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PubMed2000

The venous stasis syndrome after deep venous thrombosis or pulmonary embolism: a population-based study.

OBJECTIVES: To estimate the incidence and determine predictors of venous stasis syndrome and venous ulcers after deep venous thrombosis and pulmonary embolism. PATIENTS AND METHODS: This population-based retrospective cohort study reviewed medical records of 1527 patients with incident deep venous thrombosis or pulmonary embolism between 1966 and 1990. We recorded baseline characteristics, event type (deep venous thrombosis with or without pulmonary embolism or pulmonary embolism alone), leg side and site of deep venous thrombosis (proximal with or without distal deep venous thrombosis vs distal deep venous thrombosis alone), and venous stasis syndrome and venous ulcer. RESULTS: Two hundred forty-five patients developed venous stasis syndrome. One-year, 5-year, 10-year, and 20-year cumulative incidence rates were 7.3%, 14.3%, 19.7%, and 26.8%, respectively. By 20 years the cumulative incidence of venous ulcers was 3.7%. Patients with deep venous thrombosis with or without pulmonary embolism were 2.4-fold (95% confidence interval, 1.7-fold-3.2-fold) more likely to develop venous stasis syndrome than patients with pulmonary embolism and no diagnosed deep venous thrombosis. In patients aged 40 years or younger with proximal compared with distal-only deep venous thrombosis, venous stasis syndrome was 3.0-fold more likely (95% confidence interval, 1.6-fold-4.7-fold). In patients with unilateral leg deep venous thrombosis, venous stasis syndrome usually developed in the concordant leg (P < .001). There was a 30% (95% confidence interval, 2%-62%) increased risk for venous ulcer per decade of age at the incident venous thromboembolism. CONCLUSIONS: The cumulative incidence of venous stasis syndrome continues to increase for 20 years after venous thromboembolism. Pulmonary embolism alone is less likely to cause venous stasis syndrome.

Adult↗
PubMed2000

[Hyperhomocysteinemia and arterial or venous thrombosis. Retrospective study of 75 cases].

OBJECTIVE: Previous studies suggest that hyperhomocysteinemia may be a risk factor for arterial and venous thrombosis. We retrospectively analyzed data from 75 patients with thrombosis. PATIENTS AND METHODS: Thirty-four patients had arterial thrombosis, 22 venous thrombosis and 19 venous and arterial thrombosis. Of the 75 patients (49 men and 26 women, mean age 49 +/- 15 years) about two-thirds had recurrent episodes of thrombosis. RESULTS: Hyperhomocysteinemia was defined as serum homocysteine level above 14.1 mumol/l (mean + 2.7 SD in healthy subjects) and was found in 67 patients (89%, CI95% = 80-95). Mean total homocysteine concentration was 21.6 +/- 13.6 mumol/l for the 75 patients. About half of the patients were smokers, 35% had hypertension and 25% high serum cholesterol. There was no significant relationship between serum homocysteine level and smoking status, hypertension or serum cholesterol level. Ten patients (13%, CI95% = 7-23) had low serum cobalamin (< 150 pmol/l). Serum folates were < or = 10 nmol in 41% of the patients in the arterial thrombosis group (CI95% = 25-59), in 27% in the venous thrombosis group (CI95% = 11-50), and in 31% in the arterial and venous thrombosis group (CI95% = 13-57). Thirteen patients received vitamin B supplementation. Hyperhomocysteinemia decreased in 12/13 patients (CI95% = 64-100) and returned to normal values in 9/13 patients (69%, CI95% = 38-91). CONCLUSION: Our data show that hyperhomocysteinemia is frequently found in arterial and venous thrombosis. Further studies are needed to determine the clinical impact of homocysteine lowering therapy.

Adult↗
PubMed2001

Isotypes of anti-beta2-glycoprotein I antibodies: association with thrombosis in patients with systemic lupus erythematosus.

