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PubMed1998

Lower extremity deep venous thrombosis in cancer patients: correlation of presenting symptoms with venous sonographic findings.

We sought to determine how rates of sonographically detected deep venous thrombosis correlate with presenting symptoms in cancer patients. We performed venous sonography in 588 cancer patients with clinically suspected lower extremity deep venous thrombosis. Results were correlated with clinical findings. Deep venous thrombosis was diagnosed in 32% of patients with unilateral lower extremity symptoms and in 17% of patients with bilateral symptoms. Patients with unilateral symptoms of pain and swelling, swelling alone, or pain alone had significantly different rates of deep venous thrombosis (47%, 31%, and 16%, respectively). In patients with bilateral leg symptoms, deep venous thrombosis was significantly more likely when symptoms were not bilaterally symmetric.

Adult↗

PubMed2001

Early detection of hepatic artery thrombosis after liver transplantation by Doppler ultrasonography: prognostic implications.

We assessed the usefulness of routine Doppler ultrasonography for early detection of hepatic artery thrombosis after orthotopic liver transplantation and repercussions in patient prognosis. Seventeen confirmed cases of early hepatic artery thrombosis initially diagnosed by Doppler ultrasonography (10 of them before clinical indication) were reviewed. All patients underwent Doppler ultrasonographic studies in the first 3 days after orthotopic liver transplantation. Twelve cases of hepatic artery thrombosis (70.6%) were detected by this early Doppler ultrasonography. All 10 unsuspected cases of hepatic artery thrombosis and 5 of the 7 cases diagnosed after clinical indication were treated by revascularization. Grafts were salvaged in 80% of asymptomatic patients and in 42.8% of symptomatic patients. Furthermore, biliary complications were less serious in the first group. In conclusion, Doppler ultrasonography performed routinely in the first 3 days after orthotopic liver transplantation may permit early detection of hepatic artery thrombosis, even before clinical indications. This allows hepatic artery repermeabilization before liver function damage, improving graft rescue and patient prognosis.

Adolescent↗

PubMed2006

Prevalence of upper extremity deep venous thrombosis diagnosed by color Doppler duplex sonography in cancer patients with central venous catheters.

OBJECTIVE: The purpose of this study was to review the literature concerning upper extremity deep venous thrombosis (UEDVT) diagnosed by color Doppler duplex sonography (CDDS) in cancer patients with indwelling central venous catheters (CVCs). METHODS: From computerized databases (MEDLINE and Ovid), relevant publications regarding CDDS of the upper limb veins in cancer patients with CVCs were reviewed. RESULTS: Patients with malignancy have a higher rate of thrombosis, which is increased by the presence of CVCs. Screening CDDS in asymptomatic patients showed CVC-related UEDVT in 11.7% to 44% of patients. In symptomatic cancer patients, the range was similar to the asymptomatic ones, 6.7% to 48%. The presence of a CVC almost doubled the incidence of UEDVT in symptomatic patients. Color Doppler duplex sonography is an accurate examination for the diagnosis of UEDVT, with sensitivity ranging from 78% to 100% and specificity ranging from 82% to 100%. The main obstacle for the diagnosis of UEDVT is the presence of overlying bones, making it difficult to visualize and impossible to directly assess by compression techniques. Color and spectral Doppler sonography and the use of small transducers aid in the diagnosis. When several parameters are evaluated in combination, CDDS is a reliable method for diagnosing CVC-related thrombosis. CONCLUSIONS: Great variability in the prevalence of catheter-related thrombosis in cancer patients has been reported, although it is uniformly higher compared with patients without cancer. Color Doppler duplex sonography is the modality of choice for the diagnosis of CVC-related UEDVT in symptomatic cancer patients and for screening for asymptomatic thrombosis in this specific population.

Catheterization, Central Venous↗

PubMed1999

[Postoperative deep venous thrombosis of legs and pulmonary embolism].

