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PubMed2003

Incidence of arteriovenous thrombosis and the role of anticardiolipin antibodies in hemodialysis patients.

INTRODUCTION: Fistula thrombosis in patients on maintenance hemodialysis is an important morbidity factor. Arterial or venous thrombotic events have been described as complications in patients on regular hemodialysis and positive titers of anticardiolipin antibodies (ACLA). This study was designed to evaluate the prevalence of ACLA in hemodialysis patients and it's relation to arteriovenous fistula (AVF) thrombosis. METHODS: 218 patients with AVF on maintenance hemodialysis were studied prospectively during a period of 14 months for any episode of AVF thrombosis (AVFT), after ACLA was assayed by ELISA in 171 ones. Other risk factors for thrombosis such as presence of diabetes, hypotension during dialysis, using of erythropoietin (rEpo), fistula site, gender, age, dialysis duration, and type of dialyser membrane were accessed. RESULTS: 56% of the patients had IgG ACLA = 10 GPL which was significantly correlated with dialysis duration (23.18 +/- 24.56 months in patients with ACLA = 10 GPL vs 37.73 +/- 36.35 months in patients with 20 = IgG ACLA < 40 GPL). Within 14 months follow up, 39 episodes of AVFT occurred in 34 patients (15.8%). Dialysis duration prior to start of study was 29.16 +/- 22.04 months. In our patients radiocephalic AVFs showed more thrombosis than brachiocephalic ones (23% vs 10%, p = 0.01 by Chi-square). Age more than 50 years old was a risk factor for AVFT (p = 0.034 by Chi-square). Also erythropoietin use (p = 0.011 by chi-square) and ultrafiltration more than 3 liters (average value of 14 months) were correlated with AVFT (p = 0.042 by Chi-square), but there wasn't any correlation between diabetes, presence of ACLA, hypotension during dialysis, gender, and dialysis membranes with AVFT. Ultimately, logistic regression analysis of factors associated with thrombosis was done and only fistula site (p = 0.015, O.R. = 2.87), and Eprex use (p = 0.031, O.R. = 4.05) showed significant correlation with AVFT. CONCLUSION: Although incidence of anticardiolipin antibodies was high in our patients, we found no correlation between IgG ACLA and AVFT. Instead, we found that radiocephalic fistulas and Eprex injection were risk factors for AVFT.

Antibodies, Anticardiolipin↗
PubMed2002

Eversion thrombectomy for portal vein thrombosis during liver transplantation.

Portal vein thrombosis (PVT) has been seen as an obstacle to orthotopic liver transplantation (OLT), but recent data suggest that favorable results may be achieved in this group of patients. The aim of this study was to analyze the incidence, management, and survival of patients with PVT undergoing primary OLT with thrombectomy. Between October 1990 and August 2000, 468 liver transplantations were performed in our center and portal vein thrombosis was present in 38 patients (8.1%). Preoperative diagnosis, extension, intraoperative management, postoperative recurrence of portal vein thrombosis, and 1-year actuarial survival rates were retrospectively studied. Preoperative diagnosis was made in 17 cases (44.7%). In all patients, portal flow was restored after portal vein thrombectomy, followed by usual end-to-end portal anastomosis. All patients received preventive low-weight heparin from day 2 to hospital discharge, and then aspirin. Rethrombosis was observed in one patient with extended splanchnic thrombus. The 1-year actuarial patient survival rate was 83.7%, and did not significantly differ from the patients without portal vein thrombosis (86.7%). Our results suggest that portal vein thrombosis is often partial and thus difficult to diagnose preoperatively: it can be managed successfully during surgery by thrombectomy, except when there is complete splanchnic veins thrombosis; and it did not affect 1-year survival.

Humans↗
PubMed2005

Prevalence of inherited prothrombotic abnormalities and central venous catheter-related thrombosis in haematopoietic stem cell transplants recipients.

