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Cirrhosis in Surgery
Published in Stephen M. Cohn, Peter Rhee, 50 Landmark Papers, 2019
Cirrhotic patients with spontaneous bacterial peritonitis who received early as compared to delayed paracentesis had lower mortality (13% vs. 27%, P = 0.007) and each hour delay in paracentesis was associated with a 3.3% increase in mortality. Paracentesis performed less than 12 hours from admission may improve survival (Kim et al., 2014). In contrast to many cirrhotic complications, portal vein thrombosis can be a consequence of the progression of liver disease and may not be responsible for further progression of liver disease (Nery et al., 2015). This longitudinal study noted the cumulative incidence of portal vein thrombosis in patients with cirrhosis was 4.6%, 8.2%, and 10.7% at 1, 3, and 5 years. Although patients with more severe liver disease were at a higher risk for developing portal vein thrombosis, the progression of liver disease such as the development of ascites, reduced portal blood flow velocity, or other variables for liver decompensation were independent of the presence of portal vein thrombosis.
Gastrointestinal and hepatobiliary
Published in Dave Maudgil, Anthony Watkinson, The Essential Guide to the New FRCR Part 2A and Radiology Boards, 2017
Dave Maudgil, Anthony Watkinson
The differential diagnosis of hepatic calcification includes the following. True or false? Hydatid disease.Sarcoidosis.Portal vein thrombosis.Ovarian metastases.Chronic granulomatous disease of childhood.
Safety of direct oral anticoagulants in patients with liver disease: a systematic review and meta-analysis
Published in Acta Clinica Belgica, 2023
Yan Zhao, Liyao Zhu, Yang Yang, Han Gao, Rui Zhang
Apixaban, edoxaban and rivaroxaban belong to a family of coagulation factor X blockers [32]. Dabigatran works by antagonizing thrombin activity. Relative to VKA and LMWHs, several DOACs are more convenient for the following aspects. VKA, which inhibits the synthesis of various coagulation factors, including factors II (prothrombin), VII, IX, and X, and protein C and protein S, needs frequent coagulation monitoring and dosage adjustments [33,34]. Moreover, VKA interacts with foods that contain Vitamin K, which may interfere with VKA efficacy, leading to treatment failure. LMWH treatment showed effective therapeutic effects on portal vein thrombosis. However, there is a high risk of hemorrhage in 14.3% of the patients and two died from bleeding [35]. Thus, the risk should be discussed with patients with liver cirrhosis and histories of variceal bleeding, and the antifactory Xa activity continuously monitored [36]. Thus, DOACs are appealing alternatives for patients with liver disease because they can be given orally and do not usually require laboratory monitoring to adjust drug dosage.
Impact of cardiac and noncardiac cirrhosis on coronary revascularization outcomes from the National Inpatient Sample, 2016 to 2018
Published in Baylor University Medical Center Proceedings, 2023
Dae Yong Park, Seokyung An, Muhammad-Sheharyar Warraich, Ziad Sad Aldeen, Ibrahim Maghari, Smriti Khanal, Abdul Wahab Arif, Anas Almoghrabi
Although more known for its bleeding complications, cirrhosis is also associated with increased thrombosis.20 The liver is responsible for producing not only factors I, II, V, VII, VIII, IX, X, XI, and XII but also proteins C and S.21 Previous studies have found progressively decreasing protein C, protein S, and antithrombin levels with worsening severity of Child-Pugh class, with one study noting a 60% decrease in protein C concentrations compared to the general population.22,23 As a result, patients with cirrhosis are also at a risk of thrombosis, as demonstrated by an estimated annual incidence of spontaneous portal vein thrombosis in 5% to 10% of patients.24 These phenomena lead to a dynamic disequilibrium between thrombophilia and hemophilia, posing a significant clinical challenge in managing cirrhosis.25 Management becomes especially difficult after PCI, because stent thrombosis needs to be prevented while minimizing bleeding risks.
An overview of current advancements in pancreatic islet transplantation into the omentum
Published in Islets, 2021
Kimia Damyar, Vesta Farahmand, David Whaley, Michael Alexander, Jonathan R. T. Lakey
Type 1 Diabetes Mellitus (T1DM) is an autoimmune disorder in which insulin-producing β-cells, predominant within the islets of Langerhans in the pancreas, are destroyed. This ultimately results in blood sugar elevation and loss of glycemic control.1 The development of the Edmonton protocol in 2000 introduced islet transplantation as a method to restore glycemic control in insulin-dependent T1DM patients.2 Under the current standard of care, the liver is considered the primary site for clinical islet transplantation. The islets can be easily infused into the hepatic portal system allowing β-cells to effectively restore glycemic control to the patients. However, there are limitations associated with islet infusion into the portal system. There is a risk of portal vein thrombosis as well as the elevation of portal pressure that can lead to uncontrolled bleeding. Moreover, there is a possibility of islet loss after transplantation due to the IBMIR that can occur when islets encounter the recipient’s blood.3–6 In order to address the limitations associated with intrahepatic islet transplantation, alternative sites have been investigated including but not limited to the omentum, peritoneum, spleen, renal subcapsule, and gastric submucosa. However, some of these sites show limitations in capacity and functional outcome or introduce further complications post-transplant.3,7–12