Splanchnic vein thrombosis: Clinical manifestations, risk factors, management, and outcomes

2021 ◽  
Vol 202 ◽  
pp. 90-95
Author(s):  
Eri Kawata ◽  
Dou-Anne Siew ◽  
James Gordon Payne ◽  
Martha Louzada ◽  
Michael J. Kovacs ◽  
...  
2021 ◽  
Vol 108 (Supplement_9) ◽  
Author(s):  
K Thejasvin ◽  
Sara-Jane Chan ◽  
Chris Varghese ◽  
Wei Boon Lim ◽  
Gemisha Cheemungtoo ◽  
...  

Abstract Background There is paucity of data on the incidence, risk factors and role of anticoagulation for splanchnic vein thrombosis (SVT) in acute pancreatitis (AP). Methods A retrospective review of AP admissions between 2018-2021 across North East England was undertaken. Data on demographics, etiology, severity of AP and SVT was collected. In addition, a selective anticoagulation policy for portal vein thrombosis (PVT) and progressive splenic vein thrombosis was explored. Results 401 patients were included with a mean age of 57.0 and M:F ratio of 1.6:1. 152 patients developed intestinal oedematous pancreatitis and 249 developed necrotising pancreatitis based on Revised Atlanta criteria (RAC). 109 patients (27.2%) developed SVT of which 27 developed a PVT and splenic vein thrombus, 36 PVT only and 46 splenic vein thrombus only.  On univariate analysis, alcoholic aetiology, severe pancreatitis, necrotising pancreatitis with >50% necrosis and elevated CRP at 2 weeks were risk factors for developing SVT. On multivariable analysis, alcohol aetiology (OR 2.6, p = 0.002), and >50% pancreatic necrosis (OR 14.6,p = 0.048) increased the risk of developing SVT . 58 patients received anticoagulation for SVT, with a median duration of 90 days of anticoagulation. Recanalization rates were higher for PVT when compared to splenic vein thrombosis. 6 patients developing bleeding complications whilst on anticoagulation therapy.  Conclusions A third of patients with AP develop SVT, particularly those with severe AP secondary to alcohol and with extensive pancreatic necrosis. A selective anticoagulation policy was associated with improved recanalization rates and fewer bleeding complications.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 380-380 ◽  
Author(s):  
Sandra Régina ◽  
Olivier Herault ◽  
Louis D’lteroche ◽  
Yannick Bacq ◽  
Jorge Domenenech ◽  
...  

Abstract Introduction Many risk factors have been identified in patients with portal (PVT) and hepatic venous thrombosis (HVT), including myeloproliferative disorders (MPD), i.e. polycythemia vera (PV) and essential thrombocythemia (ET), with prevalence varying between 25% and 65%. Moreover, JAK2 mutation V617F has recently been detected in 65 to 97% of cases of PV and 23 to 57% of ET. The aim of the present study was therefore to evaluate the frequency of JAK2 mutation V617F in a cohort of consecutive patients with PVT or HVT compared to a control group comprising patients with deep vein thrombosis (DVT) of the lower limbs. Patients and Methods Forty-four patients with PVT (n=42) or HVT (n=2) diagnosed between 2001 and 2005, and 44 patients (matched for age and gender) with idiopathic DVT were included. The presence of hereditary or acquired risk factors for thrombosis (including FV Leiden and FII G20210A polymorphism, defects in coagulation inhibitors, antiphospholipid antibodies and hyperhomocysteinemia) was investigated in all patients. Bone marrow (BM) biopsy and cultures of blood and BM progenitors were performed in 18 patients with PVT for whom the etiology of thrombosis was undefined. Screening for JAK2 mutation V617F was performed on genomic DNA isolated from peripheral blood cells by an allele-specific PCR and RFLP analysis using BsaXI, as previously described (Baxter et al. Lancet2005, 365:1054), combined with nano-electrophoresis (Bioanalyzer 2100, Agilent) to increase sensitivity. HEL92.1.7 and HL60 cell lines were used as positive and negative controls, respectively. Results The 2 groups were similar in terms of blood count and conventional risk factors for thrombosis (Table). JAK2 mutation V617F was detected in 8 patients with PVT (18.2%) but in none with DVT (p=0.003). These 8 subjects had normal blood counts, and no other acquired or hereditary risk factor for thrombosis except for one case exhibiting moderate hyperhomocysteinemia. Bone marrow was hyperplastic in 6/18 patients (all JAK2 V617F positive). Cultures of progenitors showed endogenous erythroid formation in 6/18 cases (all JAK2 V617F positive). The clinical follow-up confirmed the diagnosis of MPD (1 PV and 1 ET) in 2 patients. One subject died in another context and blood counts have remained normal in the 5 other patients to date. The JAK2 mutation V617F was not detected in any patient with negative bone marrow exploration (biopsy and cultures). Conclusion The JAK2 mutation V617F is frequently and specifically detected in patients with idiopathic PVT and no other risk factor for thrombosis. Whether JAK2 mutation V617F should be screened in all subjects with splanchnic vein thrombosis and should replace BM biopsy and cultures warrants further studies. Biological data in patients with PVT/HVT or DVT PVT or HVT (n=44) DVT (n=44) n % 95% CI n % 95% CI p * * Fisher exact test FV Leiden 4 9.1 2.5–21.7 11 25 13.2–40.3 NS FII 20210A 10 22.7 11.5–37.8 6 13.6 5.2–27.4 NS AT, PC, PS deficiency 7 15.9 7.9–29.3 4 9.1 2.5–21.7 NS Antiphospholipid antibodies 5 11.4 4.9–24 8 18.2 9.5–32 NS Hyperhomocysteinemia 4 9.1 2.5–21.7 4 9.1 2.5–21.7 NS JAK2 V617 mutation 8 18.2 9.5–32 0 0 0–8 0.003