In this prospective study, we assessed the incidence of central venous catheter (CVC)-related thrombosis in haematopoietic stem cell transplant (HSCT) recipients. We determined the contribution of inherited prothrombotic abnormalities in blood coagulation to CVC-related thrombosis in these patients. The study was conducted between May 2002 and September 2004. CVCs were externalized, nontunneled, polyurethane double lumen catheters. Before catheter insertion, laboratory prothrombotic markers included factor V Leiden, the prothrombin gene Gly20210A mutation, plasma antithrombin levels, and protein C and S activity. All patients were systematically examined by ultrasonography just before, or <24 h after, catheter removal, and in case of clinical signs of thrombosis. A total of 171 patients were included during the 28-month study period. Five (2.9%) and three (1.7%) patients had evidence of protein C and protein S deficiency, respectively. Only one patient had an antithrombin deficiency (0.6%). In total, 10 patients (5.8%) were heterozygous for the factor V Leiden mutation, and one patient had heterozygous prothrombin G20210A mutation (0.6%). We observed a CVC-related thrombosis in 13 patients (7.6%). Thrombosis was diagnosed in four out of 20 patients (20%) with a inherited prothrombotic abnormality compared to nine of 151 patients (6%) who did not have a thrombophilic marker (relative risk 3.3 CI 95% 1.1-9.9). Our results suggest that inherited prothrombotic abnormalities contribute substantially to CVC-related thrombosis in HSCT recipients. In view of physicians' reluctance to prescribe prophylactic anticoagulant treatment in these patients, a priori determination of inherited prothrombotic abnormalities may form a basis to guide these treatment decisions.

Blood Coagulation Factors↗
PubMed2003

Antiphospholipid antibodies and thrombosis: strength of association.

Antiphospholipid antibodies, that is, lupus anticoagulants and anticardiolipin antibodies, are associated with thrombosis and obstetric complications in the antiphospholipid syndrome. Venous thrombosis occurs mostly in the lower limbs, with or without pulmonary embolism, and cerebral ischemia and transient ischemic attacks are the most common arterial events. Overall, the prevalence of thrombosis is about 30%, the rate of first event approximates 1%/year, and that of recurrence of patients not receiving anticoagulation is about 10-29%/year. The presence of lupus anticoagulants carries an odds ratio for thrombosis ranging from 5 to 16, and that of anticardiolipin antibodies from nonsignificant to 18. The detection of anti-beta2-glycoprotein I, but not antiprothrombin, antibodies might also help to identify antiphospholipid-positive patients at risk of thrombosis. Unfractionated or low-molecular-weight heparin followed by oral anticoagulation represents the current treatment of both arterial and venous thrombosis. However, uncertainty still exists about the optimal duration and intensity of oral anticoagulation following the first event. Several therapeutic clinical trials are currently being conducted, which soon clarify these issues. The prevalence of obstetric complications is about 15-20%. The presence of lupus anticoagulants carries an odds ratio for recurrent miscarriages and fetal death ranging from 3.0 to 4.8, whereas that of anticardiolipin antibodies goes from 0.86 to 20. Unfractionated or low-molecular-weight heparin in combination with low-dose aspirin represents the current standard of treatment of pregnant antiphospholipid-positive women to prevent recurrent obstetric complications. Upon treatment, the live birth rate increases from 0-40% to 70-80%.

Abortion, Habitual↗
PubMed1996

Failure of thrombin inhibition to prevent intracoronary thrombosis in the dog.

