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PubMed1993

Cerebral blood flow alterations in a rat model of cerebral sinus thrombosis.

BACKGROUND AND PURPOSE: Outcome from sinus vein thrombosis is very variable, with symptoms from headache to coma. Experimental findings suggest that an involvement of cortical veins is necessary to affect the cerebral microcirculation. Laser Doppler flowmetry was used to investigate the regional and temporal changes in local cortical blood flow after experimental occlusion and thrombosis of the superior sagittal sinus and tributary cortical veins in rats. METHODS: Thrombosis was induced by slow injection of kaolin-cephalin suspension after frontal and caudal ligation of the sagittal sinus in rats. Local cerebral blood flow was measured by laser Doppler flowmetry and correlated with parenchymal damage found 24 hours after induction of thrombosis. RESULTS: Local cerebral blood flow 1 hour after sinus occlusion and induction of thrombosis had decreased to 60.92 +/- 29.05% (p < 0.01); however, there was a large variability among individual animals. Only five of 12 rats showed histological damage and intracerebral hemorrhages 24 hours after induction of thrombosis. A subgroup analysis revealed that parenchymal damage occurred in concurrence with reduced blood flow values after sinus ligation and injection of the thrombogenic material. Sinus thrombosis alone, without alteration of blood flow, did not cause tissue necrosis. CONCLUSIONS: The data support the contention that sinus vein thrombosis evolves gradually, with major symptoms occurring only if the thrombus expands from the sinus into bridging and cortical veins. Collateral venous outflow pathways are thereby occluded, and local blood flow may become reduced to and below the ischemic threshold.

Animals↗
PubMed1998

Association of subclavian and jugular vein thrombosis: color doppler sonographic evaluation.

In case of clinical symptoms of subclavian vein thrombosis a phlebographic or color Doppler sonographic investigation should be performed. Phlebography is a sensitive method to exclude the thrombosis in the subclavian vein but not in the jugular vein. Color Doppler sonography additionally gives information about the surrounding tissue and the jugular vein. The authors analyze their color Doppler sonographic data, first, to evaluate the association of internal jugular and subclavian vein thrombosis and, second, to demonstrate the necessity for a color Doppler investigation. Of 213 patients who suffered from a thrombosis, 93 had a subclavian vein thrombosis, 64 had a combined thrombosis in the internal jugular and subclavian vein, and 56 had an isolated internal jugular vein thrombosis. There is a high association between subclavian and internal jugular vein thrombosis, and a color Doppler investigation of both the subclavian and internal jugular veins is necessary.

Adult↗
PubMed2004

Neonatal arterial ischemic stroke and cerebral sinovenous thrombosis are more commonly diagnosed in boys.

The risk factors for arterial ischemic stroke and cerebral sinovenous thrombosis in neonates are not well understood. We looked at gender, birthweight, and gestational age in neonates with arterial ischemic stroke and cerebral sinovenous thrombosis to see if there were trends suggesting that these were risk factors. We identified neonates with a gestational age at birth > or = 36 weeks and a diagnosis of arterial ischemic stroke or cerebral sinovenous thrombosis made by computed tomography or magnetic resonance imaging during the neonatal period from a consecutive cohort study of children with arterial ischemic stroke and cerebral sinovenous thrombosis in Ontario. Data on gender, birthweight, and gestational age were obtained by health record review. Sixty-six children with neonatal arterial ischemic stroke were identified. Forty-one (62.1%; 95% CI 49.3-73.8%) were male. Thirty-two children with neonatal cerebral sinovenous thrombosis were identified. Twenty-five (78.1%; 95% CI 60.0-90.7%) were male. One male child was identified with both arterial ischemic stroke and cerebral sinovenous thrombosis. There was a trend toward higher than average birthweights among neonates with arterial ischemic stroke and a trend toward older gestational age in female neonates with arterial ischemic stroke. Our data suggest that neonatal arterial ischemic stroke and cerebral sinovenous thrombosis are more commonly diagnosed in boys. The slightly larger size of male neonates may be contributory in arterial ischemic stroke. It is not known whether boys are at higher risk of developing arterial ischemic stroke and cerebral sinovenous thrombosis or are simply more likely to present with symptoms resulting in diagnosis. These issues need further study.

