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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The stress of injury and surgical operation results in an initial increase in the spontaneous fibrinolytic activity of the blood which is followed by a period of reduced activity in the postinjury or postoperative period. This 'fibrinolytic shutdown' is particularly marked in patients with malignant disease and occurs irrespective of whether or not they develop a deep venous thrombosis. It also occurs in patients with benign disease and in these patients is greater, though only on the first postoperative day, in those who develop deep venous thrombosis. Venous occlusion studies suggest that this reduction in spontaneous fibrinolytic activity may be the results of a reduction in the fibrinolytic capacity of the vascular endothelium resulting either from a deficiency of the enzyme plasminogen activator or an inability to release the enzyme from the endothelium. Changes in antiplasmins, the inhibitors of the fibrinolytic system, also occur as a result of the stress of operation. Plasma levels of alpha2-macroglobulin fall while those of alpha1-antitrypsin rise. These changes occur irrespective of the presence of malignant or benign disease and do not appear to influence the development of deep venous thrombosis.
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PMID:Factors affecting the fibrinolytic response to surgery. 8 46

An impaired fibrinolytic activity after a venous occlusion test is the most common abnormality associated with thomboembolic disease. To better characterize the causes of abnormal responses we have measured different fibrinolytic parameters, before and after 10 and 20 min of venous occlusion, in 77 patients with a history of idiopathic deep vein thrombosis and/or pulmonary embolism and in 38 healthy volunteers. The patients had a lower mean fibrinolytic response to venous occlusion than the controls and higher antigen levels of tissue-type plasminogen activator (t-PA:Ag) and plasminogen activator inhibitor type 1 (PAI-1:Ag). Before venous occlusion, PAI-1 levels were at a molar excess over those of t-PA in all patients and controls. After 20 min of venous occlusion, the release of t-PA from the vascular endothelium resulted in a molar excess of t-PA over PAI-1 in the majority of controls (72%) but only in a minority of patients (39%). To identify patients with fibrinolytic abnormalities, reference intervals (RI) for fibrinolytic activity, t-PA:Ag and PAI-1:Ag were established in healthy controls. None of the patients had low levels of t-PA:Ag, but 17 (22%) had elevated PAI-1:Ag levels before venous occlusion and 12 (16%) exhibited low fibrinolytic activity after 20 min of venous occlusion. Ten of these were among the 17 subjects with high PAI-1:Ag levels before venous occlusion. Thus, the measurement of PAI-1:Ag levels before venous occlusion (i.e. in samples taken without any stimulation) is a sensitive (83%) and specific (89%) assay for the detection of patients with an impaired fibrinolytic response to venous occlusion.
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PMID:Hypofibrinolysis in patients with a history of idiopathic deep vein thrombosis and/or pulmonary embolism. 163 86

Alteration of the fibrinolytic system is considered to be important in the development of deep venous thrombosis (DVT). Using specific assays for tissue plasminogen activator (t-PA) activity, t-PA inhibitor (PAI) and t-PA antigen, we measured these activities in 16 women who developed DVT during their pregnancies. A group of 24 healthy females of comparable age was studied as controls. PAI was increased in 87% of these patients compared to the healthy controls. In some of these patients a defect in release of t-PA from vascular endothelium was found as well. The site at which blood was sampled for analysis appeared to be an important criterion in the ex vivo assessment of functional t-PA reserve and PAI levels, though relatively less so for the latter measurement. The unaffected lower limbs, relative to the unaffected upper limbs, showed an increase in PAI and a demonstrable decrease in t-PA release, both representing increased risk factors for rethrombosis. The affected lower limbs showed similar but more accentuated changes in these parameters.
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PMID:Altered fibrinolysis in DVT: influence of site of sampling. 314 91

A review of a series of clinical and experimental investigations established that the incidence of deep venous thrombosis and of pulmonary embolism after total hip replacement surgery was lower in patients given continuous lumbar epidural anaesthesia than in others with general anaesthesia. The thromboprophylactic effect of continuous lumbar epidural anaesthesia is explained by its beneficial influence on all factors of the triad proposed by Virchow, viz. blood flow, factors within the blood itself, and the vascular endothelium. Continuous lumbar epidural anaesthesia is associated with hyperkinetic blood flow in the major vessels of the lower limbs, lessened tendency to coagulation of the blood and better preservation of fibrinolysis function. Other characteristics include an inhibitory action on platelet aggregation and stabilizing effect on leukocytes and endothelial cells--effects exerted by the local anaesthetics per se. The smaller blood loss and thus the lower transfusion requirements during continuous lumbar epidural anaesthesia may also play a beneficial role as a thromboprophylactic factor.
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PMID:The role of lumbar epidural anaesthesia as antithrombotic prophylaxis in total hip replacement. 393 4