1. Recurrent occlusion after thrombolysis may be caused by thrombin receptor-mediated platelet thrombosis occurring in a residual stenosis. To test the relative importance of the platelet thrombin receptor under conditions of high shear and endothelial damage (the Folts model of intracoronary thrombosis) we used the specific thrombin inhibitor recombinant hirudin. 2. A critical coronary artery stenosis overlying an area of crushed endothelium was used in a repeated measures study of eight open-chest anaesthetized dogs. In the control period, recurrent thrombosis occurred at an average rate (+/- SD) of 4.4 +/- 1.4 ml/min2. Infusion of recombinant hirudin at 1.6 mg h-1 kg-1 abolished recurrent thrombosis in three dogs, but the thrombosis rate averaged 4.7 +/- 2.9 ml/min2 in the remaining five animals. 3. Haematological measurements demonstrated the activity of recombinant hirudin: thrombin time rose from 13 +/- 3 s to > 165 s universally (P < 0.01), partial thromboplastin time rose from 14 +/- 2 s to 29 +/- 10 s (P < 0.01). Bleeding time rose from 2.3 +/- 0.8 min to 4.7 +/- 1.8 min (P < 0.05). 4. It is concluded that specific thrombin inhibition, despite affecting coagulation, is relatively ineffective in preventing intracoronary thrombosis under conditions of high shear.

Animals↗
PubMed2002

Pipobroman is safe and effective treatment for patients with essential thrombocythaemia at high risk of thrombosis.

Essential thrombocythaemia (ET) is a disease associated with an elevated risk of thrombosis. This study evaluated the efficacy and safety of pipobroman (PB) in the long-term control of ET patients who had, at diagnosis, one or more of the following currently known risk factors for thrombosis or haemorrhage (high-risk patients): age > 60 years, history of thrombosis or haemorrhage, platelets >1000 x 10(9)/l. From 1978 to 2000, with a median follow-up of 10 years, 118 previously untreated high-risk ET patients (median age 62 years, range 25-82), were treated with PB at the starting dose of 0.8-1 mg/kg/d. All patients reached a platelet count <600 x 10(9)/l and 91% achieved a platelet count <400 x 10(9)/l. During follow-up, 13 patients had thrombosis, with a 10-year cumulative risk of 14%. Acute myeloid leukaemia, myelofibrosis and solid tumours occurred in three, two and seven patients with a 10-year cumulative risk of 3%, 2% and 7% respectively. Actuarial survival at 20 years was 64% and the standardized mortality ratio was 1.1 (95% CI: 0.7-1.7), not statistically different from the general population (P = 0.54). Age was associated with a higher risk of death (P = 0.00009) and thrombosis (P = 0.003). The duration of PB treatment did not correlate with the occurrence of second malignancies. This study, with a median follow-up of 10 years, demonstrates that pipobroman is effective and well tolerated. The low cumulative 10-year risk of thrombosis, leukaemia and solid tumours indicates that pipobroman is an adequate treatment for patients with high risk ET.

Adult↗
PubMed2000

Experimental study of the influence of endoleak size on pressure in the aneurysm sac and the consequences of thrombosis.

BACKGROUND: This was an experimental study of endovascular aortic surgery, looking at the relationship between the size of an endoleak, pressure in the aneurysm sac and the effect of thrombosis produced by coagulation. METHODS: In three pigs, 16 saccular aneurysms were connected to the aorta by various side branches with different diameters and lengths ('endoleaks'). Mean and pulse pressures were measured in the systemic circulation as well as in the aneurysm sac during the experiment. Duplex ultrasonography was used to determine whether the endoleak and the aneurysm were patent or thrombosed. Thrombosis was influenced by systemic tranexamic acid, fibrinogen in the aneurysm sac, Gelfoam in both endoleak and aneurysm sac, and by Histoacryl glue in the endoleak. RESULTS: With an open endoleak, the mean pressure in the aneurysm and the aorta was identical. Mean aneurysm pressure was lower with a thrombosed endoleak and was related to the diameter of the endoleak. Pulse pressure was recorded in the aneurysm sac when there was an open endoleak and a non-thrombosed aneurysm, and was related to the diameter of the open endoleak. Thrombosed endoleaks never produced pulse pressure in the aneurysm. If Histoacryl and Gelfoam induced thrombosis of the endoleak, the decrease in mean aneurysm pressure was identical to that resulting from the spontaneous thrombosis of endoleaks. CONCLUSION: An open endoleak results in systemic arterial pressure in the aneurysm sac. Pulse pressure is detected if the aneurysm is patent, but absent if there is complete or partial thrombosis of the aneurysm. Endoleak thrombosis, either spontaneous or by embolization, is accompanied by a decrease in mean pressure and the absence of pulse pressure in the aneurysm sac. The extent to which these experimental findings are comparable to the clinical situation represents a field of further research.

