Transient changes in liver function are common following surgery due to the stresses of surgery and reduced hepatic blood flow from anesthesia. These changes are often clinically insignificant. However, if a patient develops jaundice, a more serious dysfunction is likely present and further evaluation is warranted.
There are three major factors to consider when assessing the risk of postoperative hepatobiliary dysfunction:
Elevated preoperative liver enzymes—Liver enzymes are not routinely indicated preoperatively in asymptomatic otherwise healthy patients. However, if an abnormality is detected, a thorough history and physical examination should be conducted to rule out preexisting liver disease. This process is described in detail in the previous chapter on the preoperative evaluation of hepatic dysfunction.
Preexisting liver disease—Acute hepatitis of any origin is an indication for postponement of elective surgery due to the increased morbidity and mortality from surgery. Steatosis and steatohepatitis may increase the risk of postoperative mortality. Chronic hepatitis increases the risk of liver failure and hepatic encephalopathy due to changes in hepatic perfusion during an operation. Cirrhosis is a known perioperative risk factor, and jaundice is reported in almost 50% of patients having abdominal surgery.
Type of surgery—Certain procedures entail a greater risk of postoperative liver failure. Upper abdominal surgeries may significantly reduce total hepatic blood flow. Resection of hepatocellular carcinoma poses a significant risk of liver failure from insufficient hepatic reserve following the operation. Cardiothoracic procedures pose significant risk to the liver due to decreases in hepatic blood flow.
Similar to renal dysfunction, postoperative hepatobiliary dysfunction can be broadly categorized into prehepatic, intrahepatic, and posthepatic etiologies. Jaundice may or may not be present. Patients with visible jaundice typically have serum bilirubin levels > 4 mg/dL.
Jaundice secondary to hemolysis is characterized by anemia and indirect (unconjugated) hyperbilirubinemia with preservation of normal serum alkaline phosphatase and alanine transaminase (ALT). Potential causes include breakdown of transfused erythrocytes from multiple blood transfusions, reabsorption of extravasated blood (e.g., retroperitoneal or intra-abdominal hematomas from trauma or ruptured aortic aneurysms), ABO incompatibility, hemolytic anemia, glucose-6-phosphate dehydrogenase deficiency, malaria, sickle cell anemia, and kidney diseases leading to hemolytic uremic syndrome.
Decreased hepatic clearance secondary to hepatic hypoperfusion can also cause hepatic dysfunction. Cardiogenic shock due to congestive heart failure can lead to ischemic hepatitis. This condition is characterized by rapid elevations in serum levels of AST, ALT, and LDH, often 10-fold above normal limits and potentially associated with jaundice and prolongation of prothrombin time. These elevations may last 3–11 days and rapidly return to normal thereafter. Noncardiogenic shock, such as septic shock, can also lead to hepatic dysfunction. Accidental ligation of the hepatic artery or its branches can occur during cholecystectomy, resulting in hepatic ischemia and necrosis with elevations ...