Predicting bleeding after liver biopsy using comprehensive clinical and laboratory investigations: A prospective analysis of 302 procedures.

BACKGROUND: Liver biopsy carries a small risk of bleeding complications. No validated clinical or laboratory tool helps predict liver biopsy-related bleeding. OBJECTIVES: To determine whether global hemostasis tests and/or a clinical questionnaire could identify patients at risk of liver biopsy-related bleeding. PATIENTS/METHODS: Consecutive patients scheduled for liver biopsy with an overnight hospital stay were prospectively included. Before liver biopsy, routine hemostasis tests, Platelet Function Analyzer 100, thromboelastometry, thrombin generation assay, plasma clot lysis time, and a clinical questionnaire were performed. Bleeding was defined as a liver hematoma or new free fluid on a systematic ultrasound performed 24 h after liver biopsy or a decrease in hemoglobin level of 2 g/dL or more in patients with pre-existing free fluid in the abdominal cavity. RESULTS: Three hundred two patients were included: 173 underwent percutaneous and 129 transjugular liver biopsy. There were 21 bleeding episodes (7%); 20 based on ultrasonographic criteria, 1 on laboratory criteria. None of the hemostasis tests and no item of the clinical questionnaire were associated with liver biopsy-related bleeding in the overall study group. Same results were obtained in subgroup analyses focusing on patients who underwent percutaneous liver biopsy, transjugular liver biopsy, or on patients with cirrhosis. Pain 2 h after liver biopsy was more frequent in patients with liver biopsy-related bleeding (55% vs. 23% p = .002). CONCLUSIONS: An extensive hemostasis workup, including global hemostasis assays, does not improve prediction of liver biopsy-related bleeding. Pain 2 h after liver biopsy should alert the clinician to the possibility of procedure-related bleeding.

Rivaroxaban Prophylaxis in Noncirrhotic Portal Vein Thrombosis.

Rivaroxaban Prophylaxis in Noncirrhotic PVTThis trial assessed the effects of rivaroxaban on the risk of venous thromboembolism and portal hypertension-related bleeding in patients with noncirrhotic chronic portal vein thrombosis without major risk factors for thrombosis. Daily rivaroxaban use reduced the incidence of venous thromboembolism and did not increase major bleeding events.

Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: results of a longitudinal study.

UNLABELLED: In cirrhosis, portal vein thrombosis (PVT) could be a cause or a consequence of the progression of liver disease. We analyzed data from a prospective trial of ultrasound screening for hepatocellular carcinoma in order to identify risk factors for and the impact of PVT in patients with cirrhosis. In all, 1,243 adults with cirrhosis without PVT were enrolled from 43 liver units in France and Belgium between June 2000 and March 2006. The mean follow-up was 47 months. Doppler ultrasonography was used to check the portal vein. Progression of liver disease was defined by the development of: ascites, hepatic encephalopathy, variceal bleeding, prothrombin <45%, serum bilirubin >45 µmol/L, albumin <28 g/L, and/or creatinine >115 µmol/L. G20210A prothrombin and factor V gene mutations were assessed in sera stored at three large centers. The 5-year cumulative incidence of PVT was 10.7%. PVT was mostly partial and varied over time. The development of PVT was independently associated with baseline esophageal varices (P = 0.01) and prothrombin time (P = 0.002), but not with disease progression before PVT, or prothrombotic mutations. Disease progression was independently associated with baseline age (hazard ratio [HR] 1.55; 95% confidence interval [CI]: 1.11-2.17), body mass index (HR 1.40; 95% CI: 1.01-1.95), prothrombin time (HR 0.79; 95% CI: 0.70-0.90), serum albumin (HR 0.97; 95% CI: 0.94-0.99), and esophageal varices (HR 1.70; 95% CI: 1.21-2.38) but not with the prior development of PVT (HR 1.32; 95% CI: 0.68-2.65). CONCLUSION: In patients with cirrhosis, the development of PVT is associated with the severity of liver disease at baseline, but does not follow a recent progression of liver disease. There is no evidence that the development of PVT is responsible for further progression of liver disease.

Absorption and efficacy of acetylsalicylic acid in patients with short bowel syndrome.