Aortic Dissection↗
PubMed2002

Risk factors for thrombosis in patients with immune mediated heparin-induced thrombocytopenia.

BACKGROUND: As reported by major clinical series in the literature, about 2% of patients receiving unfractionated heparin (UFH) develop immune-mediated (type II) heparin-induced thrombocytopenia (HIT) that may be complicated in 30-75% of cases by a paradoxical thrombotic syndrome (HITTS), either arterial or venous. HITTS carries relevant rates of mortality and morbidity, amongst which cerebral and/or myocardial infarction and limb amputations. It is unclear as yet why some patients suffer from isolated thrombocytopenia (HIT), whilst others have HITTS. The aim of the present study was to look for clinical and laboratory features related to the occurrence of HITTS. PATIENTS AND METHODS: We retrospectively analysed the clinical records of 56 patients with proven HIT, as diagnosed on clinical grounds and by in vitro demonstration of immunoglobulin (IgG)/IgM against the PF4/heparin complex. Thirty-four patients (61%) had HITTS (19 venous thrombosis, seven arterial thrombosis, five arterial and venous thrombosis, two skin necrosis, one diffuse intravascular coagulation), whereas 22 had uncomplicated HIT. Amongst HITTS patients, two had limb amputation, five had recurrent thrombosis and seven died. Amongst HIT patients three died from causes unrelated to HIT. RESULTS: No significant difference in sex, age, previous exposure to heparin, UFH route of administration or dose, duration of therapy, time of onset of thrombocytopenia and platelet count recovery, nor antiheparin/PF4 antibodies subtype (IgG or IgM) was detected when comparing HIT and HITTS. In contrast, in the HITTS group a higher prevalence of orthopaedic surgery (15 of 34 vs. 2/22; P=0.01), a significantly lower platelet count nadir (43 +/- 32 vs. 75 +/- 63 x 109/L; P=0.01) and a significantly higher titre of antiheparin/PF4 antibodies, expressed as optical density of enzyme-linked immunosorbent assay (ELISA); (1989 +/- 1024 vs. 1277 +/- 858; P=0.009), were observed in comparison with the HIT group. Amongst HITTS patients, the prevalence of venous thrombosis was significantly higher in orthopaedic patients and in those being treated for venous thromboembolism (18/24 vs. 1/9 patients, chi2 8.4, P=0.004), whilst arterial thrombosis (ART) occurred more often in heparin treatment for arterial disease (3/4 vs. 4/29 patients, chi2 4.6, P=0.03). CONCLUSIONS: Orthopaedic surgery, the severity of thrombocytopenia and high antiheparin/PF4 antibodies titre are adverse prognostic or concurrent factors in the development of HITTS.

Adult↗
PubMed1999

Risk factors associated with umbilical vascular catheter-associated thrombosis in newborn infants.

OBJECTIVE: To determine the risk factors associated with umbilical vascular catheter-associated thrombosis. METHODS: All consecutive inborn infants with umbilical arterial (UAC) and/or umbilical venous catheters (UVC) inserted for more than 6 h duration were included in the study. Each infant was screened for thrombosis in the abdominal aorta and inferior vena cava by 2-D abdominal ultrasonography within 48-72 h of insertion of umbilical vascular catheters. Subsequent serial scanning was performed at intervals of every 5-7 days, and within 48 h after removal of catheters. RESULTS: Upon removal of umbilical catheters, abdominal aortic thrombi were detected in 32/99 (32.3%) infants with UAC. Small thrombi were detected in the inferior vena cava of 2/49 (4.1%) infants with UVC (one of whom had both UAC and UVC). When compared with those who received only UVC (n = 18), infants who received either UAC alone (n = 68) or both UAC and UVC (n = 31) had significantly higher risk of developing thrombosis (odds ratio (OR): 7.6, 95% confidence interval (CI): 1.1, 325.5)). Logistic regression analysis of various potential risk factors showed that the only significant risk factor associated with the development of abdominal aortic thrombosis following insertion of UAC was longer duration of UAC in situ (for every additional day of UAC in situ, adjusted OR of developing thrombosis was: 1.2, 95% CI: 1.1, 1.3; P = 0.002). CONCLUSION: Umbilical arterial catheter-associated thrombosis was common. Umbilical arterial catheter should be removed as soon as possible when not needed. Upon removal of UAC, all infants should be screened for abdominal aortic thrombus by 2-D ultrasonography.