Birth Weight↗
PubMedDate not supplied

Efficacy of deep venous thrombosis prophylaxis in the medical intensive care unit.

The purpose of this study was to determine the incidence of deep venous thrombosis in medical intensive care unit patients receiving deep venous thrombosis prophylaxis. This was a prospective cohort study of 141 consecutive adult patients anticipated to remain in the medical intensive care unit for >48 hours. Deep venous thrombosis prophylaxis was provided using subcutaneous unfractionated heparin or a sequential compression device according to risk-stratified protocol. Compression ultrasound was performed. Fourteen patients (9.9%) developed deep venous thrombosis on follow-up studies. Incidence of deep venous thrombosis was 7.9% per person year (95% confidence interval, 4.8-12.8). Two of 14 developed pulmonary embolism. Eight patients required full anticoagulation with intravenous heparin or coumadin. In-hospital mortality was similar in both groups. Patients with deep venous thrombosis had a statistically higher risk of pulmonary embolism: 14.2% (95% confidence interval, 2.0-43.0) versus 0.0% (95% confidence interval, 0-3; P = .009). Incidence of deep venous thrombosis is high in medical intensive care unit patients receiving standard prophylaxis. Adherence to strict deep venous thrombosis prophylaxis protocol and exploration of other prophylaxis regimens should be pursued.

Adult↗
PubMed2000

Severity of illness, outcomes, and resource use in elderly cancer patients with deep venous thrombosis.

Low-molecular-weight heparins provide new options for outpatient management of deep venous thrombosis. Because elderly patients with cancer are at increased risk of developing deep venous thrombosis, outpatient therapy for treatment of deep venous thrombosis may be important in this population. We compared the severity of illness, outcomes, and cost of deep venous thrombosis in elderly patients with cancer to those seen in younger patients with cancer. We examined all 766 episodes of deep venous thrombosis treated at the University of Texas M.D. Anderson Cancer Center between January 1, 1994 and December 31, 1996. Severity of illness level and predicted risks of mortality and readmission were obtained from a commercially available disease staging system (Inforum System). Observed outcomes and cost were based on data collected from the 766 episodes of deep venous thrombosis at our institution. One hundred nineteen (16%) episodes of deep venous thrombosis occurred in patients 70 years of age or older. The severity of illness scale (1-5, least-most severe) were identical (3.7) in the 3 groups studied (< 70 years, 70-79, years and > or = 80 years). The predicted risk of death during hospitalization (6%, 9%, 8%, respectively, by group, P = 0.12) and readmission in 30 days (5%, 4%, 3%, respectively, P = 0.04) were similar among the groups. The observed death rates during hospitalization were 5%, 6%, and 6%, respectively (P = 0.91), and the rates of hospitalization for deep venous thrombosis recurrence were 22%, 16%, and 28%, respectively (P = 0.27). The similarities in outcomes and resource use between elderly and younger patients suggest that elderly patients with cancer are not at greater risk of serious clinical outcomes or a prolonged clinical course. There is significant potential for outpatient management of these patients.

Aged↗
PubMed2004

Venous thrombosis among patients with AIDS.

Thrombosis has been considered an uncommon complication in patients with AIDS. In a 42-month period, 28 adult male homosexuals with AIDS experienced 34 thrombotic events. All but three received HAART regimen, two a successful round of double nucleoside analog therapy, and one patient received no treatment. Median age of group was 38.5 years (range, 24 to 56 years). Median time from HIV infection to thrombosis was 40.5 months (range, 3 to 108 months). No patient had previous thrombosis, family history of thrombosis, or prothrombotic conditions. There were 31 deep vein thromboses, two pulmonary thromboembolisms, and one renal vein thrombosis. Six patients had two thrombotic events. The rate of thrombosis during the 42-month study period was 1.52% (cumulative incidence = 0.30%/year), while the rate of thrombosis in 600 patients before the era of protease inhibitor therapy was 0.33% (cumulative incidence approximately 0.055%/year) (p < 0.001). Due to high incidence of thrombotic recurrences and hemorrhagic complications while using oral anticoagulants, acetylsalicylic acid was initiated; no thrombotic episodes were recorded while using this drug. Protein C and protein S deficiency were found in nine and two patients, respectively. Two patients had lupus anticoagulant and two activated protein C resistance (APCR) without FV Leiden mutation (APCR test was negative after initial screening). Fifteen patients had no thrombophilic abnormalities. These data suggest that protease inhibitors could be a risk factor for venous thrombosis not due to thrombophilic abnormalities but likely related to abnormalities in platelets or endothelium.