324 patients operated on the organs of abdominal cavity small pelvis and retroperitoneal space were examined by the method of I-125-fibrinogen accumulation and contrast phlebography. In 109 (33.6%) patients thrombosis of deep veins of lower extremities was diagnosed, among which in 24 cases (7.5%) it was proximal. In most cases thrombosis was predisposed by postthrombotic disease and chronic venous insufficiency of lower extremities, circulatory disturbances of the 2-3 degree, tumors, obesity, preoperative thrombophilia. Combination of 2 and more risk factors increased possibility of intravascular thrombosis. The rate of clinically registered pulmonary artery embolism (14,833 general surgical patients were avau label) made up 1.2%; in 54 (0.3%) of operated patients it was the cause of death. Postoperative lethality of embolism made up 13%. Four risk levels of development of thrombo-embolic complications were established: low (common rate of thrombosis--10.3%, proximal--1.4%, clinically evidenced pulmonary artery embolism--0.7%, with lethal outcome--0.02%), medium (28.5; 6.5; 2; 0.76%, respectively), high (80.4; 17.8; 6; 2.8%, respectively) and very high (93.3; 26.6; approximately 8; approximately 4, respectively). The prevalence of thrombo-embolic complications in patients urge surgeons and reanimatologists to carrying out prophylactic to reduce the risk of intravascular thrombosis in pre- and postoperative period.

Adult↗

PubMed1999

Factor XIII Val34Leu is a genetic factor involved in the etiology of venous thrombosis.

A mutation in the factor XIII gene (FXIII Val34Leu) gene was recently reported to confer protection against myocardial infarction, but its relationship with venous thrombosis is unknown. In addition, a mutation in the 5'-untranslated region of the FXII gene (46 C->T) was identified which is associated with low plasma levels of the protein. Its prevalence in patients with venous thrombosis is also unknown. We investigated the frequency of the FXIII Val34Leu and FXII 46 C->T mutations in 189 patients with deep venous thrombosis and in 187 age-, gender- and race-matched controls. FXIII Val34Leu was detected in 38.6% of the patients and in 41.2% of the controls. Interestingly, homozygosity for the FXIII mutation was found in 1.6% of the patients and in 9.6% of the controls, yielding an odds ratio (OR) for venous thrombosis of 0.16 (95% CI: 0.05-0.5). The OR for heterozygotes was 1.1 (95% CI: 0.7-1.7). The FXII 46 C->T mutation was detected in 46.0% of the patients and in 48.6% of the controls. The OR for heterozygotes was 0.9 (95% CI: 0.6-1.4) and for homozygotes the OR was 0.8 (95% CI: 0.3-1.9). Our data indicate that the FXII 46 C->T mutation is unlikely to be a major risk factor for venous thrombotic disease. In contrast, the homozygous state for FXIII Val34Leu is a strong protective factor against venous thrombosis, which emerges as a novel genetic factor involved in the aetiology of thrombophilia.

Adolescent↗

PubMed1999

[Hyperhomocysteinemia: development of deep vein thrombosis in another location during heparin anticoagulation therapy].

A 45-year-old man was admitted complaining of chest pain and pain and edema in the left lower extremity. Ultrasonography and venography results yielded a diagnosis of left femoral vein thrombosis, and pulmonary embolism was diagnosed later. Intravenous heparin therapy (10,000 IU/day) improved the patient's clinical signs. During this therapy, however, pain and edema of the right lower extremity developed, leading to a diagnosis of right femoral vein thrombosis. The patient was admitted to our hospital. At that time, coagulation studies showed an FDP level of 44.7 micrograms/ml and an FDP-DD level of 24.5 micrograms/ml. We surmised that the bilateral deep vein thrombosis had been caused by hyperhomocysteinemia (17.8 mumol/l). Genetic and other acquired risk factors for thrombophilia were ruled out. The patient's clinical signs again improved as a result of intravenous heparin therapy (15,000 IU/day), and FDP and FDP-DD levels returned to normal. We concluded that hyperhomocysteinemia is a risk factor for thrombosis and that it can generate thrombosis in other locations even during heparin therapy.

Anticoagulants↗

PubMed1999

[Cerebral venous thrombosis in minimal change nephrotic syndrome].