Aorta, Abdominal↗
PubMed1998

Change in access blood flow over time predicts vascular access thrombosis.

BACKGROUND: Vascular access thrombosis accounts for at least $1 billion dollars in annual expenses and 25% of hospitalizations for chronic hemodialysis patients. Low vascular access blood flow (less than 800 ml/min) has been shown to modestly increase the relative risk for thrombosis in the subsequent three months. In this study, it is hypothesized that a time-dependent decrease in vascular access blood flow may be more predictive of subsequent thrombosis especially in vascular accesses with flows more than 800 ml/min, since it would indicate the development of a critical outlet stenosis in the graft. METHODS: Ninety-five accesses in 91 CHD patients were prospectively followed over 18 months. Vascular access blood flow was measured every six months by the ultrasound dilution technique. Thrombotic events were recorded during the three study periods. RESULTS: A total of 34 thrombotic events in 95 accesses were documented through the total study duration. Accesses that thrombosed had a 22% decrease in vascular access blood flow during the first observation period and a further 41% decrease during the second observation period as compared to 4% drop and 15% increase during the first and second observation periods, respectively, for accesses that did not thrombose. There was an estimated 13.6-fold (95%, confidence interval 2.68 to 69.16) increase in the relative risk of thrombosis for accesses with more than 35% decrease in vascular access blood flow compared to those accesses with no change in blood flow. There was no statistical difference in the average vascular access blood flow of all patients over the study period. CONCLUSIONS: Accesses that show a large (>15%) decrement in vascular access blood flow are associated with a high risk of thrombosis. Serial measurements of vascular access blood flow predict access thrombosis.

Adult↗
PubMedDate not supplied

Access flow measurement as a predictor of hemodialysis graft thrombosis: making clinical decisions.

Since the introduction of dilution methods for measurement of vascular access blood flow during hemodialysis, more than 170 publications addressing the accuracy, prognostic value, and economic impact of the technology have been presented. Recently researchers (Paulson et al.) have raised concerns about the accuracy of access flow measurements in predicting thrombosis. Our first objective was to address the inadequacies of the analysis by these authors. The second objective was to apply a statistically accepted three-step approach for clinical decision making to assess the utility of access flow surveillance (similar to the K/DOQI guidelines) in the prediction of thrombosis. These steps included 1) estimation of treatment thresholds based on harm-benefit analysis of fistulography-angioplasty versus thrombosis, 2) estimation of prior probability of thrombosis based on patient demographic and clinical characteristics, and 3) application of Bayes' theorem to evaluate whether flow test results provided information that could move patients across the treatment threshold, thus discriminating between patients who should be referred for fistulography-angioplasty and those who should not. These data and an analysis of recent publications show that the implementation of an access flow surveillance program decreases thrombosis rates in hemodialysis units and can significantly reduce the costs associated with hemodialysis access maintenance. We conclude that access flow monitoring (K/DOQI flow thresholds) is useful in the clinical decision-making process for thrombosis prediction across a wide range of demographic categories.

Blood Flow Velocity↗
PubMed2003

Inhibition of localized thrombosis in P2Y1-deficient mice and rodents treated with MRS2179, a P2Y1 receptor antagonist.

