Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term central venous catheters (CVCs) have considerably improved the management of cancer patients because they facilitate chemotherapy, transfusions, parenteral nutrition, and blood sampling. However, the use of long-term CVCs, especially for chemotherapy, has been associated with the occurrence of upper-limb deep venous thrombosis (UL-DVT). The incidence of clinically overt UL-DVT related to CVCs has been reported to vary between 0.3% and 28.3%. The incidence of CVC-related UL-DVT screened by venography reportedly varies between 27% and 66%. The incidence of clinically overt pulmonary embolism (PE) in patients with CVC-related UL-DVT ranges from 15% to 25%, but an autopsy-proven PE rate of up to 50% has been reported. Vessel injury caused by the procedure of CVC insertion, venous stasis caused by the indwelling CVC, and cancer-related hypercoagulability are the main pathogenetic factors for CVC-related venous thromboembolism (VTE). Several studies have assessed the benefit of the prophylaxis of UL-DVT after CVC insertion in cancer patients. According to the results of these studies, prophylaxis with low molecular weight heparin or a low fixed dose of warfarin has been recently proposed. However, the limitations of the experimental design of the prophylactic studies do not allow definitive recommendations. The recommended therapy for UL-DVT associated with CVC is based on anticoagulant therapy with or without catheter removal. This review focuses on the epidemiology, pathogenesis, diagnosis, prevention, and treatment of VTE in cancer patients with long-term CVC.
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PMID:Venous thromboembolism associated with long-term use of central venous catheters in cancer patients. 1451 99

Currently there is no cure for venous stasis syndrome, a common complication of deep vein thrombosis. Prophylaxis with anticoagulant agents, including new drugs presently under investigation, may decrease the incidence and costs associated with this condition.
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PMID:Venous stasis syndrome: the long-term burden of deep vein thrombosis. 1458 39

Venous thomboembolism (VTE) causes only about 2% of maternal deaths in the developing world but is a leading cause of direct maternal deaths in developed countries. Pregnancy increases the risk of VTE through venous stasis, changes in blood coagulability and damage to vessels. Early diagnosis of VTE depends crucially on awareness of the condition but clinical diagnosis is unreliable in pregnancy and objective testing is essential. Compression or duplex ultrasonography is used to diagnose deep venous thrombosis and a ventilation/perfusion scan for pulmonary embolism. Low molecular weight heparins are safe and effective for treatment and for thromboprophylaxis in pregnancy. All women should undergo risk assessment in early pregnancy or preferably before pregnancy. Identifying risk factors such as obesity, or a past or family history of thromboembolism, allows at-risk women to be offered thromboprophylaxis. Guidelines on thromboprophylaxis have reduced deaths after caesarean section and are now being developed for all women.
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PMID:Thromboembolism. 1471 63

We present a case of suprarenal and infrarenal absence of the inferior vena cava, combined with hyperhomocysteinemia in a 39-year-old woman who presented with symptoms of deep venous thrombosis. The patient also had a homozygous mutation of C677T methylenetetrahydrofolate reductase. Deep vein thrombosis has a multifactorial etiology involving both genetic and acquired factors. Absence of the inferior vena cava is a rare congenital anomaly, but recently it was confirmed as an important risk factor for the development of deep vein thrombosis, especially in young persons. Hypercoagulability due to hyperhomocysteinemia with a tendency toward venous stasis, mediated by congenital absence of the inferior vena cava is thought to have caused deep vein thrombosis in our patient. To our knowledge, this association has not yet been reported. The clinical features and prognosis of the entity are discussed.
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PMID:Deep venous thrombosis caused by congenital absence of inferior vena cava, combined with hyperhomocysteinemia. 1504 24

