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PubMed2004

Thromboembolism and toxic shock syndrome: a case presentation and literature update.

A case of progressive shock and multisystem organ failure is reported for an 18 year old Lebanese woman, clinically diagnosed as toxic shock syndrome (TSS). The patient developed cough and dyspnea during hospitalization; chest CT angiography revealed thromboembolism of the pulmonary artery. CBC analysis showed leukocytosis with a white cell count (WCC) with a marked increase in PT and PTT coupled with reduced protein S, antithrombin III, and protein C levels. The patient improved gradually and was discharged from the hospital 7 days later on oral anticoagulation, and was followed up for six months with no disease recurrence or complications. To our knowledge, this is the first reported case in the literature of toxic shock syndrome associated with pulmonary thromboembolism.

Adult↗
PubMed2001

[Postoperative heparin-induced thrombopenia with thromboembolism (HITT)--a rare complication of heparin therapy?].

Many surgical patients receive either unfractionated or low-molecular weight heparin in a prophylactic or therapeutic intention. Feared upon the administration of heparin is the heparin-induced thrombopenia (HIT). In HIT type 1, the heparin directly interacts with the platelets. The platelet count rarely falls below 100,000/microliter and normalizes again despite continuous administration of heparin. In HIT type 2 or HIT with thrombosis (HITT) the platelet count usually falls more than 50% and due to an antibody-dependent platelet activation, thromboembolic episodes may occur. Compared to non-surgical patients, the incidence of HITT in the postoperative phase is markedly increased. In suspicion of a HITT, heparins should immediately be stopped and replaced by an alternative coagulant because of a high risk of further thromboembolic complications. Direct thrombin-inhibitors such as the recombinant hirudins are considered to be safe and effective. They have no heparin-like immunological properties and therefore, they seem to become the therapeutic and prophylactic "gold-standard" in patients with HITT.

Heparin↗
PubMed2007

Tissue factor expression as a possible determinant of thromboembolism in ovarian cancer.

Ovarian cancer, and clear cell carcinoma in particular, reportedly increases the risk of venous thromboembolism (VTE). However, the mechanisms remain unclear. Tissue factor (TF) supposedly represents a major factor in the procoagulant activities of cancer cells. The present study examined the involvement of TF expression in VTE for patients with ovarian cancer. Subjects comprised 32 consecutive patients (mean age 49.8 years) with histologically confirmed ovarian cancer. Presence of VTE was examined using a combination of clinical features, D-dimer levels and venous ultrasonography. Immunohistochemical analysis was used to evaluate TF expression into 4 degrees. Venous thromboembolism was identified in 10 of the 32 patients (31%), including five of the 11 patients with clear cell carcinoma. Tissue factor expression was detected in cancer tissues from 24 patients and displayed significant correlations with VTE development (P=0.0003), D-dimer concentration (P=0.003) and clear cell carcinoma (P<0.05). Multivariate analysis identified TF expression as an independent predictive factor of VTE development (P<0.05). Tissue factor (TF) expression is a possible determinant of VTE development in ovarian cancer. In particular, clear cell carcinoma may produce excessive levels of TF and is more likely to develop VTE.

Adolescent↗
PubMed2001

Methionine synthase A2756G and methylenetetrahydrofolate reductase A1298C polymorphisms are not risk factors for idiopathic venous thromboembolism.

Hyperhomocysteinemia is a defined risk factor for venous thromboembolism (VTE). Several polymorphisms of genes encoding for enzymes acting in the remethylation pathway of homocysteine metabolism, ie, methionine synthase (MS) A2756G, methylenetetrahydrofolate reductase (MTHFR) C677T and MTHFR A1298C, can cause increased homocysteine levels particularly in patients with deficiencies of folic acid, vitamin B6, or B12 and hence be potential risk factors for VTE. Indeed, homozygous MTHFR C677T was shown to be a mild risk factor for VTE by some, but not by all, investigators. In this study, we assessed the risk exerted by MS A2756G and MTHFR A1298C in a cohort of patients with idiopathic venous thromboembolism. Homozygosities for MS A2756G and MTHFR A1298C were not found to be statistically significant risk factors for VTE. In addition, no interactions were observed among MS A2756G, MTHFR A1298C and MTHFR C677T in conferring a risk of VTE.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2002

Experiences of a low-intensity anticoagulation regimen for extended secondary prevention of venous thromboembolism.