Acquired Immunodeficiency Syndrome↗
PubMed2002

A new locus on chromosome 18 that influences normal variation in activated protein C resistance phenotype and factor VIII activity and its relation to thrombosis susceptibility.

Activated protein C resistance (APCR) is the most prevalent risk factor for thrombosis, accounting for 20% to 60% of familial thrombophilia. A mutation in the F5 gene, factor V Leiden (FVL), is a major determinant of pathological APCR in some populations. However, APCR predicts risk for thrombosis independently of FVL. This suggests that other genetic factors may influence risk of thrombosis through quantitative variation in APCR. To search for these unknown loci, we conducted a genome-wide linkage screen for genes affecting normal variation in APCR in the 21 Spanish families from the Genetic Analysis of Idiopathic Thrombophilia (GAIT) project. Conditional on FVL, the strongest linkage signal for APCR was found on chromosome 18 near D18S53. Bivariate linkage analyses with a genetically correlated trait, levels of clotting factor VIII, strengthened evidence for the chromosome 18 quantitative trait locus (QTL; logarithm of the odds [LOD], 4.5; P = 3.08 x 10(-5)). However, the region on chromosome 1 that contains the F5 structural gene showed little evidence of linkage to APCR (LOD, < 1). This indicates that apart from the FVL, the F5 locus itself plays a relatively minor role in normal variation in APCR, including the HR2 haplotype polymorphisms. A second bivariate analysis of APCR with thrombosis liability suggested that this QTL also influences the risk of thrombosis (P =.0016). These results indicate that a locus on chromosome 18 pleiotropically influences normal variation in the APCR phenotype and factor VIII (FVIII) levels as well as susceptibility to thrombosis. Importantly, there are no known thrombosis-related candidate genes in this region, implying that this QTL represents a completely novel thrombosis risk factor.

Activated Protein C Resistance↗
PubMed2003

Primary prophylaxis with warfarin prevents thrombosis in paroxysmal nocturnal hemoglobinuria (PNH).

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia in which venous thrombosis is the most common cause of death. Here we address the risk factors for thrombosis and the role of warfarin prophylaxis in PNH. The median follow-up of 163 PNH patients was 6 years (range, 0.2-38 years). Of the patients, 29 suffered thromboses, with a 10-year incidence of 23%. There were 9 patients who presented with thrombosis, and in the remainder the median time to thrombosis was 4.75 years (range, 3 months-15 years). The 10-year risk of thrombosis in patients with large PNH clones (PNH granulocytes > 50%) was 44% compared with 5.8% with small clones (P <.01). Patients with large PNH clones and no contraindication to anticoagulation were offered warfarin. There were no thromboses in the 39 patients who received primary prophylaxis. In comparison, 56 patients with large clones and not taking warfarin had a 10-year thrombosis rate of 36.5% (P =.01). There were 2 serious hemorrhages in more than 100 patient-years of warfarin therapy. Large PNH granulocyte clones are predictive of venous thrombosis, although the exact cut-off for clone size is still to be determined. Primary prophylaxis with warfarin in PNH prevents thrombosis with acceptable risks.

Clone Cells↗
PubMed2003

Probing antiphospholipid-mediated thrombosis: the interplay between anticardiolipin antibodies and endothelial cells.