Pulmonary embolism is common cause of morbidity and mortality in immobile patients. Approximately 100 years ago,Virchow described a classical triad of local trauma to the vessel wall, hypercoagulability and stasis as cause of venous thromboembolism. Also prolonged travel is a risk factor for venous thromboembolic disease. The sitting position is caused by venous stasis and increased blood viscosity in the legs. The vessel lesions due to compression by the seat have been suggested as a cause of thrombosis. Addition in air travel relative hypoxia in the cabin of airplane reduces fibrinolytic activity and may lead to release of vein wall relaxin factors. Protective measures should include general advice to all passengers to avoid excess alcohol and caffeine, drink plenty of water and perform leg stretching exercises. Those with risk factors for deep vein thrombosis should carried out additional protective measures such as aspirin or low molecular weight heparin.
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PMID:[Travel and pulmonary thromboembolism]. 1514 81

A 76-year-old man was admitted with a first episode of deep vein thrombosis (DVT) of his left leg. It was associated with a distended urinary bladder, due to benign prostatic hypertrophy. Screening for malignancy was negative. Laboratory testing revealed protein S deficiency. Although a distended bladder may induce venous stasis, it is not a proven risk factor for DVT. Clinical expression possibly depends on the concomitance of other risk factors, such as inherited or acquired thrombophilic defects. However, it is also possible that the association of a distended bladder with DVT of a lower limb has not been recognised yet. As a distended bladder is rather common in elderly men, a proper study is warranted to estimate the prevalence of associated DVT.
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PMID:Deep vein thrombosis associated with distension of the urinary bladder due to benign prostatic hypertrophy--a case report. 1525 85

Our hypothesis was that, due to its sympatholytic action, epidural anesthesia (EA) administered as part of anesthesia in abdominal surgery would generate a marked venous leg flow enhancement, thus aiding in the prevention of peroperative venous stasis. We studied, and comprehensively quantified the venous haemodynamic changes in the lower limb during and immediately after abdominal surgery performed under EA and general (GA) anesthesia combined, in comparison to GA alone. This is a prospective, randomized, controlled study, stratified for hypertension and smoking, comprising ASA 1-2 patients undergoing elective total abdominal hysterectomy. Those with peripheral vascular or chronic venous disease, prior DVT or BMI>35 were excluded. Eligible recruits received either GA (Group GA) (n = 10; age 36-65, median 50) alone or epidural anesthesia (EA) and GA combined (Group EA/GA) (n = 9; age 32-58, median 46). EA (L(1-2)) was administered using lignocaine 2%. Both groups had GA induced with fentanyl and propofol, maintained with N(2)O and isoflurane; larygoscopy was facilitated with vecuronium; analgesia was provided either with morphine (Group GA) or epidurally with 2% lignocaine boli (Group EA/GA). Hemodynamics were determined at the popliteal vein in the horizontal supine position at baseline (resting prior to anesthesia), post epidural (20 min after delivery of EA), post induction (15 min after laryngeal intubation), surgery (upon uterus removal) and recovery (30 min after extubation). There was no difference in the mean velocity[V(mean)] between the 2 groups at baseline (p = 0.35([Mann-Whitney])), and post induction (p = 0.5([Mann-Whitney])). However V(mean) was significantly higher in Group EA/GA than Group GA, both at surgery (point estimate[PE]: 1.8 cm/s; 95% CI: 0.01, 6.3 cm/s; p <0.05([Mann-Whitney])) and recovery (PE: 2.6 cm/s; 95% CI: 0.4, 5.1 cm/s; p = 0.02([Mann-Whitney])). Volume flow[V(Q)] was similar in the 2 groups at baseline and post induction (both, p >0.1([Mann-Whitney])), but was significantly higher in Group EA/GA at surgery (PE: 54 ml/min; 95% CI: 18, 159 ml/min; p = 0.045([Mann-Whitney])) and recovery (PE: 49 ml/min; 95% CI: 16, 129 ml/min; p=0.0037([Mann-Whitney])). Peak velocity, V(mean) and V(Q) increased significantly post epidural in Group EA/GA. Contrary to the venous leg flow attenuation in elective abdominal surgery under GA and upon its recovery, EA administered as part of GA is associated with a significant enhancement of both V(mean) and V(Q). This beneficial hemodynamic effect of EA at the vulnerable stage of recovery may be critically essential in light of enhanced blood viscosity, fibrinolytic shut-down, endothelial/platelet activation and immobility, acting in synergy with putative cardiorespiratory protection. The results of this study lend support to the preferential selection of combined EA/GA in subjects at high risk for venous thromboembolism, particularly when optimal DVT prophylaxis is practically unattainable due to limitations pertaining to the nature of surgery.
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PMID:Effects of epidural-and-general anesthesia combined versus general anesthesia alone on the venous hemodynamics of the lower limb. A randomized study. 1554 27