OBJECTIVE: To evaluate the association between isotypes of anti-beta2-glycoprotein I antibodies (anti-beta2-GPI) and thrombosis and to identify antiphospholipid antibodies (aPL) that are most associated with thrombosis in patients with systemic lupus erythematosus (SLE). METHODS: IgG anticardiolipin antibody (aCL) and isotypes of anti-beta2-GPI were measured by ELISA, and clinical evidence of thrombosis was analyzed in 270 patients with SLE. RESULTS: IgG, IgM, and IgA anti-beta2-GPI were positive in 38.1, 13.7, and 34.8% of patients, respectively. Patients with a history of thrombosis were significantly more likely to have lupus anticoagulant (LAC), IgG aCL, and the 3 anti-beta2-GPI isotypes. Arterial thrombosis was associated with the presence of IgG aCL and the 3 anti-beta2-GPI isotypes, whereas venous thrombosis was associated with LAC, IgG aCL, and IgA anti-beta2-GPI. In stepwise multivariate logistic regression analysis, the variable that was associated with thrombosis was IgA anti-beta2-GPI. The occurrence of arterial thrombosis was associated with IgG aCL and that of venous thrombosis was related to IgA anti-beta2-GPI in stepwise multivariate analysis. The IgG, IgM, and IgA anti-beta2-GPI titers were closely correlated with IgG aCL titers. The IgA anti-beta2-GPI titers were also significantly correlated with those of IgG and IgM anti-beta2-GPI. CONCLUSION: The results suggest that anti-beta2-GPI isotypes are related to the occurrence of thrombosis, and measurements of IgA anti-beta2-GPI may be useful for predicting thrombotic episodes in patients with SLE.

Antibodies, Antiphospholipid↗
PubMed2003

Left internal jugular vein thrombosis due to a lung tumor.

Deep vein thrombosis is a common disease among Caucasians but is rare in Asia. Venous thrombosis may be fatal, for example by a pulmonary embolism and right or left atrial thrombosis. Alternatively, deep vein thrombosis may follow a benign pattern such as femoral and popliteal vein thrombosis. Theories abound regarding the causes of deep vein thrombosis, with the most common theories being long-term stasis and lack of exercise. Internal jugular vein thrombosis is a rare but potentially fatal disease with various causes. In the pre-antibiotics era, this disease was frequently associated with deep neck infection. Recently however, local trauma, central catheterization, and repeated intravenous injections with drugs have become the leading causes of thrombosis. Spontaneous internal jugular vein thrombosis may occur in connection with a neoplasm, termed Trousseau's syndrome. This investigation reports a case of lung cancer associated with internal jugular vein thrombosis.

Adult↗
PubMed1992

Occurrence of arterial thrombosis in a cohort of patients with hereditary deficiency of clotting inhibitors.

Hereditary deficiency of protein C, protein S or antithrombin III has been associated with an increased incidence of venous thrombosis or pulmonary embolism. The relationship between these deficiencies and the development of arterial thrombosis is a matter of current investigation. We retrospectively studied the occurrence of arterial thrombosis in 92 symptomatic patients belonging to a group of 160 with a confirmed diagnosis of hereditary deficiency of one of the physiologic clotting inhibitors. Seventeen of them experienced at least one arterial thrombotic event. This indicates that about one out of five of the symptomatic patients had experienced arterial thrombosis. The control group consisted of 92 sex and age matched (+/- 5 years) patients with no clotting deficiency who had experienced in the same period at least one episode of deep vein thrombosis or pulmonary embolism. Only one of them had developed arterial thrombosis. Ischemic stroke, myocardial infarction, upper and lower limb arterial thrombosis, and mesenteric artery occlusion occurred regardless of the type of defect taken into account; mean age of about 37.05 +/- 23 years (mean +/- SD). In some cases, arterial thrombosis was fatal. The overall number of venous thrombotic events in the 92 symptomatic patients of this study was much higher than that of arterial thrombosis, with a ratio of 24 to 1. The use of long-term anticoagulant therapy in our group of patients seemed to be able to prevent recurrences of both arterial and venous thrombosis.

Adolescent↗
PubMed2005

Elevated levels of D-dimer and fragment 1+2 upon central venous catheter insertion and factor V Leiden predict subclavian vein thrombosis.