Extended treatment with vitamin K antagonists for more than 6 months is often used for secondary prevention of venous thromboembolism (VTE) in patients at high or moderate risk for recurrent events. The intensity of anticoagulant therapy is usually maintained at an International Normalized Ratio (INR) of 2-3. An INR of 1.5-2 might also prevent thromboembolic events with less complications of bleeding, but results from randomized trials are not yet available. In a non-prospective, uncontrolled study 40 patients with a history of VTE and an estimated high risk for recurrent events due to several previous events and/or thrombophilic defects were, after a median of 11.5 months on regular intensity anticoagulation (INR 2-3), switched to a low intensity regimen (INR 1.5-2). In six of the patients an estimated high risk for complications of bleeding contributed to this decision. After a median follow-up of 36 months (140 patient-years) recurrent events, complications of bleeding and some basic quality of life measurements regarding the new treatment were registered. No recurrent events, four minor bleedings and no major bleedings were registered. Twenty-six patients preferred an INR of 1.5-2 compared to 2-3. The main reasons for that preference were a lower risk for bleeding (13 patients) and less frequent monitoring of the INR (18 patients). No patient preferred full-dose anticoagulation at INR 2-3. In patients at a high risk for recurrence of VTE an initial period of regular intensity anticoagulation, followed by a low-intensity regimen, may provide effective and safe secondary prophylaxis.

Adult↗
PubMed2000

A comparison of the risks of venous thromboembolic disease in association with different combined oral contraceptives.

AIMS: In October 1995 in response to the results of three studies, the Committee on the Safety of Medicines advised doctors and pharmacists that oral contraceptives containing desogestrel (DSG) and gestodene (GST) were associated with around a two-fold increase in the risk of thromboembolism compared with those containing other progestogens. The objective of this study was to estimate the risk of idiopathic venous thromboembolic disease (VTE) in users of combined oral contraceptives (COCs), to compare the risk between formulations and to examine the effect of using age banding as opposed to matching by exact year of birth. METHODS: A nested case control study was conducted using the General Practice Research Database. Women with a VTE event recorded between 1992 and 1997, who were treated with an anticoagulant, from consideration of their prescription records were likely to have been using a COC prescription on the day of the event and also had no exclusion factors, were deemed cases. For comparison with the previous studies, two nested case control studies were undertaken. Study 1 used controls matched by practice and year of birth. Study 2 used controls matched by practice and within 5 years age bands. RESULTS: We found an incidence of idiopathic VTE amongst users of combined oral contraceptives of 3.8 per 10 000 exposed women years. Incidence rates increased markedly after 35 years of age. The nested case-control study using controls matched by year of birth showed no significant difference in risk between the major COC formulations. With levonorgestrel (LNG) 150 microgram and ethinyloestradiol (EE) 30 microgram as the reference, the adjusted ORs for GST 75 microgram and EE 30 microgram was 1.3 (95% CI 0.8, 2.1), for DSG 150 microgram and EE 30 microgram it was 1.0 (95% CI 0.7, 1.7) and for DSG 150 microgram and EE 20 microgram it was 0.8 (95% CI 0.4, 1.6). Using less rigorous matching criteria, matching controls to cases within 5 years age bands, the ORs increased. When a mixed group of COCs, characterized by having LNG as the progestogen component was used as the reference category, there was an elevation in the ORs for the newer products. We found a significant association between idiopathic VTE and current smoking (OR 2.0 (1.4, 2.7)), BMI over 35 (OR 3.8 (1.8, 8.0)) and asthma (OR 1.9 (1.3, 2.9)). The OR for women who had proxy evidence of general ill health (indicated by the number of prescriptions issued) was 2.2 (1.7, 3.7). CONCLUSIONS: The results of this study indicate that a number of the characteristics of the women taking COCs affect the risk of VTE. There is no evidence to support the hypothesis that there is any difference in risk between COC formulations containing under 50 microg ethinyloestradiol.

Adolescent↗
PubMed1997

Risk of venous thromboembolism associated with a G to A transition at position 20210 in the 3'-untranslated region of the prothrombin gene.