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 499-499 ◽  
Author(s):  
Walter Ageno ◽  
Nicoletta Riva ◽  
Soo-Mee Bang ◽  
Maria Teresa Sartori ◽  
Elvira Grandone ◽  
...  

Abstract Abstract 499 Background: Treatment of splanchnic vein thrombosis (SVT) is a clinical challenge due to heterogeneity of clinical presentations, increased bleeding risk and lack of evidences from clinical trials. We carried out an international registry aimed to describe current treatment strategies and factors associated with therapeutic decisions in a large prospective cohort of SVT patients. Methods: Between May 2008 and January 2012, consecutive SVT patients were enrolled in the registry and information on clinical presentation, risk factors, and therapeutic strategies was collected in an electronic database. Clinical outcomes during the first month of treatment were documented. A two-year follow up is ongoing. Results: 613 patients from 12 countries were enrolled in the registry. Mean age was 53.1 (SD ± 14.8) years (range 16–85); 62.6% were males, 74.4% Caucasians. SVT occurred in the portal vein in 470 patients, in the mesenteric vein in 266, in the splenic vein in 139, and in the supra-hepatic veins in 56; 38.8% of patients had multiple vein segments involved. In 29.8% of patients SVT diagnosis was incidental. Most common risk factors included cirrhosis (27.8%), solid cancer (22.3%), intra-abdominal inflammation/infection (11.5%), surgery (8.9%), and myeloproliferative neoplasm (MPN)(8.2%); in 27.6% of patients SVT was idiopathic. During the acute phase, 471 (76.8%) patients were treated with anticoagulant drugs: unfractionated heparin (10.4%), low molecular weight heparin or fondaparinux (66.4%), vitamin K antagonists (VKA) (48.5%). Four patients received aspirin, 9 received thrombolysis. A total of 135 patients (22.0%) remained untreated. Of patients with incidentally diagnosed SVT, 61.1% received anticoagulant treatment. Incidental diagnosis (p<0.0001), single vein thrombosis (p<0.0001), gastrointestinal bleeding (p0.008), thrombocytopenia (p0.0003), cancer (p0.009) and cirrhosis (p<0.0001) were significantly associated with no anticoagulant treatment. History of venous thrombosis (p0.003), myeloproliferative neoplasm (p0.003), surgery (p0.001), and hormonal treatment (p0.013) were significantly associated with the use of anticoagulant treatment. Decision to start patients on VKA was significantly associated with younger age (p<0.0001), symptomatic onset (p<0.0001), multiple veins involvement (p0.012) and unprovoked thrombosis (p<0.0001). Continued treatment with parenteral anticoagulants was significantly associated with anaemia (p0.013), thrombocytopenia (p<0.0001), cancer (p<0.0001), and cirrhosis (p<0.0001). During the first month after diagnosis, 2 patients on anticoagulant treatment (0.4%) and 3 untreated patients (2.2%) had thrombosis extension, 2 (0.4%) treated and 2 (1.5%) untreated patients had major bleeding, 11 patients died (7 and 4, respectively). Conclusions: Despite the increased bleeding risk and recent guidelines suggesting not to treat incidentally detected SVT, 76.8% of newly diagnosed SVT receive anticoagulant therapy in clinical practice. Treatment strategies vary according to patients characteristics, with this patient selection resulting safe and effective during the acute phase of therapy. The ongoing two-year follow up will provide additional information. Disclosures: No relevant conflicts of interest to declare.


2016 ◽  
Vol 6 (11) ◽  
pp. e493-e493 ◽  
Author(s):  
V De Stefano ◽  
A M Vannucchi ◽  
M Ruggeri ◽  
F Cervantes ◽  
A Alvarez-Larrán ◽  
...  