BACKGROUND AND OBJECTIVES: Subclavian vein thrombosis is a well-recognized complication following central venous catheter insertion. We studied whether the determination of D-dimer levels, fragment 1+2 levels and factor V Leiden can identify patients at high risk of developing subclavian vein thrombosis. DESIGN AND METHODS: The presence of central venous catheter associated thrombosis was analyzed in 235 patients undergoing allogeneic bone marrow transplantation, of whom 30 (13%) developed thrombosis. A case-control study was performed with 30 patients matched for age, gender, and type of transplantation who did not develop thrombosis. Blood was sampled 3-5 days after catheter insertion. D-dimer levels were determined using a latex microparticle assay and an enzyme linked immunosorbent assay (ELISA). An ELISA was used to determine fragment 1+2 levels. The factor V genotype was determined by polymerase chain reaction. RESULTS: The levels of D-dimer and fragment 1+2 were significantly elevated in the patients who developed thrombosis. Five patients tested positive for factor V Leiden and all 5 developed subclavian vein thrombosis. Patients with high D-dimer levels (> 1300 microg/L measured by latex agglutination and >350 microg/L measured by ELISA) had a 7.0 and 6.0 times higher risk of developing subclavian vein thrombosis, respectively. A 5.5-fold increased risk of thrombosis was observed in patients with a fragment 1+2 level higher than 1.300 nmol/L. This resulted in positive predictive values of 0.78, 0.80 and 0.83 for the fragment 1+2, D-dimer and D-dimer latex agglutination assays, respectively. The accompanying negative predictive values were 0.39, 0.40 and 0.42, respectively. INTERPRETATION AND CONCLUSIONS: We conclude that the measurement of D-dimer and fragment 1+2 levels after central venous catheter insertion, as well as factor V Leiden determination, can be used to identify patients at high risk of developing symptomatic subclavian vein thrombosis.

Adult↗
PubMed2005

Ultrasound-guided fine needle aspiration biopsy in differential diagnosis of portal vein tumor thrombosis.

BACKGROUND: Portal vein tumor thrombosis (PVTT) is a serious complication and a major metastatic way of hepatocellular carcinoma(HCC). But portal vein benign thrombosis(PVBT) always appears in patients with hepatocirrhosis, and PVTT should be differentiated from PVBT. The aim of this study was to probe the value of ultrasound-guided fine needle aspiration biopsy in differential diagnosis of PVTT. METHODS: Twenty-two HCC patients with portal vein thrombosis and 8 hepatocirrhosis patients with portal vein thrombosis were studied by ultrasound-guided fine needle aspiration biopsy. Twelve portal vein thrombosis filling portal vein embranchment of the 30 portal vein thrombosis patients were examined by 18G automatic biopsy. The positive rates of aspiration biopsy cytology and histology were calculated and compared with those of automatic biopsy. RESULTS: The positive rates of fine needle aspiration biopsy cytology and histology were 93.3% (28/30) and 90.0% (27/30), respectively. They were not different markedly from that of automatic biopsy 91.7% (11/12). In aspiration biopsy of 22 HCC patients with PVTT, HCC cellular was found in 19 portal vein thrombosis patients (86.4%) by cytology examination and in 18 portal vein thrombosis patients (81.8%) by histology examination. In total, 20 tumor thrombi were detected. The other two were diagnosed as benign thrombosis. No HCC cell and/or tissue was observed in 8 patients with hepatocirrhosis associated with portal vein thrombosis. CONCLUSIONS: Ultrasound-guided fine needle biopsy in detecting PVTT shows a high positive rate and is of diagnostic value. The positive rate is not apparently different from that of automatic biopsy. Hence the case that fails to be diagnosed by color Doppler flow imaging(CDFI) and pulsed Doppler can be detected early by ultrasound-guided fine needle aspiration biopsy.

Biopsy, Needle↗
PubMed1993

Arterial thrombosis: a rare complication of the nephrotic syndrome.

Arterial thrombosis is a rare complication of the nephrotic syndrome, occurring mainly in men. Two cases of arterial thrombosis are described, the first affecting a 54-year-old man in whom aortic thrombosis initiated the nephrotic syndrome and who relapsed 1 year later resulting in graft thrombosis, the second affecting a 15-year-old male patient with extensive popliteal and distal arterial thrombosis, followed by recurrent venous bypass thrombosis. A review of the literature shows that arterial thrombosis occurs primarily in the femoropopliteal, renal and coronary arteries. The genesis of arterial thrombosis in patients with nephrotic syndrome involves increased blood viscosity, platelet adhesion and aggregation, high levels of fibrinogen, low levels of serum antithrombin III, diuretic agents and steroid therapy. For high-risk patients with low levels of plasma albumin or those receiving steroids, anticoagulation therapy should be introduced to prevent thrombosis. Urine protein should be evaluated in patients with arterial thrombosis of unknown origin.