The odds ratio for the FII 20210G/A mutation in 504 patients with venous thromboembolism compared to controls was 2.0 (95% CI 1.0-4.0) and, for factor V Leiden, 5.8 (95% CI 3.3-10.3). 3/504 patients were heterozygous for both mutations. None of the patients had combined natural anticoagulant deficiency and the FII 20210G/A mutation. We conclude that the FII 20210G/A mutation is present in 2.6% of the population and the relative risk of venous thromboembolism in carriers is 2.0.

Factor V↗
PubMed1998

A common polymorphism in the tumour necrosis factor-alpha gene associated with high TNF levels is not a risk factor for venous thromboembolism.

The odds ratio of homozygosity or heterozygosity for the TNF2 polymorphism in 575 patients with venous thromboembolism compared to controls was found to be 1.0 (95% CI 0.4-2.1) and 1.1 (95% CI 0.8-1.4) respectively. Comparing subgroups of patients and controls with the factor V Leiden mutation the odds ratio for the TNF2 polymorphism was 0.7 (95% CI 0.2-2.2). Despite evidence of a link between high tumour necrosis factor (TNF) levels and hypercoagulability, our results do not indicate a link between the genetic regulation of TNF production and venous thromboembolic disease.

Adolescent↗
PubMed1998

Effect of the MTHFRC677T variant on risk of venous thromboembolism: interaction with factor V Leiden and prothrombin (F2G20210A) mutations.

Odds ratios for the MTHFRC677T variant were determined in a large case-control study of 558 unselected patients with venous thromboembolism and 500 control subjects. The odds ratios for MTHFRC677T heterozygosity and homozygosity were 1.07 (95%CI 0.84-1.36) and 0.71 (95%CI 0.48-1.03). In patients with the factor V Leiden or the F2G20210A mutations there was no apparent increase in risk of venous thromboembolism due to the MTHFRC677T polymorphism. Thrombophilia testing should not include genotyping for the MTHFRC677T polymorphism.

Adolescent↗
PubMed2003

Thromboembolic events in patients with myelodysplastic syndrome receiving thalidomide in combination with darbepoietin-alpha.

A phase II trial was conducted to explore the efficacy and tolerability of combining thalidomide (100 mg/d p.o.) with an erythropoietic growth factor (darbepoietin-alpha 2.25 micro g/kg/d s.c.) in patients with low-to-intermediate-risk myelodysplastic syndromes (MDS). However, the trial had to be discontinued early because of an unexpectedly high incidence of thromboembolic events. Of the first seven patients enrolled, two developed deep-vein thrombosis and one died of massive pulmonary embolism. We concluded that thalidomide might significantly increase the thromboembolic risk of erythropoietic proteins in MDS patients. Careful clinical surveillance and thrombosis prophylaxis (heparin or oral anticoagulation) should be considered for MDS patients undergoing combined treatment with thalidomide and erythropoietic growth factors.

Aged↗
PubMed2002

Revascularization of the superior mesenteric artery after acute thromboembolic occlusion.

BACKGROUND: The outcome and prognostic factors after revascularization of acute thromboembolic occlusion of the superior mesenteric artery (SMA) are poorly documented. METHODS: Sixty patients with acute thromboembolic occlusion of the SMA had revascularization procedures at 21 hospitals from 1987 to 1998. They were registered prospectively in the Swedish Vascular Registry. Patient files were analysed retrospectively. RESULTS: The median age of the patients was 76 years; 73 per cent suffered from cardiac disease and 23 per cent had previous vascular surgery. Onset of symptoms was classified as sudden (30 per cent), acute (33 per cent) or insidious (37 per cent). The occlusions were thought to be either embolic (67 per cent) or thrombotic (33 per cent). The diagnosis was suspected on first examination in 32 per cent of patients, a group whose median time to operation was shorter (P = 0.01). Fifty-eight patients had an exploratory laparotomy and subsequent revascularization, and two were treated with thrombolysis alone. Second-look laparotomy was performed in 41, and third look in eight patients; 19 required an additional bowel resection. The overall mortality rates were 43, 52, 60 and 67 per cent at 30 days, discharge, 1 and 5 years, respectively. No patient was dependent on intravenous nutrition after 1 year. Previous vascular surgery resulted in a higher institutional mortality rate (79 per cent; P = 0.02). Patients who had a sudden onset of symptoms outside hospital had a better outcome (mortality rate 27 per cent; P = 0.02). CONCLUSION: Many non-diagnostic radiological examinations were performed and a routine second-look is warranted. The results suggest that attempts at revascularization procedures for acute mesenteric ischaemia may improve the outcome.