The association of antiphospholipid (aPL) antibodies with thrombosis in patients with antiphospholipid syndrome (APS) is well documented in humans and in animal studies. However, the mechanisms by which aPL antibodies induce thrombosis are the subject of much current study. It has been suggested that aPL may activate endothelial cells (ECs), thus creating a hypercoagulable state that precedes and contributes to thrombosis in patients with APS. Several studies have shown that aPL upregulate ECs' adhesion molecules (CAMs): intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (E-sel) or induce tissue factor (TF) in monocytes in vitro. Similarly, the incubation of EC with antibodies reacting with beta2glycoprotein I (beta2GPI) has been shown to induce EC activation with concomitant upregulation of CAMs, IL-6 production and alteration of prostaglandin metabolism. Our group has shown that aPL-mediated upregulation of adhesion molecules on ECs correlates with an increased adhesion of leukocytes to endothelium in the microcirculation of mouse cremaster muscle, a n indication of EC activation in vivo, andwith enhanced thrombosis in vivo. In another series of studies, investigators have shown that upregulation of expression of adhesion molecules by some murine monoclonal anti-beta2glycoprotein I (anti-beta2GPI) antibodies correlated with fetal resorption in mice in vivo. More recently, one study showed that the anti-hypercholesterolaemic drug fluvastatin inhibited the aPL-mediated enhanced adhesion of monocytes to ECs in vitro. Data from our laboratories indicate that fluvastatin also reverses thrombus formation and activation of EC induced by aPL in an in vivo mouse model. As additional support for the hypothesis that aPL antibodies activate ECs and may create an hypercoagulable state in APS patients, two recent studies indicated that levels of soluble ICAM-1 and VCAM-1 were significantly increased in the plasma of patients with APS and recurrent thrombosis. Furthermore, studies utilizing knockout mice and specific monoclonal anti-VCAM-1 antibodies have demonstrated that expression of ICAM-1, P-selectin, E-selectin and VCAM-1 are important in in vivo aPL-mediated thrombosis and EC activation in mice. Recent data suggests that aPL antibodies also induce expression of TF not only in monocytes but in ECs. Hence, the interference of aPL with the TF mechanism may be another important mechanism by which these antibodies create a hypercoagulable state and prone patients to thrombosis. Specifically, how aPL alters EC activation state and the molecular and intracellular mechanisms involved have not yet been defined. APL may interact with specific cell surface receptors (proteins and/or lipids) induce signals that have consequences downstream, and that ultimately will result in upregulation of cell surface proteins (i.e., CAMs and TF) and subsequently induce EC activation. In that regard, our group recently showed that aPL-mediated upregulation of adhesion molecules in ECs is preceded by activation of the nuclear factor kappa B (NFkappaB). Other intracellular mechanisms triggered by aPL are not completely understood and are the subject of current investigation. In conclusion, studies suggest that activation of ECs by aPL is an important mechanism that may precede thrombus formation in patients with APS. Hence, the interplay between aPL antibodies and ECs is important inthe pathogenesis of thrombosis in APS.

Animals↗
PubMed2005

Thrombophilia and the risk for hemodialysis vascular access thrombosis.

Vascular access thrombosis is the most common and costly complication in hemodialysis patients. The role of thrombophilia in access thrombosis is not established. A case-control study was conducted of 419 hemodialysis patients to determine whether thrombophilia was associated with arteriovenous fistula or graft thrombosis. Participants were enrolled from three in-center and five satellite dialysis units associated with a Canadian academic health science center that provides dialysis services in a catchment area of one million. Patients were tested for factor V Leiden, prothrombin gene mutation, factor XIII genotype, methylenetetrahydrofolate reductase genotype, lupus anticoagulant, anticardiolipin antibody, factor VIII, homocysteine, and lipoprotein (a) concentrations. Overall, 59 (55%) patients with access thrombosis had at least one thrombophilia compared with 122 (39%) patients without access thrombosis (unadjusted odds ratio [OR], 1.91; 95% confidence interval [CI], 1.23 to 2.98). After controlling for important risk factors, the association between any thrombophilia and access thrombosis remained (adjusted OR, 2.42; 95% CI, 1.47 to 3.99). For each additional thrombophilic disorder, the odds of access thrombosis increased significantly (adjusted OR, 1.87; 95% CI, 1.34 to 2.61). This study suggests that thrombophilia is associated with access thrombosis in dialysis patients. Large, multicenter, prospective cohort studies are needed to confirm the observations from this case-control study.

Aged↗
PubMed1998

Comparison of the use of a foot pump with the use of low-molecular-weight heparin for the prevention of deep-vein thrombosis after total hip replacement. A prospective, randomized trial.