2008 ◽  
Vol 14 (2) ◽  
pp. 168-173 ◽  
Author(s):  
Gulfer Okumus ◽  
Esen Kiyan ◽  
Orhan Arseven ◽  
Levent Tabak ◽  
Reyhan Diz-Kucukkaya ◽  
...  

The aim of this study was to investigate the hereditary thrombophilic risk factors in patients with venous thromboembolism (VTE) and whether these risk factors play a different role in patients with isolated pulmonary embolism (PE) as compared with patients with deep vein thrombosis (DVT) and patients with PE + DVT. The protein C (PC), protein S, antithrombin activities, homocysteine levels, and factor V Leiden (FVL) G1691A and prothrombin G20210A mutations were evaluated in 191 patients with VTE and 191 controls. The prevalence of FVL and PC deficiency were higher in patients ( P = .003 and P = .02, respectively). There was no significant difference for the other risk factors. The combination of thrombophilic risk factors was significantly higher in patients with DVT + PE as compared with patients with isolated PE or DVT ( P = .04). In conclusion, the most important hereditary risk factors for VTE in this study were the FVL mutation and PC deficiency.


2012 ◽  
Vol 129 ◽  
pp. S93-S96 ◽  
Author(s):  
Marco P. Donadini ◽  
Francesco Dentali ◽  
Walter Ageno

2010 ◽  
Vol 103 (06) ◽  
pp. 1136-1144 ◽  
Author(s):  
Valerio De Stefano ◽  
Ida Martinelli

SummaryVenous thrombosis typically involves the lower extremity circulation. Rarely, it can occur in the cerebral or splanchnic veins and these are the most frightening manifestations because of their high mortality rate. A third site of rare venous thrombosis is the deep system of the upper extremities that, as for the lower extremity, can be complicated by pulmonary embolism and post-thrombotic syndrome. The authors conducted a narrative review focused on clinical manifestations, risk factors, and treatment of rare venous thromboses. Local risk factors such as infections or cancer are frequent in thrombosis of cerebral or portal veins. Upper extremity deep-vein thrombosis is mostly due to local risk factors (catheter- or effort-related). Common systemic risk factors for rare venous thromboses are inherited thrombophilia and oral contraceptive use; chronic myeloproliferative neoplasms are closely associated with splanchnic vein thrombosis. In the acute phase rare venous thromboses should be treated conventionally with low-molecular-weight heparin. Use of local or systemic fibrinolysis should be considered in the case of clinical deterioration in spite of adequate anticoagulation. Anticoagulation with vitamin K-antagonists is recommended for 3–6 months after a first episode of rare venous thrombosis. Indefinite anticoagulation is recommended for Budd-Chiari syndrome, recurrent thrombosis or unprovoked thrombosis and permanent risk factors. In conclusion, the progresses made in the last couple of decades in diagnostic imaging and the broadened knowledge of thrombophilic abnormalities improved the recognition of rare venous thromboses and the understanding of pathogenic mechanisms. However, the recommendations for treatment mainly derive from observational studies.


2020 ◽  
pp. 112972982098320
Author(s):  
Karolina Chojnacka ◽  
Zbigniew Krasiński ◽  
Katarzyna Wróblewska-Seniuk ◽  
Jan Mazela

Introduction: Newborns treated in a neonatal intensive care unit (NICU) are susceptible to several complications one of them being vein thrombosis. Aim: The study aims to evaluate risk factors of catheter-related venous thrombosis, clinical manifestations, treatment, and the outcomes of thrombotic events (TE) during the neonatal period. Methods: This work is a case-control retrospective study performed on patients in the tertiary NICU between January 2013 and June 2016. The analysis includes data from infants with CVC diagnosed with thrombosis and infants with CVC, not being diagnosed with thrombosis (control group). Statistica 10 software was used for statistical analysis. Results: Vein thrombosis was diagnosed in 19 NICU infants including 16 cases of catheter-related vein thrombosis (84% of complicated cases). Other statistically significant risk factors were asphyxia, infection, and the duration of CVC use. The incidence of thrombosis in our population increased during the study which may result from a statistically significant increase in the number of inserted CVC (294 vs 435), and more frequent diagnosis of incidental thrombosis (1 vs 9). Conclusion: Vein catheterization, asphyxia, infection, and prolonged CVC use are critical risk factors for thrombosis in the neonatal period. Given the hereinbefore mentioned increased number of central line catheterizations in the NICU, it would be useful to conduct a prospective study with a scheduled routine ultrasound protocol applied not only as a tool to diagnose thrombosis but also to prevent it by determining a proper catheter for a particular vein.


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