Patients with brain tumors are at considerable risk for the formation of venous thromboemboli. One method of preventing these complications is mechanical prophylaxis in which an external pneumatic compression device and graduated elastic compression stockings are used. Evidence indicates that these devices prevent deep venous thrombosis (DVT) and pulmonary embolism (PE) by limiting venous stasis and increasing fibrinolytic activity at both the local and systemic levels. The authors present evidence for the occurrence of both mechanisms and discuss the use of mechanical compression in the setting of surgery for brain tumors. They also present data proving the efficacy of these devices in patients who undergo craniotomy with motor mapping for resection of glioma and in whom the contralateral leg receives no prophylaxis. Finally, they comment on the use of anticoagulation therapy both in addition to and in place of mechanical prophylaxis.
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PMID:Efficacy of mechanical prophylaxis for venous thromboembolism in patients with brain tumors. 1563 89

Thrombotic events are an increasingly recognized complication of treatment with intravenous immunoglobulins (IVIg). We aimed to define clinical characteristics, risk factors and outcome for venous thrombosis as opposed to arterial thrombosis following administration of IVIg. Six patients with post-IVIg venous thrombosis were identified at our institution. In addition, a review of the literature revealed 65 reported cases. Arterial thrombosis (stroke and myocardial infarction) was four times more common than venous thrombosis (deep vein thrombosis and pulmonary embolism). The incidence rate was estimated at 0.15-1.2% per treatment course, but the large increase in reported cases in 2003 suggests that the true incidence may be significantly greater. The following differences were found between arterial and venous events: arterial thrombosis occurred early after IVIg administration (49% within 4 h, 77% within 24 h) and was associated with advanced age and atherosclerotic vascular disease; venous thrombosis occurred later (54% more than 24 h after IVIg administration) and was associated with factors contributing to venous stasis (obesity and immobility). Thirteen patients died (mortality 20%), 11 of whom had arterial thrombosis. In conclusion, IVIg-associated thrombosis is more common than previously recognized, and is associated with significant mortality. The different characteristics of arterial and venous events may reflect different pathophysiological mechanisms. A better understanding of these mechanisms should aid in defining a risk-benefit ratio for the individual patient.
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PMID:Venous and arterial thrombosis following administration of intravenous immunoglobulins. 1660 87

The epidemiology of venous thromboembolism (VTE) in the community has important implications for VTE prevention and management. This review describes the disease burden (incidence), outcomes (survival, recurrence and complications) and risk factors for deep vein thrombosis and pulmonary embolism occurring in the community. Recent comprehensive studies of the epidemiology of VTE that reported the racial demography and included the full spectrum of disease occurring within a well-defined geographic area over time, separated by event type, incident vs. recurrent event and level of diagnostic certainty, were reviewed. Studies of VTE outcomes had to include a relevant duration of follow-up. VTE incidence among whites of European origin exceeded 1 per 1000; the incidence among persons of African and Asian origin may be higher and lower, respectively. VTE incidence over recent time remains unchanged. Survival after VTE is worse than expected, especially for pulmonary embolism. Thirty percent of patients develop VTE recurrence and venous stasis syndrome. Exposures can identify populations at risk but have a low predictive value for the individual. An acquired or familial thrombophilia may predict the subset of exposed persons who actually develop symptomatic VTE. In conclusion, VTE is a common, lethal disease that recurs frequently and causes serious long-term complications. To improve survival and prevent complications, VTE occurrence must be reduced. Better individual risk stratification is needed in order to modify exposures and target primary and secondary prophylaxis to the person who would benefit most.
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PMID:Venous thromboembolism: disease burden, outcomes and risk factors. 1610 26


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