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The aim of this study is to investigate the pathophysiological mechanisms underlying the formation of posthepatectomy ascites with a focus on the significance of changes in portal venous hemodynamics after hepatic resection. By evaluation of other factors that may be involved in the formation of ascites this study may help to show to what extent the increase of portal venous pressure contributes to ascites formation. Detailed knowledge about pathogenetic factors concerning the formation of postoperative ascites might help preventing protracted hospital stay and further inconveniences to the patient.
The mechanisms underlying the development of large-volume ascites after hepatectomy remain poorly understood. While studies on animal models suggest an increase of portal venous pressure after hepatectomy that may in turn favor the transudation of fluid into the peritoneal cavity further factors may be critically involved in the postoperative formation of ascites. These factors may include a drop in serum protein levels (and colloid osmotic pressure), a transient impairment in renal function and a surgery-induced capillary leakage. However, a better knowledge of the pathophysiology represents the prerequisite for efficient treatment.
In the present study the impact of changes in hepatic hemodynamics after hepatectomy on development of ascites will be investigated. Enrolled patients will receive measurement of portal venous flow and pressure as well as hepatic artery flow before and after hepatic resection. Associations of changes in these parameters with development of postoperative ascites and further postoperative complications will be evaluated.
Observational Model: Cohort, Time Perspective: Prospective
Portal venous pressure, Portal venous flow, Hepatic artery flow
Department of General, Visceral and Transplantation Surgery
Enrolling by invitation
University of Heidelberg
Published on BioPortfolio: 2014-07-23T21:10:02-0400
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The venous pressure measured in the PORTAL VEIN.
Abnormal increase of resistance to blood flow within the hepatic PORTAL SYSTEM, frequently seen in LIVER CIRRHOSIS and conditions with obstruction of the PORTAL VEIN.
Dilated blood vessels in the ESOPHAGUS or GASTRIC FUNDUS that shunt blood from the portal circulation (PORTAL SYSTEM) to the systemic venous circulation. Often they are observed in individuals with portal hypertension (HYPERTENSION, PORTAL).
Impaired venous blood flow or venous return (venous stasis), usually caused by inadequate venous valves. Venous insufficiency often occurs in the legs, and is associated with EDEMA and sometimes with VENOUS STASIS ULCERS at the ankle.
Surgical venous shunt between the portal and systemic circulation to effect decompression of the portal circulation. It is performed primarily in the treatment of bleeding esophageal varices resulting from portal hypertension. Types of shunt include portacaval, splenorenal, mesocaval, splenocaval, left gastric-caval (coronary-caval), portarenal, umbilicorenal, and umbilicocaval.
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