A 46-year old man presented with an eight-day history of edema and was found to be nephrotic, with a plasma albumin level of 1.1 g/dl and urine protein excretion of 13.3 g/24 hrs. The level of plasma creatinine was normal at 1.0 mg/dl. A finding of renal biopsy was consistent with minimal change glomerulopathy. On the 6th hospital day, he suddenly developed a severe headache and was noted to have bilateral papilledema. Lumbar puncture revealed an opening pressure of 250 mm of water. Magnetic resonance venography showed an irregular flow in the superior sagittal sinus and right transverse sinus, a finding consistent with thrombus. The diagnosis of cerebral venous thrombosis was made, and the patient was given both Warfarin 2 mg/day and prednisolone 60 mg/day. A complete recovery from nephrotic syndrome was achieved within eight weeks. Nephrotic syndrome causes a hypercoagulable state, leading to both venous and arterial thrombosis. The most common clinical features are renal vein thrombosis, femoral vein thrombosis, and pulmonary embolism, however, cerebral venous sinus thrombosis is rare in patients with nephrotic syndrome. It is important to be aware of this complication, since prompt treatment with anticoagulation and control of nephrotic syndrome can lead to a successful outcome.

Anti-Inflammatory Agents↗

PubMed1999

[Coach-class thrombosis--a potential risk for long distance-travelers].

Prolonged non-stop flights imply the hazard of thromboses in the deep veins of the leg. Since more than a billion passengers each year travel by air, the economy class syndrome (coach class thrombosis) has become a rather frequent complication among travellers. For various reasons it is difficult to investigate the economy class syndrome in a methodological way. Therefore, we approached the subject of travellers' thrombosis by using standardised questionnaires and, using this method, we reviewed 121 patients with traveller's thromboses and its complications (50 males, 71 females, mean age 55 years). Seventy-seven patients of this sample suffered from deep venous thromboses, 39 suffered from pulmonary embolism as a consequence of manifest thromboses and 4 were found to have "isolated" pulmonary embolism. The journeys had a mean duration of 12 hours and the first symptoms were observed 3.1 days after the migration. Specific risk factors for thrombosis were identified in no more than 41 patients. Based on our data, a Consensus Conference on travellers' thrombosis was held in 1995, in which the diagnosis, prophylaxis and treatment of deep vein thrombosis associated with migration were investigated and established.

Adolescent↗

PubMed1999

[Primary antiphospholipid syndrome presented with portal vein thrombosis].

Antiphospholipid Antibody Syndrome (APS) is defined by arterial and venous thrombosis, recurrent spontaneous abortions and thrombocytopenia associated with persistence of antiphospholipid antibodies. Thrombosis may involve virtually all arterial or venous sites, but deep vein thrombosis of the lower limbs are the most common; however, unusual thrombi that involve the portal vein have been described. We report females with documented portal vein thrombosis and primary APS. The treatment of these patients is difficult because of the risk of bleeding and the recurrent thrombosis if they don't receive appropriate long-term anticoagulant therapy.

Adult↗

PubMed1999

[Left branch portal vein thrombosis associated with hyperhomocysteinemia].

A 34 year-old man, who was a smoker, was hospitalised because of severe epigastric and right upper quadrant pain. An isolated left branch portal vein thrombosis was diagnosed using ultrasonography and arteriography. Two thrombogenic pathologies were found: i) a latent myeloproliferative syndrome with spontaneous presence of erythroid colony forming unit (CFU-E) in bone marrow culture, normal blood cell count, platelet count and medullogram; ii) a hyperhomocysteinemia associated with low serum folate levels and a methyl tetrahydrofolate reductase mutation. The association of these two factors probably resulted in portal vein thrombosis. This is the first adult case of a portal vein thrombosis associated with hyperhomocysteinemia. Increased homocysteine serum levels could be a previously unrecognized factor for portal vein thrombosis. Homocysteinemia should be systematically investigated in patients with idiopathic portal vein thrombosis since folate supplements could prevent deleterious vascular effects of hyperhomocysteinemia.