We conducted a prospective, randomized trial to compare the safety and effectiveness of the A-V Impulse System foot pump with that of low-molecular-weight heparin for reducing the prevalence of deep-vein thrombosis after total hip replacement. Of 290 patients who were to have a primary total hip replacement, 143 were randomized to receive enoxaparin (forty milligrams daily) for seven days after the operation and 147, to use the foot pump for seven days. The primary outcome measure was the prevalence of deep-vein thrombosis, as determined by venography on the sixth, seventh, or eighth postoperative day. Secondary outcome measures included transfusion requirements, intraoperative blood loss, postoperative drainage, blood-loss index, appearance of the site of the wound according to a subjective visual-analog scale, and swelling of the thigh. The patients' compliance with the regimen for use of the foot pump was monitored with an internal timing device, and their acceptance of the device was assessed with a questionnaire. Symptoms consistent with pulmonary embolism were investigated with ventilation-perfusion scanning. The patients were contacted later for detection of symptoms of venous thromboembolism that may have occurred during the first three months after discharge from the hospital. Venography was performed on 274 patients: 136 who used the foot pump and 138 who received enoxaparin. Deep-vein thrombosis was detected in twenty-four (18 per cent) of the patients who used the foot pump compared with eighteen patients (13 per cent) who received enoxaparin (95 per cent confidence interval for the difference in proportions, -3.9 to +13.0 per cent). Thrombosis in the calf was found in seven patients (5 per cent) in the former group compared with six patients (4 per cent) in the latter (95 per cent confidence interval for the difference, -4.2 to +5.8 per cent), and proximal thrombosis was observed in seventeen patients (13 per cent) in the former group compared with twelve patients (9 per cent) in the latter (95 per cent confidence interval for the difference, -3.5 to +11.1 per cent). None of these differences was significant. No patient in either group had major proximal deep-vein thrombosis; all proximal thrombi were isolated entities involving the femoral valve cusp and were of unknown importance. One patient who used the foot pump had a non-fatal pulmonary embolism. One patient who received enoxaparin had a symptomatic deep-vein thrombosis during hospitalization. Two patients (one from each group [0.7 per cent]) were readmitted to the hospital because of a symptomatic deep-vein thrombosis despite normal venographic findings at the time of discharge. There was no difference in the transfusion requirements or the intraoperative blood loss between the two groups. There were more soft-tissue side effects in the patients who received enoxaparin than in those who used the foot pump: there was more bruising of the thigh and oozing of the wound (p < 0.001 for each), postoperative drainage (578 compared with 492 milliliters; p = 0.014), and swelling of the thigh (twenty compared with ten millimeters; p = 0.03). Of 124 patients who used the foot pump and were asked about the acceptability of the device, fourteen (11 per cent) said that it was uncomfortable, twenty-one (17 per cent) reported sleep disturbance, and four (3 per cent) stated that they had stopped using the device. Conversely, ten (8 per cent) found it relaxing. We concluded that the foot pump is a suitable alternative to low-molecular-weight heparin for prophylaxis against thromboembolism after total hip replacement and that it produces fewer soft-tissue side effects. Tolerance of the device is a problem for some patients.

Aged↗
PubMed2006

Proximal deep vein thrombosis after hip replacement for oncologic indications.

BACKGROUND: Patients with cancer who undergo surgery about the hip are at increased risk for the development of deep vein thrombosis. We implemented a program of chemical and mechanical prophylaxis to prevent this problem. This study was performed to assess the effectiveness of that program. METHODS: Eighty-seven consecutive patients with an active malignant tumor who underwent hip replacement surgery at our institution over a two-year period were included in the study. All patients were treated with intermittent pneumatic compression devices. Seventy-eight patients received anticoagulants, and nine did not. Postoperative surveillance for proximal deep vein thrombosis was routinely performed on all patients with duplex Doppler ultrasonography. RESULTS: Four patients had proximal deep vein thrombosis, and one patient, who did not receive anticoagulation, had a nonfatal pulmonary embolism. The use of prophylactic low-molecular-weight heparin (dalteparin) was associated with a 4% rate of proximal deep vein thrombosis (three of seventy-eight patients). Proximal deep vein thrombosis developed in three of eight patients with pelvic disease, one of nineteen patients with femoral disease, and zero of sixty patients with hip disease (p < 0.00001). The prevalence of proximal deep vein thrombosis was significantly higher (p < 0.02) following replacements in patients with sarcoma (three of twenty-one) than it was after replacements in patients with carcinoma (zero of fifty-seven) or hematologic malignant disease (one of nine). On multivariate analysis, only the location of the disease (the pelvis, femur, or hip) was found to be independently significant for an association with deep vein thrombosis. A wound complication developed in four of twenty-one patients with sarcoma and no patient with carcinoma or hematologic malignant disease (p < 0.001). The pathologic type was the only factor studied that was independently significant for an association with wound complications on multivariate analysis. CONCLUSIONS: The rate of proximal deep vein thrombosis in patients who had undergone hip replacement for oncologic indications was low when the use of an intermittent pneumatic compression device was supplemented with prophylaxis with low-molecular-weight heparin.

