Validation of color Doppler ultrasound and computed tomography in the radiologic assessment of non-malignant acute splanchnic vein thrombosis

Introduction International guidelines propose color Doppler ultrasound (CDUS) and contrast-enhanced computed tomography (CT) as primary imaging techniques in the diagnosis of acute splanchnic vein thrombosis. However, their reliability in this context is poorly investigated. Therefore, the aim of our study was to validate CDUS and CT in the radiologic assessment of acute splanchnic vein thrombosis, using direct transjugular spleno-portography as gold standard. Materials and methods 49 patients with non-malignant acute splanchnic vein thrombosis were included in a retrospective, multicenter analysis. The thrombosis’ extent in five regions of the splanchnic venous system (right and left intrahepatic portal vein, main trunk of the portal vein, splenic vein, superior mesenteric vein) and the degree of thrombosis (patent, partial thrombosis, complete thrombosis) were assessed by portography, CDUS and CT in a blinded manner. Reliability of CDUS and CT with regard to portography as gold standard was analyzed by calculating Cohen’s kappa. Results Results of CDUS and CT were consistent with portography in 76.6% and 78.4% of examinations, respectively. Cohen’s kappa demonstrated that CDUS and CT delivered almost equally reliable results with regard to the portographic gold standard (k = 0.634 [p < 0.001] vs. k = 0.644 [p < 0.001]). In case of findings non-consistent with portography there was no clear trend to over- or underestimation of the degree of thrombosis in both CDUS (60.0% vs. 40.0%) and CT (59.5% vs. 40.5%). Conclusions CDUS and CT are equally reliable tools in the radiologic assessment of non-malignant acute splanchnic vein thrombosis.

A Case of Extensive Splanchnic Vein Thrombosis in a COVID-19 Patient and a Review of the Literature

: Splanchnic vein thrombosis is one of the rare complications of coronavirus disease 2019 (COVID-19). A 43-year-old woman presented with splanchnic vein thrombosis as a rare extrapulmonary complication of COVID-19. She was previously healthy without a medical history of coagulopathy before hospital admission. She complained of epigastric pain, along with nausea and vomiting. Enhanced abdominopelvic CT scan demonstrated extensive acute thrombosis in the portal, superior mesenteric, and splenic veins with total occlusion. Intestinal ischemia or infarction was not clinically observed. All thrombophilia screening tests yielded negative results. Under anticoagulation therapy, she recovered dramatically and was discharged from the hospital. Imaging findings can be used to confirm splanchnic vein thrombosis when a COVID-19 patient has abdominal symptoms.

P-P31 Splanchnic vein thrombosis in acute pancreatitis: Incidence, risk factors and long term outcomes

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 &gt;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 &gt;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.