Focus in this discussion of pulmonary embolism is on the following: risk factors (age, heredity and blood type, obesity, estrogen and oral contraceptive use/pregnancy, cardiovascular disease, cancer, and other risk factors); pathophysiology and presenting symptoms; laboratory procedures and findings (radiography, electrocardiography, lung scanning, and evaluation of lower extremity veins); treatment modalities (heparin therapy, thrombolysis, and surgery); and prevention. Pulmonary embolism may be the primary cause or a major contributory cause in as many as 200,000 deaths per year in the US. Most of these deaths occur in patients in whom the diagnosis is not suspected and, thus, not treated. The mortality rate for untreated pulmonary embolism is approximately 30%. 90% of patients survive the initial embolic event, but the correct diagnosis is made in no more than 2/3 of cases. Risk factors for the development of deep venous thrombosis are based upon the Virchow-Aschoff postulates, which include: trauma or disruption of the vein wall; stasis of blood flow in the veins; and increased coagulability of the blood. More than 85-90% of all pulmonary emboli originate from deep venous thromboses in the popliteal and femoral deep veins. Other important, although less frequent, sites of origin of venous thromboembolism include the pelvic veins, the renal and hepatic veins, the axillary veins in the upper extremities, and the right atrium. Accurate diagnosis and effective prevention and treatment depend on the clinician's awareness of risk factors for development of deep vein thrombosis. Estrogen may accelerate intimal proliferation in arteries and veins, and it may also increase permeability of venous vascular endothelium. The risk of thromboembolism increases as the dose of estrogen increases. Both pregnancy and oral contraceptive use significantly decrease venous tone and the velocity of blood flow in the calf of the leg. Appropriate treatment includes thrombolytic therapy for patients with massive pulmonary embolism, which results in hypotension or shock. Anticoagulant therapy with herapin followed by an oral anticoagulant is the primary treatment for most patients with submassive emboli in which there is less cardiovascular compromise. When thrombolytic therapy is used, it should always be followed by anticoagulant therapy. Prevention of primary or recurrent deep vein thrombosis is directed toward improving venous blood flow and reducing hypercoagulability.
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PMID:Pulmonary embolism: incidence, diagnosis, prevention, and treatment. 398 Feb 63

Low molecular weight heparins (LMWHs) are now considered to be the drugs of choice for prophylaxis against deep venous thrombosis (DVT) in post operative patients undergoing both general and orthopaedic surgical procedures. Despite extensive research, the exact mechanism of the antithrombotic activity of LMWHs remains unclear. These agents have been shown to activate the fibrinolytic system and to directly inhibit both the activity and the generation of factor Xa and thrombin. New evidence suggests that LMWHs also stimulate the release of endogenous tissue factor pathway inhibitor (TFPI) from the vascular endothelium. This study was designed to investigate the role of TFPI in mediating the antithrombotic activity of LMWHs. We measured the plasma levels of TFPI in a group of post orthopaedic surgery patients treated with daily subcutaneous injections of LMWH and a group of patients treated with placebo. In the placebo group (n = 25), the plasma TFPI levels were slightly elevated immediately after surgery but returned to their baseline value by the fifth post operative day. In contrast, in the group of patients treated with LMWH (n = 34), the plasma levels of TFPI increased significantly and remained elevated for up to 7 days following surgery. However, the TFPI levels in both groups showed wide patient to patient variability. These results indicate that LMWHs stimulate the release of TFPI into the bloodstream of post surgical patients. This suggests the importance of TFPI in mediating the antithrombotic activity of LMWHs.
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PMID:Role of tissue factor pathway inhibitor in post surgical deep venous thrombosis (DVT) prophylaxis in patients treated with low molecular weight heparin. 802 8

Three cases of deep venous thrombosis following varicella infection are described which were successfully treated with bed rest and anticoagulants. Two of these patients had severe pulmonary manifestations of varicella and the third was complicated by pulmonary embolism. Deep vein thrombosis is an uncommon systemic manifestation of varicella, possibly associated with vascular endothelium wall damage caused by varicella zoster virus infection.
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PMID:Three cases of varicella thrombophlebitis as a complication of varicella zoster virus infection. 846 61