Aged, 80 and over↗
PubMed2004

Hypercoagulability in renal transplant recipients. Identifying patients at risk of renal allograft thrombosis and evaluating strategies for prevention.

Renal transplantation improves survival and quality of life for patients with end-stage renal disease (ESRD). Improvements in immunosuppressive therapy have reduced early allograft loss due to acute rejection to very low levels. Early allograft loss, due to acute thrombotic complications, remains a constant and proportionally increasing complication of renal transplantation. Identifying risk factor(s) for thrombosis amenable to preventive strategies has been elusive. Epidemiological studies have attempted to define risk in terms of modifiable (drugs, dialysis modality, surgical procedure) and non-modifiable (age, diabetes mellitus, vascular anomalies) factors, or identify changes in coagulation or fibrinolysis promoting a more thrombotic state. Most recently the evolution of thrombophilia research has established the potential for inherited hypercoagulability to predispose to acute allograft thrombosis. Inheritance of the factor V Leiden (FVL), prothrombin G20210A mutation, or the presence of antiphospholipid antibodies (APA) may increase the risk of renal allograft thrombosis approximately 3-fold in selected patients. Patients with ESRD due to systemic lupus erythematosus (SLE) appear at particularly high risk of thrombosis, especially if they have either APA or detectable beta(2)-glycoprotein-1. Data for other hypercoagulable states such as hyperhomocystinemia or the C677T polymorphism of the methylenetetrahydrofolate reductase gene are deficient. Patients with APA, FVL, or prothrombin G20210A mutation also appear to have greater graft loss due to vascular rejection, possibly reflecting immunological injury upon the vascular wall exacerbated or induced by the prothrombotic state. While substantial in vitro data suggest cyclosporine is prothrombotic, an independent clinical association with allograft thrombosis is unproven. Interventions to reduce thrombotic risk including heparin, warfarin, and aspirin have been evaluated in both selected high-risk groups (heparin and warfarin) and unselected populations (heparin and aspirin). In unselected patients at low clinical risk, aspirin (75-150 mg/day) with or without a short period of unfractionated heparin (5000U twice a day for 5 days) appears to reduce the risk of renal allograft thrombosis significantly with a low risk of bleeding, especially when compared with low molecular weight heparins which risk accumulation in renal failure. In high-risk groups (identified thrombophilic risk factor, previous thrombosis, or SLE) longer period of heparin, with or without aspirin and maintenance with warfarin, should be considered. Re-transplantation following graft loss due to vascular thrombosis can be undertaken with a low risk of recurrence. Further prospective studies evaluating both putative risk factors and intervention strategies are required to determine whether routine clinical screening for thrombophilic factors is justified.

Antibodies, Antiphospholipid↗
PubMed1999

Assessment of deep venous thrombosis using routine pelvic CT.