Adult↗

PubMedDate not supplied

[Renal vein partial thrombosis in 3 recipients of kidney transplantation].

OBJECTIVE: To report on three patients with partial graft renal vein thrombosis diagnosed by ultrasound. METHODS: The vascular complications diagnosed by ultrasound in 400 transplants performed from 1995-1998 were reviewed. RESULTS: Three patients with partial graft renal vein thrombosis were found. Two patients were treated with anticoagulant therapy. No thrombosis could be detected in all three patients on subsequent US control evaluation. CONCLUSIONS: Unlike complete thrombosis, partial graft renal vein thrombosis presents late, without significant clinical features and can be managed conservatively.

Adult↗

PubMed2000

[Thalidomide and thrombosis].

BACKGROUND: Teratogenicity and neuropathy are the well known serious side effects induced by thalidomide. We describe 5 cases of thrombotic events occurring within a brief delay after the onset of thalidomide in a manner that suggests that thalidomide could have acted as a precipiting or as a starting factor in these events. OBSERVATIONS: Five patients including 4 patients with lupus erythematosus (1 discoid lupus, 1 subacute lupus and 2 systemic lupus erythematosus) and one patient with a severe atopic dermatitis, all without previous history of vascular events, developed an arterial thrombosis (2 cases) or a venous thrombosis (3 cases), severe in 4 cases, few days or weeks after the onset of thalidomide treatment (50 to 100 mg daily). DISCUSSION: All the patients had risk factors of thrombosis: the presence of antiphospholipids and/or anticardiolipin antibodies in lupus erythematosus patients and a trauma in the atopic case. However the absence of a previous story of thrombosis, its rapid occurrence after the onset of thalidomide and its severity are intriguing. In addition, recent studies demonstrate that thalidomide has various effects that would act, among other things, on angiogenesis. Thus, we think that a doubt exists on a negative effect of thalidomide in thrombosis risk factors patients and that this hypothesis has to be confirmed.

Adult↗

PubMed2000

Recurrent venous thrombosis and markers of inflammation.

Inflammatory processes may play a key role in venous thrombosis, by inducing a procoagulant state through the action of cytokines and chemokines on monocytes and endothelial cells. Plasma concentrations of three inflammatory mediators, interleukin 6 (IL-6), interleukin 8 (IL-8) and monocyte chemotactic protein 1 (MCP-1), that mediate the cross-talk between inflammation and coagulation, were measured in 182 subjects with recurrent venous thrombosis and 350 healthy subjects recruited through a general practice. Elevated levels of IL-6 (>90th percentile of the control group) were detected in 25.8% of the patients with venous thrombosis in comparison with 10% (by definition) of the controls [odds ratio 2.4 (95%CI 1.5-3.8)]. In 21.5% of the patients elevated plasma levels of IL-8 (>90th percentile) were determined [odds ratio 2.0 (95%CI 1.2-3.5)]. Elevated levels of MCP-1 (>90th percentile) were detected in 24.1% of the patients [odds ratio 1.9 (95%CI 1.2-3.2)]. This is the first large clinical study showing that an increase in inflammatory mediators is associated with venous thrombosis. Future prospective studies are necessary to clarify the causal nature of the inflammatory process with respect to venous thrombosis.

Adult↗

PubMed2000

Comparison between critical pathway guidelines and management of deep-vein thrombosis: retrospective cohort study.