Adolescent↗
PubMed1999

Low levels of heparin-releasable tissue factor pathway inhibitor in young patients with thrombosis.

An association between deficiency of tissue factor pathway inhibitor (TFPI) and thrombosis has not been clearly demonstrated in humans, but previous studies have focused on the measurement of plasma TFPI, which is only a small part of the total body TFPI. The major fraction of this natural anticoagulant can be measured in plasma after release by heparin injection. To investigate if deficiency of heparin-releasable TFPI is associated with thrombosis. we measured TFPI activity in plasma before and 10 min after intravenous injection of 7500 IU unfractionated heparin in 64 young patients with venous thrombosis, 49 young patients with arterial thrombosis and 38 healthy individuals. Post-heparin TFPI activity levels were significantly lower in the group of patients with venous thrombosis than in controls (mean+/-SD: 230%+/-39 vs 260%+/-34, p = 0.0002), whereas there was no difference for patients with arterial thrombosis. Defining the normal range as the mean+/-2 SD of TFPI activity in controls, twelve patients had low post-heparin TFPI activity levels, seven with venous and five with arterial thrombosis. Low levels of TFPI activity were confirmed by immunoassay in six of the seven patients with venous thrombosis and two of the five patients with arterial thrombosis, and were present also in at least one first degree relative of six patients, suggesting that the defect might be inheritable. However, the causative role of low heparin-releasable TFPI remains uncertain, because co-segregation of the defect with thrombotic symptoms could not be demonstrated in the small number of families studied.

Adolescent↗
PubMed1991

Deep venous thrombosis and pulmonary embolism.

All surgical patients are at risk for the development of deep venous thrombosis and subsequent pulmonary embolism or postphlebitic syndrome. The evolution of ultrasonographic imaging has increased the awareness of prevention, diagnosis, and treatment of deep venous thrombosis. Duplex imaging and Doppler color flow imaging have made the diagnosis of deep venous thrombosis relatively simple, painless, inexpensive, and definitive. These procedures have gained acceptance by both patients and physicians. Several risk factors have been identified that increase the chance of the development of deep venous thrombosis. These factors include a history of deep venous thrombosis, presence of a malignant process, increasing age, cigarette smoking, obesity, prolonged bed rest, and general anesthesia. The greater the number of risk factors, the more aggressive prophylaxis should be. Means of prophylaxis have improved, and surgeons now generally agree that some form of prophylaxis is required. Heparin and intermittent compression devices appear to be equally effective in preventing deep venous thrombosis. The addition of venous monitoring in high-risk patients permits immediate identification of the presence of deep venous thrombosis. During the last decade, the treatment of patients with deep venous thrombosis has changed little. Heparin followed by warfarin remains the treatment of choice. A small group of patients receive fibrinolytic therapy for deep venous thrombosis. Although the incidence of postoperative deep venous thrombosis has decreased during the last decade, it remains a significant complication.

Humans↗
PubMed2003

Plasma levels of D-dimer and soluble fibrin polymer in patients with hepatocellular carcinoma: a possible predictor of tumor thrombosis.