OBJECTIVE: The purpose of this study was to assess routine pelvic CT both for accuracy in diagnosis of deep venous thrombosis and for frequency of detection of clinically unsuspected pelvic thrombi. MATERIALS AND METHODS: We reviewed the CT records of patients who had undergone pelvic CT during a 6-month period and cross-referenced these records to reports on lower extremity venous sonography to identify patients who had undergone this test within 1 week of pelvic CT. We compared the frequency and location of venous thrombosis revealed through these two tests. To identify unsuspected deep venous thrombosis detected on pelvic CT, we reviewed the charts of patients for whom a clot was reported to determine if it had been clinically suspected before CT. RESULTS: Among the 52 patients who underwent both CT and lower extremity venous sonography, the findings were in agreement for 49 (94%). The techniques disagreed for three patients; two patients had deep venous thrombosis detected on sonography but not on CT and the other had a clot detected on CT but not on sonography. The prevalence of unsuspected deep venous thrombosis detected by CT was 1.1%, and 73% of these patients underwent anticoagulation therapy without further confirmatory tests. CONCLUSION: Unsuspected deep venous thrombosis is commonly seen on routine pelvic CT and should be carefully sought during such examinations. CT appears to be relatively accurate in the detection of deep venous thrombosis. Thus, CT venography combined with pulmonary CT angiography may significantly increase the percentage of patients who are appropriately treated for thromboembolic disease because both deep venous thrombosis and pulmonary emboli can be identified by this combined test.

Contrast Media↗
PubMed2002

Deep vein thrombosis: can a second sonographic examination be avoided?

OBJECTIVE: Our objective was to determine the prevalence of deep vein thrombosis in symptomatic patients and its distribution based on the assessment of prior clinical probability. We evaluated whether repeated sonography is necessary in patients with either intermediate or high clinical probability for deep vein thrombosis after an initial examination with negative findings. SUBJECTS AND METHODS: We prospectively evaluated 438 consecutive patients with clinical suggestion of deep vein thrombosis of the lower limbs, classified according to the prior clinical probability (high, intermediate, low). Sonography with positive findings was diagnostic for deep vein thrombosis. Negative findings in low-risk patients excluded thrombosis. Patients with intermediate or high clinical risk whose initial sonographic examination showed negative findings underwent a second examination after 1 week. RESULTS: Of the 438 patients with clinical symptoms, 112 patients (26%) had positive findings on sonography, and 326 (74%) had negative findings. Of the 202 intermediate- and high-risk patients with negative initial sonography, 140 patients underwent a single follow-up sonographic examination 1 week later. In three cases, findings were positive for deep vein thrombosis. Two other patients developed pulmonary embolism. Sonographic follow-up increased the detection of deep vein thrombosis in the patients with intermediate or high probability from 32.5% to 33.5%; the prevalence of thromboembolic disease in this group was 34%. CONCLUSION: The prevalence of deep vein thrombosis studied by sonography in the patients with intermediate or high clinical risk was 33.5%. Initial sonography revealed a 32.5% prevalence, and a second examination 1 week later detected an additional 1%. Sonography did not reveal 0.5% of thromboembolic events. Our results do not justify a routine second scanning at 1 week.

Adolescent↗
PubMed2004

Relationship between various patterns of transient increased hepatic attenuation on CT and portal vein thrombosis related to acute cholecystitis.

OBJECTIVE: We sought to investigate the prevalence of portal vein thrombosis in patients with acute cholecystitis and the relationship between portal vein thrombosis and the various patterns of transient increased hepatic attenuation on CT. MATERIALS AND METHODS: We studied 72 of 107 patients with acute cholecystitis who, during a 3-year period, underwent dual-phase contrast-enhanced CT before percutaneous cholecystostomy or cholecystectomy. CT scans were retrospectively reviewed for the presence of portal vein thrombosis and location of the thrombi and for patterns of transient increased hepatic attenuation, which were classified as either pericholecystic, segmental, or mixed. RESULTS: Portal vein thrombi (two in hepatic segment IV, three in the left portal vein, and one in the right posterior portal vein) were found in six (8.3%) of 72 patients, and in those patients, transient increased attenuation with a segmental (five patients) or mixed (one patient) pattern was seen on CT. The pattern of transient increased attenuation in the 54 patients without portal vein thrombosis was pericholecystic in 41 (75.9%) and mixed in 13 (24.1%). Nineteen patients had segmental distribution (segmental or mixed pattern) that in 31.6% (6/19) of the patients was associated with portal vein thrombosis. Segmental distribution was more frequently found in those patients who had acute cholecystitis with portal vein thrombosis than in those who had only acute cholecystitis (p = 0.001). CONCLUSION: In patients with acute cholecystitis, portal vein thrombosis is not uncommon. Patterns of transient increased hepatic attenuation were found to vary, depending on the presence or absence of portal vein thrombosis.