AIM: To compare the key steps of standard deep-vein thrombosis management with the critical pathway practice guidelines, and to assess the outcome of the treatment after 6 months. METHOD: This retrospective cohort study (from January 1, 1997 to December 31, 1998) included 172 patients with uncomplicated deep-vein thrombosis of lower extremities, consecutively admitted via emergency room. The data were collected from the entry register in emergency room and medical charts. The outcome of therapy was assessed 6 months after the acute event. RESULTS: A bolus dose of heparin was administered to 81 (46%) patients. The recommended initial heparin infusion rate at 1250 U/h was employed in only 26 (15%) patients. Time to activated partial thromboplastin time >60 s was met in 29 (17%) patients. All patients but one received heparin therapy longer than 96 h. The recommended time to a therapeutic international normalized ratio of less than 120 h was achieved in 134 (78%) patients, but the average length of a stay in the hospital exceeded the recommended 5. 5 days by 86%. Six months later, compressive ultrasonography revealed 44 (28.9%) cases of complete vein obstruction, 67 (44.1%) cases of partial recanalization and 41 (27%) cases with a normal finding. Recurrent thrombosis developed in 16 patients (10.5%) and acute pulmonary embolism in 4 (2.6%) patients. CONCLUSION: Our results considerably differ from the critical pathway guidelines due to the lower initial heparin doses and longer diagnostic assessment of thrombosis etiology. Our approach to deep-vein thrombosis treatment was a combination of the critical pathway guidelines and the conventional regimen. The clinical outcome in our series did not differ significantly from the outcome after the conventional way of treatment.

Cohort Studies↗

PubMed2000

Vascular release of plasminogen activator inhibitor-1 impairs fibrinolysis during acute arterial thrombosis in mice.

The role of plasminogen activator inhibitor-1 (PAI-1) in the plasma, blood platelets, and vessel wall during acute arterial thrombus formation was investigated in gene-deficient mice. Photochemically induced thrombosis in the carotid artery was analyzed via transillumination. In comparison to thrombosis in C57BL/6J wild-type (wt) mice (113 +/- 19 x 10(6) arbitrary light units [AU] n = 15, mean +/- SEM), thrombosis in PAI-1(-/-) mice (40 +/- 10 x 10(6) AU, n = 13) was inhibited (P <.01), indicating that PAI-1 controls fibrinolysis during thrombus formation. Systemic administration of murine PAI-1 into PAI-1(-/-) mice led to a full recovery of thrombotic response. Occurrence of fibrinolytic activity was confirmed in alpha(2)-antiplasmin (alpha(2)-AP)-deficient mice. The sizes of thrombi developing in wt mice, in alpha(2)-AP(+/-) and alpha(2)-AP(-/-) mice were 102 +/- 35, 65 +/- 8.1, and 13 +/- 6.1 x 10(6) AU, respectively (n = 6 each) (P <.05), compatible with functional plasmin inhibition by alpha(2)-AP. In contrast, thrombi in wt mice, t-PA(-/-) and u-PA(-/-) mice were comparable, substantiating efficient inhibition of fibrinolysis by the combined PAI-1/alpha(2)-AP action. Platelet depletion and reconstitution confirmed a normal thrombotic response in wt mice, reconstituted with PAI-1(-/-) platelets, but weak thrombosis in PAI-1(-/-) mice reconstituted with wt platelets. Accordingly, murine (wt) PAI-1 levels in platelet lysates and releasates were 0.43 +/- 0.09 ng/10(9) platelets and plasma concentrations equaled 0.73 +/- 0.13 ng/mL. After photochemical injury, plasma PAI-1 rose to 2.9 +/- 0.7 ng/mL (n = 9, P <.01). The plasma rise was prevented by ligating the carotid artery. Hence, during acute thrombosis, fibrinolysis is efficiently prevented by plasma alpha(2)-AP, but also by vascular PAI-1, locally released into the circulation after endothelial injury.

Animals↗

PubMed2000

Isolated thrombosis of the external jugular vein.