INTRODUCTION: Fibrin formation and removal occurs continuously during the development of malignancy. Moreover, plasma D-dimer is indicative of ongoing fibrinolysis, and soluble fibrin polymer (Thrombus precursor protein, TpP) represents thrombogenic activity. We evaluated the relationship between the levels of plasma D-dimer and TpP and tumor thrombosis in patients with hepatocellular carcinoma (HCC), and examined these markers as possible predictors of tumor thrombus in the portal or the hepatic vein. MATERIALS AND METHODS: Plasma levels of D-dimer and TpP were measured in 66 HCC patients (38 without tumor thrombosis, 28 with tumor thrombosis) and 29 healthy controls, by enzyme immunoassay using an Asserachrom D-Di kit (Diagnostica Stago, France) and a TpP kit (American Biogenetic Sciences, USA). RESULTS: The plasma levels of D-dimer and TpP in HCC patients were found to be significantly higher than those in healthy controls, and these values were also significantly higher in patients with tumor thrombosis than those without tumor thrombosis. Positive D-dimer (>367 ng/ml) correlated weakly with the presence of tumor thrombosis, whereas positive TpP (>5.4 microg/ml) correlated strongly with the presence of tumor thrombosis. By multivariant logistic analysis, positive TpP level was found to be a significant predictor of the presence of tumor thrombosis. In contrast, positive D-dimer level was not found to be a significant predictor for predicting tumor thrombosis. CONCLUSIONS: Increased D-dimer and TpP levels in HCC may suggest that fibrinolysis and coagulation occur continuously during tumor progression. This study shows that a positive TpP level is a predictor of tumor thrombosis in HCC, which suggests that TpP may be useful for identifying tumor thrombus in the portal and hepatic veins.

Biomarkers↗
PubMed1986

Clinical features and diagnosis of venous thrombosis.

The clinical diagnosis of venous thrombosis is inaccurate because the clinical findings are both insensitive and nonspecific. The sensitivity of clinical diagnosis is low because many potentially dangerous venous thrombi are clinically silent. The specificity of clinical diagnosis is low because the symptoms or signs of venous thrombosis all can be caused by nonthrombotic disorders. For these reasons, a practical approach for the diagnosis of venous thrombosis is important. A current approach to the diagnosis of clinically suspected venous thrombosis favors the use of impedance plethysmography over Doppler ultrasonography as the main test for this disorder. This is because impedance plethysmography is precise and objective, whereas the interpretation of Doppler ultrasonography is subjective and requires considerable skill and experience to form reliable diagnoses. The use of serial impedance plethysmography has been evaluated recently in a prospective study. The rationale of repeated impedance plethysmography evaluation is based on the premise that calf vein thrombi are only clinically important when they extend into the proximal veins, at which point detection with impedance plethysmography is possible. Therefore, by performing repeated examinations with impedance plethysmography in patients with clinically suspected venous thrombosis, it is possible to identify patients with extending calf vein thrombosis who can be treated appropriately. Impedance plethysmography is performed immediately on referral; if it is positive in the absence of clinical conditions that are known to produce falsely positive results, the diagnosis of venous thrombosis is established, and the patient is treated accordingly. If the result of the initial impedance plethysmography evaluation is negative, anticoagulant therapy is withheld, and impedance plethysmography is repeated the following day, again on day 5 to 7 and on day 10 to 14. If impedance plethysmography becomes positive during this time, a diagnosis of venous thrombosis is made and anticoagulant therapy is commenced. Positive impedance plethysmography in the presence of conditions known to produce a false positive result (for example, congestive cardiac failure) should be confirmed by venography. If noninvasive tests for the diagnosis of venous thrombosis are not available, a clinical suspicion of venous thrombosis should be objectively confirmed or excluded by performing ascending venography.

Diagnosis, Differential↗
PubMed1997

[Pseudoexfoliation syndrome in patients with retinal vein branch and central vein thrombosis].

BACKGROUND: Pseudoexfoliation syndrome is a frequent cause of secondary open-angle glaucoma due to deposition and in situ-production of abnormal extracellular matrix proteins in the trabecular meshwork. Glaucomas itself are a known risk factor for retinal vein thrombosis. In this retrospective study the prevalence of pseudoexfoliation syndrome in patients with branch and central retinal vein thrombosis was investigated. PATIENTS AND METHODS: The records of 332 unselected patients with branch retinal vein thrombosis and 159 with central retinal vein thrombosis, which were seen in our laser out-patient clinic between January 1990 and July 1996, were analysed retrospectively. RESULTS: 6.0% of patients with branch and 6.9% of patients with central retinal vein thrombosis revealed pseudoexfoliation syndrome. The full picture of pseudoexfoliation syndrome was seen in 4.2% of patients with branch and in 4.4% of patients with central retinal vein thrombosis. The prevalence of pseudoexfoliation syndrome increased with age. Twenty percent of patients with branch and 27% of patients with pseudoexfoliation syndrome and branch or central retinal vein thrombosis. The branch retinal vein thrombosis was significantly more often localised at the disk in patients with glaucoma and in patients with pseudoexfoliation syndrome. CONCLUSIONS: Pseudoexfoliation syndrome is a risk factor for retinal vein thrombosis. Pathogenetically the secondary open-angle glaucoma caused by pseudoexfoliation syndrome could be causative for the venous thrombosis.

