order to investigate if routine bedside questioning and examination by the visiting doctor could reveal deep vein thrombosis in the legs of patients who had received a hip replacement. 258 patients were evaluated. Thromboprophylaxis (dextran-70, low molecular weight heparin and graded elastic stockings) was given during the first week after operation. Bilateral venography was performed in all patients on day seven after operation, and showed an overall deep vein thrombosis incidence of 16%. The visiting doctors had not suspected deep vein thrombosis in any of the patients. This may have been because postoperative painful and swollen legs effectively masked any signs and symptoms of deep vein thrombosis. Our results show that deep vein thrombosis during the first week after hip replacement surgery cannot be discovered by clinical diagnostics. The high subclinical frequency of deep vein thrombosis indicates the importance of improving thromboprophylaxis in order to further minimise the occurrence of deep vein thrombosis and the risk of thromboembolic complications.

Aged↗
PubMedDate not supplied

The utility and cost-effectiveness of D-dimer measurements in the diagnosis of deep vein thrombosis.

BACKGROUND AND OBJECTIVE: The potential utility of D-dimer measurements for the diagnosis of deep vein thrombosis became evident soon after the development of reliable commercial assays. The purpose of this review is to outline some critical aspects affecting cost-effectiveness of D-dimer measurements in the diagnosis of deep vein thrombosis (DVT). METHODS: The authors have been working in this field contributing original papers whose data have been used for this study. In addition, the material analyzed in this article includes papers published in the journals covered by the Science Citation Index and Medline. RESULTS: D-dimer levels are very sensitive to the process of fibrin formation/dissolution occurring with ongoing thrombosis. However, they may not be highly specific for venous thromboembolism as they are influenced by the presence of comorbid conditions potentially elevating plasma D-dimer (cancer, surgery, infectious diseases). In addition, commercially available ELISA assays, although quantitative and reproducible, cannot be used under emergency conditions because they are time-consuming and suited for batch-processing of plasma samples. Recently, new assays have been introduced which permit fast and quantitative D-dimer estimations in individual patients. We have evaluated the utility of two new rapid assays (LPIA D-dimer. Mitsubishi, and VIDAS D-DIMER, bio-Merieux) in combination with compression real-time-B-mode ultrasonography for the detection of deep vein thrombosis in asymptomatic patients following elective hip replacement and in patients with clinically suspected deep vein thrombosis. In both settings, we identified cut-off values with optimal sensitivity which allow exclusion of deep vein thrombosis in a considerable percentage of patients, with substantial sparing of economic resources. In fact, based on a cost-effectiveness analysis, a diagnostic algorithm combining D-dimers measurement and compression ultrasonography would result in cost-savings ranging from 5% to 55% in patients with high or low clinical pretest probability respectively. However, the specificity of D-dimer measurements for deep vein thrombosis was much higher in symptomatic than in asymptomatic patients. Choice of the cut-off value proved to be dependent on the method as well as on the patient populations studied. CONCLUSIONS: The cost-effectiveness of D-dimers measurement in the diagnosis of asymptomatic DVT remains questionable. Conversely, our data strongly support the utility of D-dimers determinations in the diagnosis of symptomatic DVT. In terms of sparing economic resources, the introduction in the clinical laboratory of the rapid quantitative assays would be highly convenient, because they avoid a source of bias in the interpretation of D-dimers results, are easy to perform and do not require dedicated personnel or instrumentation. Prospective management studies validating the utility of D-dimer measurement in the diagnosis of deep vein thrombosis are urgently needed.

Costs and Cost Analysis↗
PubMed2000

Antithrombotic and hemostatic capacity of factor Xa versus thrombin inhibitors in models of venous and arteriovenous thrombosis.

Thrombin plays a central role in venous and arterial thrombosis. We utilized two different rabbit models of in vivo thrombosis to investigate the effect of inhibitors of thrombin generation and thrombin activity. The agents tested were specific inhibitors of factor Xa (fXa) [N2-[(phenylmethyl)sulfonyl]-D-arginyl-N-[(1S)-4-[(aminoiminomethyl++ +)a mino]-1-(2-thiazolylcarbonyl)butyl]-glycinamide (C921-78)] and thrombin [D-phenylalanyl-N-[4-[(aminoiminomethyl)amino]-1-(chloroacetyl)but yl]-L-prolinamide (PPACK)], as well as drugs that affect both thrombin and fXa, unfractionated and low molecular weight (enoxaparin) heparin. The agents administered as constant intravenous infusion were evaluated for antithrombotic efficacy in anesthetized rabbits. All four agents were capable of dose dependent inhibition of thrombosis in venous and arteriovenous thrombosis models. However, due to the more aggressive nature of thrombotic stimulation in the arteriovenous shunt model, complete cessation of thrombus growth was not achieved for any of the agents at the doses tested. Comparison between the agents focused on the differences in extension of coagulation parameters (activated partial thromboplastin time, prothrombin time, thrombin clotting time), changes in hematological parameters, and extension of rabbit cuticle bleeding time at doses required to produce maximum inhibition in the thrombosis models. In the venous thrombosis model at the maximally effective dose, C921-78 had minimal extension of ex vivo clotting parameters, while enoxaparin and unfractionated heparin demonstrated a two to sevenfold increase in activated partial thromboplastin times, and PPACK had a threefold extension of thrombin clotting times. In addition, unlike the other three agents, which exhibited no significant changes in hematological parameters, PPACK demonstrated dose dependent thrombocytopenia. A standardized cuticle bleeding time was used as a measure of perturbation of hemostasis. The agents were evaluated for significant increases in bleeding time at doses up to eight times that needed to completely inhibit venous thrombus formation. Unfractionated heparin displayed a significant bleeding time effect at the dose required to inhibit venous thrombosis (100 u/kg+2 u/kg/min). Enoxaparin and PPACK caused significant bleeding time extensions at four times the fully efficacious venous dose (800 u/kg+8 u/kg/min and 30 microg/kg/min). By contrast, C921-78 did not significantly increase bleeding time even at eight times the maximally effective dose (240 microg/kg+7.2 microg/kg/min). Our results demonstrate that specific inhibition of fXa can be utilized to derive potent antithrombotic activity without disrupting extravascular hemostasis.

Amino Acid Chloromethyl Ketones↗
PubMed1998

Antithrombotic effects of YM-60828 in three thrombosis models in guinea pigs.

The antithrombotic effects of a novel factor Xa inhibitor, YM-60828 ([N-[4-[(1-acetimidoyl-4-piperidyl)oxy]phenyl]-N-[(7-amidino-2-nap hthyl)methyl]sulfamoyl]acetic acid dihydrochloride), in three thrombosis models in guinea pigs were studied in comparison with its effect on bleeding time. The antithrombotic effects of YM-60828 were most pronounced in the venous thrombosis and the arterio-venous shunt models but YM-60828 showed 10-fold weaker effects in the carotid thrombosis model. However, YM-60828 prolonged bleeding time at a much higher dose than that required in all thrombosis models. In conclusion, YM-60828 exerted its antithrombotic effects without prolonging bleeding time in all thrombosis models and may be of clinical value not only in venous thrombosis but also in arterial thrombosis.

Animals↗