Thrombosis of the external jugular vein (EJV) is an infrequent clinical condition that has been associated with central venous catheterization, head and neck infections, intravenous drug abuse, and compression at the affected site. The authors report a case of thrombotic obstruction of the EJV in the late postoperative period after laparoscopic anterior lumbar interbody fusion. A 40-year-old morbidly obese woman with a depressive syndrome was diagnosed with L5-S1 discopathy and was submitted to laparoscopic anterior isthmic fusion. The operation lasted approximately 6 hours, during which the patient remained in a supine decubitus and Trendelenburg position. The left radial artery, peripheral veins, and right internal jugular vein were canalized. The internal jugular vein catheter was electively withdrawn 24 hours after the intervention. The postoperative period was satisfactory, and the patient was started on prophylaxis with low-molecular-weight heparin. She sat up and began walking at 24 hours and was discharged to her home 4 days after the procedure. Eight days after discharge she returned, experiencing right cervical pain. Palpation revealed a painful induration and erythematous area under the anterior edge of the sternocleidomastoid muscle. Results of otoscopy and laryngoscopy were normal. Cervical echo-Doppler disclosed an image consistent with EJV thrombosis. The most frequent causes of jugular vein thrombosis are mentioned above. A higher incidence has been described after upper abdomen and pelvic surgery; other contributing factors are age, obesity, and associated illness. There are few references in the literature to position-induced EJV thrombosis in the late postoperative period. The authors' patient presented signs and symptoms of EJV thrombosis (probably because of various factors), which was confirmed by echo-Doppler study and treated with 10 days of calcic heparin.

Adult↗

PubMed2000

Functional analyses of patient-derived IgG monoclonal anticardiolipin antibodies using in vivo thrombosis and in vivo microcirculation models.

Antiphospholipid antibodies (aPL) have been associated with thrombosis and pregnancy losses in patients diagnosed with antiphospholipid syndrome (APS) and enhance thrombus formation in vivo in mice, but the mechanism of thrombosis by aPL is not completely understood. It has been proposed that aPL may affect endothelial cell (EC) function and/or induce their activation, transforming their anticoagulant surface into procoagulant, thus predisposing to thrombosis. It has been proposed that aPL may affect EC cell function and/or induce their activation, transforming their anticoagulant surface into procoagulant, thus predisposing to thrombosis. This study proposes to test the hypotheses that some IgG anticardiolipins (IgG aCL) with thrombogenic properties in mice, exert their effects through activation of endothelium. We studied seven patient-derived monoclonal aCL for their thrombogenic properties in an in vivo pinch-induced thrombosis model, and their functional activities in activating EC by analyzing in vivo leukocyte adhesion to endothelium in microcirculation in venules in exposed murine cremaster muscle and in vitro adhesion molecule expression in cultured EC. The binding of the monoclonal aCL to EC was also tested. In addition to the previous identified thrombogenic IS2, four of the five new more IgG monoclonal aCL (from two patients) were found to be thrombogenic. Of these five thrombogenic aCL, three caused more in vivo leukocyte adhesion to EC in microcirculation, as compared to that induced by the H2 control human monoclonal IgG, and enhanced expression of adhesion molecules (particularly VCAM-1) on cultured EC. These data show that about 2/3 patient-derived IgG monoclonal aCL are thrombogenic and suggest that some thrombogenic IgG aCL exert their effects through activating EC.

Adult↗

PubMed2000

Use of low molecular weight heparin for prevention of deep vein thrombosis in total knee arthroplasty--a study of its efficacy in an Asian population.

INTRODUCTION: The aims of this paper were to study the incidence of deep vein thrombosis following total knee replacement in an Asian population and to evaluate the role of low molecular weight heparin for deep vein thrombosis in this setting. MATERIALS AND METHODS: We prospectively studied two groups of 100 consecutive patients undergoing total knee replacement separately. Group 1 did not receive any low molecular weight heparin and group 2 received low molecular weight heparin, nodraparin calcium (Fraxiparine) according to body weight. The sex distribution, age group, weight, preoperative knee and function scores, and postoperative rehabilitation were similar for both groups. A single ultrasound technician performed ultrasound duplex scan of both lower limbs on the seventh postoperative day. RESULTS: The incidence of deep vein thrombosis in group 1 was 14% (14 patients, 5 proximal vein thromboses and 9 distal vein thromboses) while in group 2, no patients developed deep vein thrombosis. There was no increased incidence, either local or systemic, of major bleeding complications with the use of low molecular weight heparin. CONCLUSION: While the incidence of deep vein thrombosis following total knee replacement in an Asian population appears lower compared to Western populations, the use of low molecular weight heparin for thromboprophylaxis appears to further reduce the incidence without major bleeding complications.

Activities of Daily Living↗