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  • 1. Introduction The liver is the most metabolically complex organ. Hepatocytes (liver parenchymal cells) perform the liver's metabolic functions: formation and excretion of bile; regulation of carbohydrate homeostasis; lipid synthesis and secretion of plasma lipoproteins; control of cholesterol metabolism; formation of urea, serum albumin, clotting factors, enzymes, and numerous other proteins; and metabolism or detoxification of drugs and other foreign substances. At the cellular level, the portal triads consist of adjacent and parallel terminal branches of bile ducts, portal veins, and hepatic arteries that border the hepatocytes (see Fig. 1: Approach to the Patient With Liver Disease: Organization of the liver. ). Terminal branches of the hepatic veins are in the center of hepatic lobules. Because blood flows from the portal triads past the hepatocytes and drains via vein branches in the center of the lobule, the center of the lobule is the area most susceptible to ischemia. Fig. 1 Organization of the liver. Liver disorders can result from a wide The liver is organized into lobules around terminal branches of the hepatic vein. Between the lobules are portal triads. Each triad consists of branches of a bile duct, portal vein, and hepatic artery. variety of insults, including infections, drugs, toxins, ischemia, and
  • 2. autoimmune disorders. Occasionally, liver disorders occur postoperatively (see Sidebar 1: Approach to the Patient With Liver Disease: Postoperative Liver Dysfunction ). Most liver disorders produce some degree of hepatocellular injury and necrosis, resulting in various abnormal laboratory test results and, sometimes, symptoms. Symptoms may be due to liver disease itself (eg, jaundice due to acute hepatitis) or to complications of liver disease (eg, acute GI bleeding due to cirrhosis and portal hypertension).
  • 3. Sidebar 1 Postoperative Liver Dysfunction Mild liver dysfunction sometimes occurs after major surgery even in the absence of pre-existing liver disorders. This dysfunction usually results from hepatic ischemia or poorly understood effects of anesthesia. Patients with pre-existing well- compensated liver disease (eg, cirrhosis with normal liver function) usually tolerate surgery well. However, surgery can increase the severity of some pre-existing liver disorders; eg, laparotomy may precipitate acute liver failure in a patient with viral or alcoholic hepatitis. Postoperative jaundice: Diagnosis of postoperative jaundice requires liver laboratory tests. Timing of symptoms also aids in diagnosis. Multifactorial mixed hyperbilirubinemia is the most common reason for postoperative jaundice. It is caused by increased formation of bilirubin and decreased hepatic clearance. This most often occurs after major surgery or trauma requiring multiple transfusions. Hemolysis, sepsis, resorption of hematomas, and blood transfusions can increase the bilirubin load; simultaneously, hypoxemia, hepatic ischemia, and other poorly understood factors impair hepatic function. This condition is usually maximal within a few days of operation. Hepatic insufficiency is rare, and hyperbilirubinemia typically resolves slowly but completely. Liver laboratory tests can often differentiate multifactorial mixed hyperbilirubinemia from Despite hepatitis; in multifactorial mixed hyperbilirubinemia, severe hyperbilirubinemia with mild aminotransferase and alkaline phosphatase elevations are common. In hepatitis, aminotransferase levels are usually very high. Ischemic postoperative “hepatitis” results from insufficient liver perfusion, not inflammation. The cause is transient perioperative hypotension or hypoxia. Typically, aminotransferase levels increase rapidly (often > 1000 units/L), but bilirubin is only mildly elevated. Ischemic hepatitis is usually maximal within a few days of operation and resolves within a few days. Halothane-related hepatitis can result from use of anesthetics