Previous studies in experimental models revealed a role for the P2Y1 platelet ADP receptor in systemic vascular thromboembolism models. In the present work, we used models of localized arterial and venous thrombosis to assess the role of the P2Y1 receptor in these processes. Arterial thrombosis was induced in one mesenteric arteriole of a mouse using FeCl3, while venous thrombosis was studied in a Wessler model adapted to rats. P2Y1-deficient mice and mice treated with the P2Y1 antagonist MRS2179 displayed significantly less arterial thrombosis than their respective controls. Combination of P2Y1 deficiency with P2Y12 inhibition led to a significant additive effect. Venous thrombosis was slightly but significantly inhibited in MRS2179-treated rats. These results demonstrate a role for the P2Y1 receptor in both arterial and venous thrombosis, further establishing this receptor as a potential target for antithrombotic drugs.

Adenosine Diphosphate↗
PubMed2002

[Travel-induced thrombosis: an update].

Travel-related disorders are a well known problem. In the last years many cases of deep venous thrombosis (DVT) and pulmonary thromboembolism (VTE) were published after several hours lasting journeys by airplane, but also by car, bus and railway. This condition was termed "travel-thrombosis" or "economy class syndrome" for long haul flights. At present the precise incidence for travel-thrombosis is not known. Accepted contributing factors for the development of travel-thrombosis are sitting in a cramped position for several hours, low humidity due to climatisation with the risk for dehydration and increased blood viscosity, reduced fluid intake as well as travellers related risk factors. Whether the special situation in the cabin of an airplane, e.g. mild hypoxia, is an essential contributing factor for DVT and VTE, is controversially discussed. This review will present very recent guidelines of an expert meeting concerning the risk groups for travel-thrombosis (low, moderate and high risk). In addition recommendations for prophylaxis of travel-thrombosis adapted to the different risk groups (leg exercise, adequate fluid intake, compression stockings, low molecular weight heparins) are given.

Aerospace Medicine↗
PubMed2001

Current outcome of portal vein thrombosis in adults: risk and benefit of anticoagulant therapy.

BACKGROUND & AIMS: The outcome of portal vein thrombosis in relation to associated prothrombotic states has not been evaluated. We assessed current outcome and predictors of bleeding and thrombotic events in a cohort of 136 adults with nonmalignant, noncirrhotic portal vein thrombosis, of whom 84 received anticoagulant therapy. METHODS: Multivariate Cox model analysis for event-free survival and analysis taking into account multiple events were used. RESULTS: Median follow-up was 46 months. The incidence rate of gastrointestinal bleeding was 12.5 (95% confidence interval [CI], 10-15) per 100 patient-years. Large varices were an independent predictor for bleeding. Anticoagulant therapy did not increase the risk or the severity of bleeding. The incidence rate of thrombotic events was 5.5 (95% CI, 3.8-7.2) per 100 patient-years. Underlying prothrombotic state and absence of anticoagulant therapy were independent predictors for thrombosis. In patients with underlying prothrombotic state, the incidence rates of splanchnic venous infarction were 0.82 and 5.2 per 100 patient-years in periods with and without anticoagulant therapy, respectively (P = 0.01). Two nonanticoagulated patients died of bleeding and thrombosis, respectively. CONCLUSIONS: In patients with portal vein thrombosis, the risk of thrombosis is currently as clinically significant as the risk of bleeding. The benefit-risk ratio favors anticoagulant therapy.

Adolescent↗
PubMed2000

Inferior vena cava and right atrial thrombosis in children with nephroblastoma: diagnostic and therapeutic problems.

