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Esophageal Varices: Pathophysiology, Approach, and Clinical Dilemmas International Journal of Hepatology Esophageal Varices: Pathophysiology, Approach, and Clinical Dilemmas Guest Editors: Nir Hilzenrat, Marc Bilodeau, and Averell H. Sherker Esophageal Varices: Pathophysiology, Approach, and Clinical Dilemmas International Journal of Hepatology Esophageal Varices: Pathophysiology, Approach, and Clinical Dilemmas Guest Editors: Nir Hilzenrat, Marc Bilodeau, and Averell H. Sherker Copyright © 2012 Hindawi Publishing Corporation. All rights reserved. This is a special issue published in “International Journal of Hepatology.” All articles are open access articles distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Editorial Board Chul Ahn, USA Shannon Glaser, USA Guy W. Neff,USA Antonio Ascione, Italy Fredric D. Gordon, USA Lun-Xiu Qin, China Matthias Bahr, Germany Claus Hellerbrand, Germany MiguelA.Serra,Spain Simon Bramhall, UK Masahiko Hirota, Japan Pierluigi Toniutto, Italy Maria Buti, Spain Paloma Jara, Spain Takuji Torimura, Japan Umberto Cillo, Italy Claus Kremoser, Germany Roberto I. Troisi, Belgium Heather Francis, USA Roberto Lupi, Italy Dirk Uhlmann, Germany Hikaru Fujioka, Japan Shigeru Marubashi, Japan Yo-ichi Yamashita, Japan Junji Furuse, Japan Kojiro Michitaka, Japan Matthias Glanemann, Germany Daisuke Morioka, Japan Contents Esophageal Varices: Pathophysiology, Approach, and Clinical Dilemmas, Nir Hilzenrat and Averell H. Sherker Volume 2012, Article ID 795063, 2 pages Etiology and Management of Hemorrhagic Complications of Portal Hypertension in Children, Alejandro Costaguta and Fernando Alvarez Volume 2012, Article ID 879163, 8 pages Clinical Manifestations of Portal Hypertension, Said A. Al-Busafi, Julia McNabb-Baltar, Amanda Farag, and Nir Hilzenrat Volume 2012, Article ID 203794, 10 pages Role of Self-Expandable Metal Stents in Acute Variceal Bleeding, Fuad Maufa and Firas H. Al-Kawas Volume 2012, Article ID 418369, 6 pages The Transjugular Intrahepatic Portosystemic Shunt in the Treatment of Portal Hypertension: Current Status, Gilles Pomier-Layrargues, Louis Bouchard, Michel Lafortune, Julien Bissonnette, Dave Guerette,´ and Pierre Perreault Volume 2012, Article ID 167868, 12 pages Endoscopic Management of Portal Hypertension, Said A. Al-Busafi, Peter Ghali, Philip Wong, and Marc Deschenes Volume 2012, Article ID 747095, 12 pages Management of Anticoagulation for Portal Vein Thrombosis in Individuals with Cirrhosis: ASystematicReview,Genevieve` Huard and Marc Bilodeau Volume 2012, Article ID 672986, 6 pages Pathophysiology of Portal Hypertension and Esophageal Varices, Hitoshi Maruyama and Osamu Yokosuka Volume 2012, Article ID 895787, 7 pages Prevention and Management of Gastroesophageal Varices in Cirrhosis, Yen-I Chen and Peter Ghali Volume 2012, Article ID 750150, 6 pages Towards Noninvasive Detection of Oesophageal Varices,KaraRye,RobertScott,GerriMortimore, Adam Lawson, Andrew Austin, and Jan Freeman Volume 2012, Article ID 343591, 9 pages Hindawi Publishing Corporation International Journal of Hepatology Volume 2012, Article ID 795063, 2 pages doi:10.1155/2012/795063 Editorial Esophageal Varices: Pathophysiology, Approach, and Clinical Dilemmas Nir Hilzenrat1 and Averell H. Sherker2 1 McGill University, Montreal, QC, Canada 2 Liver Diseases Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, USA Correspondence should be addressed to Nir Hilzenrat, [email protected] Received 30 September 2012; Accepted 30 September 2012 Copyright © 2012 N. Hilzenrat and A. H. Sherker. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Portal hypertension is one of the most significant complica- significant increase in the blood flow through the portal vein tions of both acute and chronic liver diseases. It generally which further contributes to portal hypertension. Esophageal develops as a result of an increase in vascular resistance varices appear and may bleed when the HVPG exceeds at the prehepatic, intrahepatic, or postherpetic level. An 12 mmHg. increase in portal blood flow may also contribute. The A comprehensive review of the clinical manifestations dominant cause of portal hypertension relates to liver of portal hypertension is presented by S. A. Al-Busafi et al. cirrhosis which increases resistance through the hepatic Portal hypertension is a common clinical syndrome defined sinusoids. Gastroesophageal varices are the most important as the elevation of hepatic venous pressure gradient (HVPG) clinical manifestation of this syndrome and are associated above 5 mmHg. Its gastrointestinal manifestations include with a high risk of upper gastrointestinal hemorrhage and the