Adult↗
PubMed1989

Risk factors for thrombosis in lupus patients.

Lupus anticoagulant, concentrations of anticardiolipin antibodies, antithrombin III, plasminogen, (free) protein S, protein C, prothrombin, platelet counts, and bleeding times were determined in 74 lupus patients (58 with systemic lupus erythematosus; 16 with lupus-like disease) to establish the presence of risk factors for thrombosis in these patients. Of the variables evaluated, lupus anticoagulant had the strongest association with a history of thrombosis. Both positive anticardiolipin antibody concentrations and the presence of (mild) thrombocytopenia were significantly associated with a history of thrombosis and the presence of lupus anticoagulant. Reduced concentrations of antithrombin III, plasminogen, (free) protein S, and protein C were found in some patients but were not associated with either thrombosis or lupus anticoagulant. Mean concentrations of total protein S were significantly lower in patients with thrombosis than in those without and in patients with lupus anticoagulant than in those without. The antigenic concentration of prothrombin was reduced in 3/74 (4%) lupus patients. These three patients had lupus anticoagulant but no history of thrombosis, which suggests that a low prothrombin concentration protects patients with lupus anticoagulant from the development of thrombosis. A prolonged bleeding time was associated with the presence of lupus anticoagulant but not with a history of thrombosis. Analysis by stepwise logistic regression did not disclose additional risk factors for thrombosis in lupus patients with lupus anticoagulant. Increased antithrombin III concentrations and decreased free protein S concentrations are often found in lupus patients, unrelated to lupus anticoagulant or thrombosis.

Adolescent↗
PubMed1994

Deep venous thrombosis and occult malignancy: an epidemiological study.

OBJECTIVE: To determine the risk of subsequent cancer in patients with deep venous thrombosis confirmed by venography. DESIGN: Follow up of all patients who had venography for suspected deep venous thrombosis during 1984-88. Patients were traced through a cancer registry up to 1 January 1991. SUBJECTS: 4399 patients who had phlebography in one hospital. SETTING: General hospital in Malmö, Sweden, serving a population of 230,000. MAIN OUTCOME MEASURE: Number of cancers recorded. RESULTS: 4399 patients had venography for suspected deep venous thrombosis; 604 were known to have a malignancy at the time of venography and were excluded from further analysis. 1383 had deep venous thrombosis, 150 of whom subsequently developed cancer. 182 of the 2412 patients without thrombosis developed cancer. During the first six months after venography 66 patients with thrombosis developed malignancy compared with 37 patients without thrombosis (P < 0.0001). 38 of the cancers in the deep venous thrombosis group were detected by history, physical examination, and laboratory tests. Three patients had postoperative or post-traumatic deep venous thromboses. Only two of the remaining patients would have benefited from early detection by extensive screening. After six months the incidence of cancer was identical in patients with and without thrombosis. CONCLUSION: Deep venous thrombosis is associated with a significantly higher frequency of malignancy during the first six months after diagnosis. Malignancies can be found with simple clinical and diagnostic methods and extensive screening is not required.

Adult↗
PubMed1994

Postoperative surveillance for deep venous thrombosis with duplex ultrasonography after total knee arthroplasty.