JAK2 GGCC (46/1) Haplotype in Unprovoked Venous Thrombotic Events

Background: JAK2 GGCC 46/1 haplotype can be represented by four main SNPs (rs3780367, rs10974944, rs12343867, and rs1159782) which replace one cytosine and three thymidines by two guanosines and two cytosines, generating a "GGCC" combination. These four SNPs located on JAK2 introns 10, 12, 14, and 15, respectively, and are always inherited together, being in complete linkage disequilibrium. The 46/1 component of the name came from Jones et al. study where the haplotype structure of the JAK2 gene was mapped using 14 SNPs genotyped by the Wellcome Trust Case Control Consortium (WTCCC) in 1500 healthy blood donors. Two haplotypes (numbers 46 and 1) were found to be identical except for one SNP, and they have a combined frequency of 0.24 in healthy individuals. Numerous observational studies associate this haplotype with myeloproliferative neoplasms (MPNs), as well as splanchnic vein thrombosis (SVT) and non-splanchnic vein thrombosis (non-SVT). In contrast to 24% frequency noted in healthy population, the frequency goes up to 40-80% in JAK2 V617F mutated MPN, and in 64% of those with JAK2 exon 12 mutations (Anelli et al. IJMS, 2018). We herein report our study of JAK2 GGCC (46/1) Haplotype in unprovoked Venous Thrombotic Events (VTE) in patients with negative thrombophilia workup, including negative JAK2 V617F mutation. Methods: We retrospectively identified patients positive for one of the two SNPs (rs12343867 and rs10974900) and unprovoked venous thrombotic among adult patients with negative thrombophilia workup (including JAK2 mutation) treated at tertiary care center from January 2018 to January 2021. Results: We have identified 8 patients, Table (1), that were positive for JAK2 46/1 haplotype SNPs, of whom 62.5% were homozygous 2/2, 25% heterozygous 1/2, while only 12.5% harbor homozygous 1/1 (a normal variant of JAK2 haplotype). The median age 48.5 years (23-65), and the majority (87.5%) were females. Thrombosis site was noted to be SVT in half of the patients, while non-SVT was noted in the other half (12.5% had cerebral vein thrombosis, 12.5% had deep venous thrombosis, 12.5% had a pulmonary embolism, and 12.5% had jugular vein thrombosis). Half of the patients had more than one site venous thrombosis and the other half had only one site. Around 37.50% of the patients had recurrent venous thrombosis on top of therapeutic anticoagulation. Two patients (25%) had high hemoglobin (17.4/16.7) g/dl, but did not fulfill the criteria for polycythemia vera diagnosis (of whom one is a male smoker and one was a female). None of the patients had leukocytosis or thrombocytosis. By imaging, one patient had mild splenomegaly which could be related to SVT. Conclusion: We report on a potential correlation between unprovoked thrombotic events, mainly venous thrombotic events, with JAK2 46/1 haplotype in patients with a negative thrombophilia workup, a finding that merit further investigation. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Prior History of Thrombosis, Meld, BMI and the Presence of Esophageal Varices Predict Thrombus Progression in Patients with Untreated Splanchnic Vein Thrombosis

Background: Splanchnic vein thrombosis (SVT) occurs in a heterogenous group of patients secondary to a variety of risk factors including acute and chronic liver disease, malignancy, and myeloproliferative neoplasms. There is equipoise on the utility of anticoagulation in many patients with SVT given the perceived risks of bleeding and unclear benefits. We sought to determine which clinical factors predict new or progressive thrombosis in a cohort of patients with SVT. Methods: We undertook a retrospective cohort study of patients over 18 years of age identified to have an SVT at the Oregon Health & Science University from 01/01/2015 - 12/31/2020, including only patients who were not initially treated with anticoagulation at the time of their initial VTE diagnosis. Relevant clinical variables were selected apriori. The primary study endpoint was imaging-confirmed progression of SVT, development of cavernous transformation, intestinal ischemia, or new venous or arterial thrombosis. Chart demographics, patient history, and relevant lab values at the time of initial SVT were extracted for the analysis. Descriptive analysis, univariate logistic regression, and multivariable logistic regression were performed in STATA version 12.1 and R (R core team 2019). Results: Seventy-eight patients were included in the analysis (mean age 60 years old, 74% male). The most common SVT in the cohort was isolated portal vein thrombosis (N=60) followed by thrombosis of multiple splanchnic veins (N=14). The most prevalent causes of liver disease in the cohort were viral hepatitis (N=33) alcoholic cirrhosis (N=20) and non-alcoholic steatohepatitis (N=12). 66% of patients had known varices at diagnosis. 33% had thrombosis directly associated with a tumor. The mean platelet count and INR were 105 x 109/L and 1.55 respectively. Twenty-two patients (28%) developed the primary endpoint of thrombus progression. Univariate logistic regression found that prior history of thrombosis (OR 6, P= 0.04) and the presence of varices at diagnosis (OR 4.4, P= 0.02) were associated with progression. We then created a multivariable logistic regression model and observed that total bilirubin (ORadj = 0.34, p = 0.03), MELD score (ORadj = 1.33, p = 0.04), the presence of varices (ORadj = 11.7, 0.03), and BMI (ORadj = 1.14, p = 0.047) were significant predictors of our composite outcome while controlling for age, glomerular filtration rate, INR, and prior history of VTE. Discussion: In our heterogenous cohort of patients with SVT not treated with anticoagulation, one in four patients developed the composite endpoint of SVT progression, development of cavernous transformation, intestinal ischemia, or new venous or arterial thrombosis. Several common clinical variables appear to be predictive for thrombus progression, suggesting that predictive models may be feasible to determine which patients with SVT are likely to benefit from anticoagulation. Disclosures Shatzel: Aronora Inc,: Consultancy.