Adult↗
PubMed1999

Oral anticoagulation in venous thromboembolism: decisions based on more than mere feelings.

Although there is a very limited scientific basis for the recommendation to target the intensity of oral anticoagulation after venous thromboembolism at an international normalized ratio (INR) of 2.0-3.0, this has been widely adopted. It seems possible from the DURAC I and II trials that a slight lowering of the upper limit could further reduce the risk of major haemorrhage. The optimal duration of anticoagulation in this group of patients has been extensively investigated. For the majority of patients a treatment duration of 6 months eliminates the high risk of relatively early recurrences without yielding an increase in the incidence of major haemorrhages. Patients with a distal deep vein thrombosis and a temporary risk factor or those with poor compliance should have a shorter treatment duration, whereas further prolongation is warranted in patients with certain biochemical abnormalities or recurrent thromboembolic episodes. The optimal treatment regimen is individualized, taking into account a variety of risk factors, and re-evaluated regularly in case of prolonged therapy.

Administration, Oral↗
PubMed2003

Safety from thromboembolism using intravenous immunoglobulin therapy in Kawasaki disease: Study of whole-blood viscosity.

BACKGROUND: High-dose intravenous infusions of immunoglobulin (IVIG) are well established as a standard therapy for Kawasaki disease (KD) for reducing the risk of coronary artery aneurysms. IVIG therapy might increase the blood viscosity both in vitro and in vivo, which has been reported as a risk factor for cardiovascular or cerebrovascular thromboembolism in adults. METHODS: We measured the whole-blood viscosity in vitro, serum IgG and albumin, and blood hematocrit in 10 patients with KD and 10 with non-KD (five with acute encephalitis, one with sepsis, one with idiopathic thrombocytopenic purpura, one with Guillain-Barré syndrome, one with insulin-dependent diabetes mellitus, and one with Evans syndrome) before and after IVIG therapy. RESULTS: The blood viscosity increased significantly after IVIG therapy in the patients with non-KD, but did not increase in those with KD. CONCLUSION: The results of the present study suggest that the use of IVIG therapy for KD might be relatively safe, with no risk of thromboembolism due to hyperviscosity.

Blood Viscosity↗
PubMed2001

Management of venous thromboembolic disease in the lower limb.

Thromboembolic disease continues to cause significant morbidity and mortality in our community, despite extensive research into the aetiological factors and significant resources invested in the development of pharmacological agents for treating this condition. Development of more sensitive and specific modalities for identifying venous thromboses has improved their early detection, particularly in the commonest site, the lower limb. A rational evidence-based management pathway has not been formulated as debate continues over the most appropriate method of treatment. This review outlines the pathophysiology of the disease, provides a clinical pathway for the management of lower limb thromboembolic disease using reliable available evidence and briefly discusses the efficacy of drug therapy.

Fibrinolytic Agents↗
PubMedDate not supplied

Retrospective survey of unselected hospital patients with and without cancer comparing outcomes following venous thromboembolism.

BACKGROUND: Cancer patients are at risk of venous thromboembolism (VTE). Currently, management of these patients is based on studies performed in the general population. AIMS: To determine whether the natural history of VTE in cancer patients differs sufficiently from patients in general such that a specific management approach is required. METHODS: A retrospective survey was conducted using case records from three tertiary referral hospitals (1993-2001). One hundred and forty-seven VTE patients with cancer and 82 control patients matched for age and gender were followed for a median of 24 months (0-104 months). RESULTS: The overall prevalence of cancer among patients with VTE was 19.3% (vs 4% in patients with arterial thromboembolic events). In the follow-up groups, cancer conferred a significantly worse functional status, although other risk factors for VTE were similar. Proximal sites of VTE were twice as common in cancer as in non-cancer patients. The majority of patients in both groups were treated with oral anticoagulants. Complications were more common in cancer patients (40% vs 23%) and occurred more frequently despite apparently adequate anticoagulation. Following VTE, cancer patient survival (median 4.1 months, 127 deaths) was markedly worse than non-cancer patients (median not reached, eight deaths). Thirty-five cancer deaths occurred within 5 weeks of VTE. Eleven deaths in cancer patients were directly related to VTE compared to three in patients without cancer. CONCLUSIONS: Cancer patients with VTE fare extremely poorly compared to the general hospital population. Prospective treatment studies, specifically in cancer patients with VTE, are needed.