Duplex ultrasonography of the lower extremity was used for routine non-invasive screening for asymptomatic proximal and distal deep venous thrombosis, for monitoring of potential propagation of deep venous thrombosis from distal to proximal, and for confirmation of the resolution of proximal deep venous thrombosis after treatment. In the first part of the study, to substantiate the accuracy of duplex ultrasonography, 130 lower limbs (seventy-nine patients) were studied with that modality as well as with venography after a total hip or total knee arthroplasty. Compared with venography, duplex ultrasonography demonstrated 100 per cent sensitivity, specificity, and accuracy for the detection of proximal deep venous thrombosis and 88 per cent sensitivity, 98 per cent specificity, and 98 per cent accuracy for the detection of distal deep venous thrombosis. In the second part of the study, 100 patients who had had a total knee arthroplasty and had been managed with pneumatic stockings and aspirin for prophylaxis against deep venous thrombosis had screening of both lower extremities with duplex ultrasonography on the fourth postoperative day. Duplex ultrasonography demonstrated proximal deep venous thrombosis in seven patients and distal deep venous thrombosis in twenty-two patients; all twenty-nine patients were asymptomatic. The patients who had distal deep venous thrombosis had surveillance with serial duplex ultrasonography on the seventh and fourteenth postoperative days; five of these patients were found to have had propagation of the thrombosis to the proximal deep veins.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1997

Cost of long-term complications of deep venous thrombosis of the lower extremities: an analysis of a defined patient population in Sweden.

BACKGROUND: Little information is available on the epidemiology and economic effect of long-term complications developing after deep venous thrombosis. OBJECTIVE: To determine the extent of, timing of, and treatment costs associated with long-term complications developing after deep venous thrombosis of the lower extremities. DESIGN: 15-year retrospective cohort study. SETTING: County hospital in Sweden. PATIENTS: 257 patients with deep venous thrombosis and 241 age- and sex-matched controls without deep venous thrombosis. MEASUREMENTS: Data on use of health care resources and costs of inpatient and outpatient care, pharmaceutical agents, and treatment of complications. RESULTS: After 15 years of follow-up, 35% of the patients with thrombosis and 57% of the controls were alive. Two hundred forty-two complications were reported among the patients with thrombosis, and 25 similar events were reported among the controls. The average expected present value of the health care cost of treating complications of thrombosis was estimated to be about $4659 in the patients with thrombosis and $375 in the controls. In controls, primary deep venous thrombosis cost about $6000; thus, the additional long-term health care cost of post-thrombotic complications is about 75% of the cost of primary deep venous thrombosis. CONCLUSIONS: The economic effect of post-thrombotic complications is considerable. The use of measures to prevent thromboembolism and its long-term complications are justified on both clinical and economic grounds.

Follow-Up Studies↗
PubMed1998

Increased risk for venous thrombosis in carriers of the prothrombin G-->A20210 gene variant.

BACKGROUND: A mutation in the prothrombin gene (G-->A20210) has been associated with higher plasma prothrombin levels and an increased tendency for venous thrombosis. OBJECTIVE: To determine whether the prothrombin A20210 allele is independently associated with the occurrence of venous thrombosis. DESIGN: Case-control study. SETTING: Two thrombosis centers in southern Italy. PATIENTS: 281 consecutive patients with venous thrombosis confirmed by objective tests and 850 controls. MEASUREMENTS: Medical history was collected on standardized questionnaires. The presence of prothrombin G-->A2020 and factor V Leiden mutations was determined by polymerase chain reaction. The presence of anticoagulant factors and prothrombin activity was determined by tests of function. RESULTS: In 150 controls, increased prothrombin activity (P < 0.001) was associated with the prothrombin A20210 allele. This allele was more frequent in patients than in controls (8.01% compared with 2.29%; P < 0.001) and was associated with an increased risk for thrombosis (odds ratio, 3.88 [95% CI, 2.23 to 6.74]). The increased prevalence of this allele was independent of the presence of the factor V Leiden mutation. After adjustment for sex, age, arterial thrombosis, and factor V Leiden mutation, the risk was still significantly elevated (odds ratio, 3.13 [CI, 1.89 to 5.21]). Moreover, the overall prevalence of inherited coagulation abnormalities was significantly higher in patients with thrombosis of the lower extremities than in patients with thrombosis of the upper extremities (odds ratio, 3.77 [CI, 1.10 to 12.93]). Fourteen patients carried both the prothrombin G-->A20210 and factor V Leiden mutations. CONCLUSIONS: The prothrombin A20210 allele is independently associated with the occurrence of venous thrombosis, particularly in patients with a history of thrombosis of the lower extremities.

Adolescent↗