BACKGROUND: The patients with a short bowel (SB) frequently require antiplatelet therapy. Resection of the bowel is likely to modify the absorption and first-pass effect of drugs. No data on the absorption and efficacy of the cardiovascular dose of aspirin (75-160 mg) in these patients have been published. OBJECTIVE: To evaluate the efficacy of a low dose of aspirin in patients with SB caused by mesenteric ischemia. METHODS: The efficacy of a low dose of aspirin was assessed in 10 consecutive SB patients, both 1 hour and 24 hours after administration (peak and trough value, respectively). The primary criterion was the inhibition of platelet aggregation, as assessed by light transmission aggregometry, triggered with 0.5 mg/mL arachidonic acid. Biological efficacy of aspirin was also evaluated by serum thromboxane B2 value and by platelet function analyzer-100. RESULTS: At its peak value, aspirin had the expected efficacy, as demonstrated both by light transmission aggregometry and the other methods. However, 24 hours after administration, as many as 30% of patients had lost the pharmacological efficacy of their aspirin. CONCLUSION: We show for the first time that with at least 30 cm of small intestine, all patients with SB absorb sufficient oral aspirin in a cardiovascular dose to rapidly exert the expected level of antiplatelet activity. But given only once daily, aspirin does not provide stable 24-hour antiplatelet protection in 30% of patients, because of increased platelet turnover, as usually observed in patients with extensive vascular pathology, diabetes, or inflammation.

Type 2 diabetes mellitus as a risk factor for intestinal resection in patients with superior mesenteric vein thrombosis.

BACKGROUND & AIMS: The most serious complication of acute mesenteric vein thrombosis (MVT) is acute intestinal ischaemia requiring intestinal resection or causing death. Risk factors for this complication are unknown. To identify risk factors for severe intestinal ischaemia leading to intestinal resection in patients with acute MVT. METHODS: We retrospectively analysed consecutive patients seen between 2002 and 2012 with acute MVT in 2 specialized units. Patients with cirrhosis were excluded. We compared patients who required intestinal resection to patients who did not. RESULTS: Among 57 patients, a local risk factor was identified in 14 (24%) patients, oral contraceptive use in 16 (29%), and at least one or more other systemic prothrombotic condition in 25 (44%). Five (9%) patients had diabetes mellitus (DM), 33 (58%) had overweight or obesity, 9 (18%) had hypertriglyceridemia and 10 (19%) had arterial hypertension. Eleven patients (19%) underwent intestinal resection. DM was significantly associated with intestinal resection (P = 0.02) while local factors or prothrombotic conditions were not. Computed tomography (CT) scans performed at diagnosis found that occlusion of second order radicles of the superior mesenteric vein was more frequently observed in patients who underwent intestinal resection (P = 0.009). CONCLUSIONS: In acute MVT, patients with underlying DM have an increased risk of requiring intestinal resection. Neither local factors nor systemic prothrombotic conditions are associated with intestinal resection. When CT scan shows the preservation of second order radicles of the superior mesenteric vein, the risk of severe resection is low.

Extrahepatic portal venous system thrombosis in recurrent acute and chronic alcoholic pancreatitis is caused by local inflammation and not thrombophilia.

OBJECTIVES: Extrahepatic portal venous system thrombosis (EPVST) occurs in 13% of patients with either recurrent acute (AP) or chronic (CP) alcoholic pancreatitis. The role of thrombophilia has never been assessed in this entity. METHODS: All consecutive patients with alcoholic AP or CP were included in a prospective study. All patients underwent a computerized tomography (CT) scan of the pancreas to evaluate EPVST as well as thorough testing for thrombophilia (protein C, S, and antithrombin deficiency, factor II, factor V, and JAK2 gene mutations, homocystein, biological antiphospholipid syndrome). RESULTS: A total of 119 patients (male, n=100 (84%); smokers, n=110 (92%)) were included. EPVST was found in 41 patients (35%). The portal, superior mesenteric, or splenic veins were involved in 34%, 24%, and 93% of patients, respectively. Thrombophilia was identified in 18% (n=22), including the biological antiphospholipid syndrome, factor V Leiden mutation, and factor II G20210A gene mutation in 21 (17.6%), 2 (1.6%), and 1 patient (0.8%), respectively. On univariate analysis, the factors associated with EPVST were smoking (RR=1.6 (1.38-1.85), P=0.03), pseudocysts (RR=2.91 (1.29-6.56), P=0.008), a pseudocyst in the pancreatic tail (P=0.03), a high CT severity index for AP (P=0.007), and pancreatic parenchymal necrosis (P=0.02). The presence of hemostatic risk factors was not associated with an increased risk of EPVST. On multivariate analysis, only pseudocysts were associated with EPVST (hazard ratio: 6.402; 95% confidence interval (1.59-26.54), P=0.009). CONCLUSIONS: EPVST is found in 35% of patients with acute/chronic alcoholic pancreatitis. Local inflammation appears to be the major predisposing condition. The presence of some form of thrombophilia does not increase the risk of EPVST and should not be systematically searched for in case of EPVST.