We have observed a deep venous thrombosis with pulmonary embolism in a young woman receiving low-dose oral contraceptives; this adverse drug effect was not associated with some risk factor and, in particular, with a demonstrable congenital or acquired clotting abnormality. It is reported that EP can induce deep venous thrombosis with different mechanisms, as hemorheological changes with subsequent poor clearance of locally activated clotting factors, or an increase of platelet or leukocytes aggregation, or a direct effect on some clotting factor; furthermore, it is well known that oral contraceptives may induce antibodies to synthetic hormones, with detection of circulating immune complexes, that might produce thrombosis by damaging the vascular endothelium or interfering with clotting factors or platelet aggregation. Moreover, only a familial history of thrombosis or a past history of recurrent deep venous thrombosis, especially in young age, may justify a broad and highly expensive screening of latent clotting abnormalities, that may significantly increase the risk of vascular thrombosis with the use of oral contraceptives.
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PMID:[Low-dose oral contraceptives and pulmonary embolism: a case report]. 876 50

Deep vein thrombosis (DVT) is a frequent event in patients with spinal cord injury, even with prophylactic anticoagulant therapy. Lower limb paralysis is a known major risk factor for venous thrombosis, supposedly due to the venostasis in relation with total immobility. The main goal of this study was to evaluate the endothelial response to anoxia to determine whether recovery of fibrinolytic potential occurs in patients subjected to forced bedrest because of a spinal cord injury and whether this recovery is related to the incidence and/or evolution of DVT. We evaluated vascular endothelium reactivity in the lower limbs no longer submitted to the hydrostatic pressure of the erected position in 15 patients with paraplegia or tetraplegia and in 10 normal volunteers after venous occlusion produced by the application of 10 cm Hg pressure to the lower limb for 15 min comparatively to the upper limb used as reference. Among the 15 patients, 10 whose spinal cord injury had occurred 1 to 6 months earlier were still receiving prophylactic anticoagulant therapy, whereas the five other patients were not receiving prophylactic anticoagulants because the injury dated back 6 months or more. After venostasis, tissue plasminogen activator (tPA) increased significantly in both patients and controls in the upper limb (tPA levels twofold and threefold respectively in controls and patients) but showed no significant changes in the lower limb; prolonged immobility did not allow recovery in the lower limbs of a level of fibrinolytic responsiveness identical to that in the upper limbs. The plasminogen activator inhibitor (PAI1) remained unchanged after anoxia, although wide interindividual variations were seen. Natural coagulation inhibitors and circulating blood stigmates of hypercoagulability were measured. None of the patients had abnormally low levels of coagulation inhibitors (ie, antithrombin III, protein C and protein S levels were normal). Seventy-five per cent of patients (prophylactically anticoagulated or not) had very high levels of fibrin degradation products (D. Dimer levels sevenfold to eightfold those of the controls), but all patients had normal levels of thrombin-antithrombin complexes and prothrombin fragments 1 + 2. The permanence of the thrombotic process characterized by an increase in D. Dimer levels without recovery of fibrinolytic potential suggests a proposal for the patients an indefinite antithrombotic treatment at curative doses.
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PMID:Endothelial fibrinolytic reactivity and the risk of deep venous thrombosis after spinal cord injury. 907 65

We examined hemostatic molecular markers in various thrombotic disorders. The efficacy of treatment in relation to the disseminated intravascular coagulation (DIC) score when the treatment was begun showed that greater efficacy was achieved in Pre-DIC than in DIC patients. The outcome was poorer with increasing DIC score, suggesting that early treatment is important. The sensitivity in some of molecular markers was high for both DIC and Pre-DIC. Receiver operating characteristic analysis suggest that soluble fibrin monomer level could be the most useful marker for the diagnosis of DIC. In examination of these markers in deep vein thrombosis, pulmonary embolism, acute myocardial infarction, and cerebral infarction, plasminogen activator inhibitor-1 and activated protein C-protein C inhibitor complex were useful marker for the diagnosis. Increased plasma GMP-140 was suggested to be the activation of platelets. The patients with high levels of plasma thrombomodulin (TM) considered to be a marker of vascular endothelial injuries became poor outcome. We will term these patients with high TM as systemic vascular endothelium injuries syndrome, and treat those by protecting the vascular endothelium.
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PMID:[Study of hemostatic molecular marker]. 913 93


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