Secondary Venous Thrombosis Research Articles

Totally implanted central venous access devices inserted by the femoral route: A narrative review and the proposal of a novel approach, the FICC-port.

Femoral ports are used in patients with indication to a totally implanted venous access device but with contraindication to chest-ports and brachial ports because of obstruction of the superior vena cava. In the last three decades, femoral ports have been implanted almost exclusively by cannulation of the common femoral vein at the groin, while the position of the tip has been assessed by X-ray. We report our experience with a new approach to femoral ports, which includes recent methods and techniques developed in the last few years. These novel femoral ports, which we call "FICC-ports," are characterized by (a) long femoral 5 Fr polyurethane catheter inserted by ultrasound-guided puncture of the superficial femoral vein at mid-thigh; (b) intraprocedural location of the tip in the sub-diaphragmatic inferior vena cava, using ultrasound visualization by the transhepatic and/or the subcostal view; (c) low-profile or very low-profile reservoir implanted above the quadriceps muscle, at mid-thigh. In the last 3 years, we have implanted 47 FICC-ports in young adults with mediastinal lymphoma compressing the superior vena cava. We had no immediate/early complication, and only three late complications (one kinking of the catheter in the subcutaneous tissue; one tip migration with secondary venous thrombosis; one persistent withdrawal occlusion due to fibroblastic sleeve). If there is indication to a femoral port, the implantation of a "FICC-port"-as described above-is to be strongly considered in terms of safety, effectiveness, and cost-effectiveness: no immediate-early complications, minimal late complications, no X-ray exposure, low invasiveness, low cost.

A systematic review of the utility of residual vein obstruction studies in primary and secondary venous thrombosis.

Background. Residual vein obstruction (RVO), the persistence of venous thrombosis with time and often after anticoagulation, may indicate a systemic prothrombotic condition. Prior studies have shown varying efficacy in using RVO as a risk factor for future venous thromboembolic (VTE) recurrence. Methods. To assess whether positive RVO imaging predicts recurrent VTE events, we performed a meta-analysis on studies in which patients with documented VTEs, anticoagulated for a minimum of 4 weeks, had repeat sonography to assess RVO and were subsequently followed for recurrent events. Results. Thirteen studies met inclusion criteria: 3531 patient VTE events with 3474 evaluable results were analyzed. The presence of RVO was associated with recurrence in all VTE (OR 1.93; 95% CI: 1.29, 2.89) and secondary VTE (OR 2.78; 95% CI: 1.41, 5.5) but not for primary VTE (OR 1.35; 95% CI: 0.87, 2.08). When cancer patients were eliminated from the secondary VTE group, there was no longer a significant association of RVO with VTE recurrence (OR 1.73; 95% CI: 0.81, 3.67) while in the subset of cancer patients, presence of RVO was associated with an increase in VTE recurrence risk (OR 5.14; 95% CI: 1.59, 16.65, P < 0.006). Conclusions. We conclude that the presence of RVO is associated with recurrence in secondary VTE but not in primary VTE and that association may be driven by the subset with cancer.

The role of CT in acute mesenteric ischemia

Results Only 12 patients (37.5%) performed a preoperative diagnostic CT study, whereas in 20 cases (62.5%) the intestinal ischemia was diagnosed during surgical exploration. The acute mesenteric ischemia caused primarily by occlusive superior mesenteric artery in 26 cases (81.2%) and by venous thrombosis in 6 cases (18.7%). Most of the embolus are located approximately 3–10 cm from superior mesenteric artery emergence. An arterial embolus can be detected like filling defect or like an abrupt interruption of vascular enhancement. Frequently a secondary venous thrombosis follows the arterial occlusion. CT shows a moderate intestinal wall thickening and inclusions in air signs of intestinal gangrene. Only 19 (59.3%) of 32 patients survived the acute intestinal ischemia (in hospital mortality was 40.6%), delayed diagnostic and operation caused higher mortality. In 12 cases a preoperative diagnostic CT was performed the mortality was 32.5%.

Venous thromboembolism and the risk of subsequent symptomatic atherosclerosis.

Recently, we reported an association between asymptomatic carotid atherosclerosis and venous thromboembolism (VTE) of unknown origin. We hypothesized that patients with VTE of unknown origin would be at a higher risk of developing symptomatic atherosclerosis than patients with VTE induced by known risk factors. To examine this hypothesis, we studied 1,919 consecutive patients followed prospectively after their first VTE episode. The primary outcome was non-fatal and fatal symptomatic atherosclerotic disease in patients with VTE of unknown origin as compared to those with secondary VTE. An independent committee assessed all study outcomes, and adjusted hazard ratios (HR) were calculated using the Cox's proportional hazards model. After a median follow-up of 48 and 51 months, respectively, at least one symptomatic atherosclerotic complication was detected in 160 of the 1,063 patients (15.1%) with VTE of unknown origin, and in 73 of the 856 (8.5%) with secondary VTE. After adjusting for age and other risk factors of atherosclerosis, the HR for symptomatic atherosclerotic complications in patients with VTE of unknown origin compared to those with secondary VTE was 1.6 (95% confidence intervals; CI: 1.2-2.0). When the analysis was restricted to patients without previous symptomatic atherosclerosis, the HR became 1.7 (95% CI: 1.1-2.4). Patients with VTE of unknown origin have a 60% higher risk of developing symptomatic atherosclerotic disease than do patients with secondary venous thrombosis.

Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men.

A specific point mutation in the gene coding for coagulation factor V is associated with resistance to degradation by activated protein C, a recently described abnormality of coagulation that may be associated with an increased risk of venous thrombosis. Whether this mutation also predisposes patients to arterial thrombosis is unknown, as is the value of screening for the mutation in order to define the risk of venous thrombosis among unselected healthy people. Among 14,916 apparently healthy men in the Physicians' Health Study who provided base-line blood samples, 374 had myocardial infarctions, 209 had strokes, and 121 had deep venous thrombosis, pulmonary embolism, or both, during a mean follow-up of 8.6 years. We determined whether a mutation at nucleotide position 1691 of the factor V gene was present or absent in these 704 men and in an equal number of matched participants who remained free of vascular disease. The prevalence of heterozygosity for the mutation among men who had myocardial infarctions (6.1 percent, P = 0.9) or strokes (4.3 percent, P = 0.4) was similar to that among men who remained free of vascular disease (6.0 percent). However, the prevalence of the mutation was significantly higher among men who had venous thrombosis, pulmonary embolism, or both (11.6 percent, P = 0.02). In adjusted analyses, the relative risk of venous thrombosis among men with the mutation was 2.7 (95 percent confidence interval, 1.3 to 5.6; P = 0.008). This increased risk was seen with primary venous thrombosis (relative risk, 3.5; 95 percent confidence interval, 1.5 to 8.4; P = 0.004) but not with secondary venous thrombosis (relative risk, 1.7; 95 percent confidence interval, 0.6 to 5.3; P = 0.3), and it was most apparent among older men. Specifically, the prevalence of the mutation among men over the age of 60 in whom primary venous thrombosis developed was 25.8 percent (relative risk, 7.0; 95 percent confidence interval, 2.6 to 19.1; P < 0.001). In a large cohort of apparently healthy men, the presence of a specific point mutation in the factor V gene was associated with an increased risk of venous thrombosis, particularly primary venous thrombosis. The presence of the mutation was not associated with an increased risk of myocardial infarction or stroke. This mutation appears to be the most common inherited factor thus far recognized that predisposes patients to venous thrombosis.

Deep-Vein Thrombosis and the Incidence of Subsequent Symptomatic Cancer

In contrast to the established relation between overt cancer and subsequent venous thromboembolism, it is unclear whether symptomatic deep-vein thrombosis is associated with a risk of subsequent overt malignant disease. Two hundred sixty consecutive patients with symptomatic, venographically proved deep-vein thrombosis were enrolled in a study, of whom 250 were followed during a two-year period. Among those assessed during follow-up, the incidence of subsequently detected cancer in the 105 patients with secondary venous thrombosis (i.e., thrombosis associated with a well-recognized risk factor other than cancer) was compared with the incidence of cancer in the 145 patients with idiopathic venous thrombosis. Routine examination at the time of diagnosis of the venous thrombosis revealed cancer in 5 of the 153 enrolled patients with idiopathic venous thrombosis (3.3 percent) and in none of the 107 enrolled patients with secondary venous thrombosis. During follow-up, overt cancer developed in 2 of the 105 patients with secondary venous thrombosis (1.9 percent) and in 11 of the 145 patients with idiopathic venous thrombosis (7.6 percent; odds ratio, 2.3; 95 percent confidence interval, 1.0 to 5.2; P = 0.043). Of the 145 patients with idiopathic venous thrombosis, 35 had confirmed recurrent thromboembolism. Overt cancer subsequently developed in 6 of the 35 (17.1 percent). The incidence of cancer in the patients with recurrent idiopathic venous thrombosis was higher than that in the patients with secondary venous thrombosis (P = 0.008; odds ratio, 9.8; 95 percent confidence interval, 1.8 to 52.2) or in the patients with idiopathic venous thrombosis that did not recur (P = 0.024; odds ratio, 4.3; 95 percent confidence interval, 1.2 to 15.3). There is a statistically significant and clinically important association between idiopathic venous thrombosis and the subsequent development of clinically overt cancer, especially among patients in whom venous thromboembolism recurs during follow-up.

About epifascial gangrene

The occurrence of epifascial gangrene in the scrotal region is caused by anatomical and physiological features of this region. The absence of anastomoses of scrotal skin arteries with the underlying anatomical formations, which worsens the local blood supply conditions, draws attention. Triggering mechanisms causing epifascial gangrene (surgical and domestic trauma, skin diseases, etc.) cause vasomotor reaction of blood circulation at the level of arterioles, lymph circulation with evident ischemia and secondary venous thrombosis. This creates conditions for intensive development, accumulation and manifestation of pathogenic properties of microbial flora naturally vegetating on the surface or penetrating into the subcutaneous tissue from the thoracic and abdominal cavity during surgery.

Cutaneous and Venous Complications of Pentazocine Abuse

A 55-year-old man with a two-year history of intramuscular pentazocine abuse had classical cutaneous findings as well as secondary venous thrombosis, which, to our knowledge, is previously undescribed. Histologic evaluation, including direct immunofluorescent microscopy, did not establish the mechanism of tissue destruction.