Aged↗
PubMed2003

Thromboembolic risk of patients referred for radiofrequency catheter ablation of typical atrial flutter without prior appropriate anticoagulation therapy.

BACKGROUND: Radiofrequency catheter ablation of isthmus dependent atrial flutter is considered the therapy of choice. There is, however, controversy with regard to the thrombogenicity of atrial flutter in comparison with atrial fibrillation. METHODS: Consecutive patients scheduled for catheter ablation of documented typical atrial flutter receiving insufficient (INR < 2.0) or no anticoagulation during the three weeks preceding the procedure underwent multiplane transesophageal echocardiography (TEE). Patients with exclusive documentation of atrial flutter were classified as group I, whereas patients with additional documentation of atrial fibrillation were classified as group II. RESULTS: The study included 201 patients, 62 of whom were not on therapeutic anticoagulation (mean age 64 +/- 9 years, 87% men). In 10 of these 62 patients (16%), TEE detected a left atrial (LA) appendage thrombus in 4, or dense spontaneous echo contrast (SEC) in 6 patients. Comparison of patients with versus without SEC or thrombus, revealed a higher incidence of valvular heart disease (60% vs 26%, P = 0.05), but no differences with respect to age, gender, LA diameter, left ventricular end-diastolic diameter, or left ventricular ejection fraction. The incidence of positive TEE findings in group I was 1 in of 36 versus 9 of 26 in group II (3% vs 35%, P < 0.001), and the relative risk for thromboembolism in group II versus group I was 12.5 (95% CI: 3-55, P < 0.001). CONCLUSION: There is a significant risk for thromboembolism in patients referred for ablation of typical atrial flutter who have not been appropriately anticoagulated.

Anticoagulants↗
PubMed2000

Prevention of thromboembolism in atrial fibrillation. A meta-analysis of trials of anticoagulants and antiplatelet drugs.

OBJECTIVE: Appropriate use of drugs to prevent thromboembolism in patients with atrial fibrillation (AF) involves comparing the patient's risk of stroke and risk of hemorrhage. This review summarizes the evidence regarding the efficacy of these medications. METHODS: We conducted a meta-analysis of randomized controlled trials of drugs used to prevent thromboembolism in adults with nonpostoperative AF. Articles were identified through the Cochrane Collaboration's CENTRAL database and MEDLINE until May 1998. MAIN RESULTS: Eleven articles met criteria for inclusion in this review. Warfarin was more efficacious than placebo for primary stroke prevention (aggregate odds ratio [OR] of stroke = 0.30, 95% confidence interval [CI] 0.19, 0.48), with moderate evidence of more major bleeding (OR 1.90; 95% CI 0.89, 4.04). Aspirin was inconclusively more efficacious than placebo for stroke prevention (OR 0.56, 95% CI 0.19, 1.65), with inconclusive evidence regarding more major bleeds (OR 0.81, 95% CI 0.37, 1.77). For primary prevention, assuming a baseline risk of 45 strokes per 1,000 patient-years, warfarin could prevent 30 strokes at the expense of only 6 additional major bleeds. Aspirin could prevent 17 strokes, without increasing major hemorrhage. In direct comparison, there was evidence suggesting fewer strokes among patients on warfarin than among patients on aspirin (aggregate OR 0.64, 95% CI 0.43, 0.96), with only suggestive evidence for more major hemorrhage (OR 1.60, 95% CI 0.77,3.35). However, in younger patients, with a mean age of 65 years, the absolute reduction in stroke rate with warfarin compared with aspirin was low (5.5 per 1,000 person-years) compared with an older group (15 per 1,000 person-years). CONCLUSION: In general, the evidence strongly supports warfarin for patients with AF at average or greater risk of stroke. Aspirin may prove to be useful in subgroups with a low risk of stroke, although this is not definitively supported by the evidence.

Anticoagulants↗