Acute Disease↗
PubMed2002

Residual venous thrombosis as a predictive factor of recurrent venous thromboembolism.

BACKGROUND: The optimum duration of anticoagulant therapy after an episode of deep venous thrombosis (DVT) is controversial. Contributing to the controversy is uncertainty about whether residual venous thrombosis, as assessed by repeated ultrasonography over time, increases the risk for recurrent thromboembolism. OBJECTIVE: To determine the risk for recurrent thromboembolism in patients who have persistent residual thrombosis compared with patients who have early vein recanalization. DESIGN: Prospective cohort study. SETTING: A university hospital in Padua, Italy. PATIENTS: 313 consecutive symptomatic outpatients with proximal DVT who received conventional short-term anticoagulation. MEASUREMENTS: Ultrasonographic assessment of the common femoral and popliteal veins was performed 3 months after acute DVT in all patients and at 6, 12, 24, and 36 months in patients found to have residual venous thrombosis. Veins were considered recanalized if they were 2.0 mm or less in diameter on a single test or 3.0 mm or less in diameter on two consecutive tests. Recurrent thromboembolism was assessed during a 6-year period. RESULTS: The cumulative incidence of normal results on ultrasonography was 38.8% at 6 months, 58.1% at 12 months, 69.3% at 24 months, and 73.8% at 36 months. Of 58 recurrent episodes, 41 occurred while the patient had residual thrombosis. The hazard ratio for recurrent thromboembolism was 2.4 (95% CI, 1.3 to 4.4; P = 0.004) for patients with persistent residual thrombosis versus those with early vein recanalization. CONCLUSIONS: Residual venous thrombosis is an important risk factor for recurrent thromboembolism. Ultrasonographic assessment of residual venous thrombosis may help clinicians modify the duration of anticoagulation in patients with DVT.

Adult↗
PubMed2005

A randomized trial of diagnostic strategies after normal proximal vein ultrasonography for suspected deep venous thrombosis: D-dimer testing compared with repeated ultrasonography.

BACKGROUND: With suspected deep venous thrombosis and normal results on proximal vein ultrasonography, a negative d-dimer result may exclude thrombosis and a positive D-dimer result may be an indication for venography. OBJECTIVE: To evaluate and compare the safety of 2 diagnostic strategies for deep venous thrombosis. DESIGN: Randomized, multicenter trial. SETTING: Four university hospitals. PATIENTS: 810 outpatients with suspected deep venous thrombosis and negative results on proximal vein ultrasonography. INTERVENTIONS: Erythrocyte agglutination D-dimer testing followed by no further testing if the result was negative and venography if the result was positive (experimental) or ultrasonography repeated after 1 week in all patients (control). MEASUREMENTS: Symptomatic deep venous thrombosis diagnosed initially and symptomatic venous thromboembolism during 6 months of follow-up. RESULTS: Nineteen of 408 patients (4.7%) in the D-dimer group and 3 of 402 patients (0.7%) in the repeated ultrasonography group initially received a diagnosis of deep venous thrombosis (P < 0.001). During follow-up of patients without a diagnosis of deep venous thrombosis on initial testing, 8 patients (2.1% [95% CI, 0.9% to 4.0%]) in the D-dimer group and 5 patients (1.3% [CI, 0.4% to 2.9%]) in the repeated ultrasonography group developed symptomatic venous thromboembolism (difference, 0.8 percentage point [CI, -1.1 to 2.9 percentage points]; P > 0.2). Venous thromboembolism occurred in 1.0% (CI, 0.2% to 2.8%) of those with a negative D-dimer result. LIMITATIONS: Seventy patients (8.6%) deviated from the diagnostic protocols, and 9 patients (1.1%) had inadequate follow-up. CONCLUSION: In outpatients with suspected deep venous thrombosis who initially had normal results on ultrasonography of the proximal veins, a strategy based on D-dimer testing followed by no further testing if the result was negative and venography if the result was positive had acceptable safety and did not differ from the safety of a strategy based on withholding anticoagulant therapy and routinely repeating ultrasonography after 1 week.

Female↗