BACKGROUND: The neoplastic thrombus in Wilms' tumor rarely can extend in to the inferior vena cava or to the right atrium. The neoplastic thrombus usually is diagnosed concurrently with the tumor, although in some cases the diagnosis of the thrombus may precede the diagnosis of nephroblastoma. METHODS: Among 90 children with Wilms' tumor who were treated in the authors' unit, 4 had extensive tumor thrombosis of the inferior vena cava or the right atrium. One of these patients was found with a life-threatening thrombosis of the inferior vena cava and the right atrium, which was treated surgically; in this case, the diagnosis of nephroblastoma was made postoperatively. As for the 3 remaining patients the diagnosis of neoplastic thrombosis and Wilms' tumor was made simultaneously. RESULTS: In the first case, the patient underwent surgical excision of the thrombus with cardiopulmonary bypass and a short period of hypothermic cardiopulmonary arrest. In the other 3 cases the thrombus resolved with chemotherapy only. CONCLUSIONS: Surgical excision of extensive neoplastic thrombosis is suggested in the case of life-threatening thrombosis even with cardiopulmonary bypass. Chemotherapy is suggested in cases lacking clinical symptoms of thrombosis.

Child↗
PubMed2002

Portal vein thrombosis after variceal endoscopic sclerotherapy in cirrhotic patients: role of genetic thrombophilia.

BACKGROUND AND STUDY AIMS: Portal vein thrombosis is a rare event in patients with liver cirrhosis in the absence of a related neoplasm. Endoscopic sclerotherapy of esophageal varices has been anecdotally associated with the development of portal vein thrombosis. We tested the hypothesis that genetic thrombophilia plays a role in the development of portal vein thrombosis in patients with liver cirrhosis undergoing endoscopic sclerotherapy. PATIENTS AND METHODS: From June 1998 to December 1999, 61 consecutive patients underwent multiple sessions of endoscopic sclerotherapy for bleeding esophageal varices. Doppler ultrasound of the portal vein was performed before sclerotherapy and every 3 months thereafter. Antiphospholipid antibodies, factor V Leiden (FVL) mutation, prothrombin mutation G20210A (PTHRA20210) and mutation TT677 of methylenetetrahydrofolate reductase (MTHFR C677T) were evaluated in all patients. RESULTS: Portal vein thrombosis developed in 16 % of the patients (10 of 61) after a mean follow-up period of 16 months. A genetic cause for thrombosis was found in 70 % of patients with liver cirrhosis who developed portal vein occlusion, but only in 8 % of patients without this complication. CONCLUSIONS: Endoscopic sclerotherapy of esophageal varices may represent a trigger factor for portal vein thrombosis in cirrhotic patients with genetic thrombophilia.

Aged↗
PubMed2004

[Benign or malignant thrombosis of the jugular vein? - Differentiation with colour-Doppler sonography].

Thrombosis can lead to physical impairment and cost-intensive investigations. In some cases, a thrombosis is caused by infiltration of an adjacent tumour. It is therefore important to differentiate between a benign or malignant thrombosis. We report the case of a woman with a malignant thrombosis of the jugular vein. She was hospitalised for suspected malignant disease of unknown origin. Her family doctor had made the diagnosis of a "partially organised thrombosis". At sonography, vessels with an arterial blood flow were detected in the thrombus. A carcinoma of the thyroid gland was therefore suspected and confirmed by histology. This case report demonstrates that the differentiation between a benign and malignant thrombosis is possible with colour-Doppler sonography.

Aged↗
PubMed2003

Thrombosis in pediatric cardiac patients.

Cardiac disease and thrombosis are intimately related in adults, but primary myocardial infarction in children is rare. Homozygous familial hyperlipidemia occurs in approximately 1 million children, and causes severe coronary artery disease during childhood. Kawasaki's disease is an acquired inflammatory disorder, which, if untreated, leads to coronary artery aneurysms and subsequent myocardial infarction. The current understanding of the pathophysiology and management of these conditions is discussed. More commonly, the relationship between cardiac disease in children and thrombosis is that children being treated for congenital structural cardiac disease develop iatrogenic thrombosis, most commonly precipitated by central venous access. The epidemiology of common treatment-induced thrombosis is described, and management guidelines presented. Finally, many cardiac surgical procedures increase the risk of thrombosis, and prophylactic antithrombotic therapy is commonly used. The current evidence for prophylaxis in different clinical situations is presented. Additional study is required in all areas to improve the outcome for children affected by cardiac disease and thrombosis.

Anticoagulants↗