development of esophageal varices, gastric varices, and its attendant high mortality. intestinal vasculopathy. Approximately 5–15% of cirrhotics This special issue includes nine evidence-based reviews. develop esophageal varices annually. The majority of patients They discuss the pathophysiology of portal hypertension as with cirrhosis are expected to develop this condition over well as its clinical manifestations and management. Selected their lifetime. Beyond its gastrointestinal effects, portal topics and controversies related to esophageal varices are hypertension may also affect other vital organs resulting in covered, including noninvasive diagnostic methods, bleeding extrahepatic manifestations. prophylaxis in adults and children, rescue treatments, and Y.-I. Chen and P. Ghali present an overview of strategies the clinical dilemma of portal vein thrombosis. to prevent and manage portal hypertension. The one-year H. Maruyama and O. Yokosuka review the current rate of first variceal hemorrhage is 5% for small varices and concepts of the pathophysiology of portal hypertension and 15% for large varices. Six-week mortality rate following an esophageal varices. Portal hypertension is initially caused by episode of bleeding varies between 15 and 20%. Clearly, distortion of the hepatic vascular bed, which in turn leads to a strategy of prophylaxis to prevent the first episode of increased resistance to portal blood flow. This phenomenon bleeding may reduce morbidity and mortality. In this is associated with intrahepatic endothelial dysfunction with a respect, nonselective beta blockers and new types of beta resultant imbalance between vasodilators such as nitric oxide blockers play a major role. The overall approach and the and prostaglandins vasoconstrictors including endothelin. current pharmacological therapy of acute hemorrhage and An important consequence of increased resistance to portal of recurrent bleeding (i.e., secondary prophylaxis) are based blood flow is splanchnic vasodilatation with consequent on understanding the pathophysiology of esophageal varices. sodium and water retention. As a result of the plasma’s Early diagnosis of esophageal varices prior to the first expansion, and the reduction in peripheral resistance, a episode of bleeding is essential. Studies of primary prophy- hyperdynamic circulation develops. Consequently, there is a laxis clearly show that the risk of first variceal haemorrhage 2 International Journal of Hepatology can be reduced significantly. Upper GI endoscopy remains Portal hypertension in children represents a particular the gold standard for screening, but this test is not without its challenge in both diagnosis and management. A. Costaguta own limitations. K. Rye et al. review the utility of noninvasive and F. Alvarez describe the progress that has been achieved tests to predict esophageal varices. Unfortunately, current recently in the treatment of children with portal hyperten- clinical, biochemical, and radiological parameters are not sion. Two main factors influence therapeutic decisions: the accurate enough to detect varices without a screening age of the patient and the etiology of the liver disease. In endoscopy, but assessment of systemic hemodynamics and this special issue, one can find a summary of the current other serum markers may hold promise for the future. knowledge and an expert opinion on the subject. Variceal rupture is governed by Laplace’s law. Increased Finally, nonneoplastic portal vein thrombosis (PVT) wall tension is the end result of increased intravariceal can be found in up to 25% of individuals with liver pressure, increased diameter of the varices, and reduced wall cirrhosis. The major risk factor of having PVT is severe liver thickness. The variceal wall thickness can be evaluated visu- disease and portal hypertension. Recently, it was found that ally by the presence of red wale markings. These markings procoagulant imbalance in individuals with advanced liver reflect areas where the wall is especially thin. Variceal rupture disease contributes to the development of PVT. The clinical often occurs at the level of the gastroesophageal junction impact of PVT on liver function is not clear. Nevertheless, where the varices are very superficial and thus have thinner it is a predictive factor for mortality among cirrhotics, inde- walls. S. A. Al-Busafi et al. discuss the role of endoscopic pendent of MELD score. PVT may be the cause of various management of esophageal varices. They emphasized the fact life-threatening conditions. It increases portal hypertension that gastroscopy allows direct visualization and is an excellent
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