Postoperative Liver Dysfunction

Introduction

• Bilirubin is a byproduct of the breakdown of heme from red blood cells. Under normal conditions, the liver conjugates the bilirubin to make it water-soluble and secretes it into the gastrointestinal tract as bile. Jaundice, which is the result of hyperbilirubinemia, occurs when there is a breakdown anywhere along the normal bilirubin uptake, metabolism, or excretion processes.
• The combined stresses of anesthesia and surgery frequently produce some degree of hepatic dysfunction, often manifested as jaundice. At the mildest end of the spectrum, the POLD is short-lasting and leads to a mild elevation in bilirubin and liver enzyme levels, while at the most severe end, a sustained deterioration in the metabolic and synthetic functions of the liver culminating in postoperative liver failure.
• The effects of anesthesia and surgery often result in a fall in hepatic blood flow leading to a reduction in O₂ delivery, which can be as much as 30-40%.² It is thought that ischemia and the subsequent reperfusion injury is responsible for much of the POLD reported.

Causes of Postoperative Jaundice

• It is useful to categorize the causes of jaundice and liver dysfunction into three main groups: prehepatic, intrahepatic, and posthepatic.³
• Prehepatic jaundice usually arises when the quantity of heme delivered to the liver surpasses its ability to conjugate it all.
  • This presents as an unconjugated hyperbilirubinemia that resolves fully over time.
  • In most cases, the excess heme is produced by hemolysis following bleeding during surgery or the use of blood transfusions.
• Intrahepatic jaundice is due to either the hepatocyte’s inability to conjugate bilirubin (hepatocellular dysfunction), or obstruction of the intrahepatic bile ducts resulting in a failure to transport the bile out of the liver (as in cirrhosis).
  • It usually presents as an increase in both conjugated and unconjugated bilirubin.
  • Hepatocellular dysfunction can be a result of hepatocyte failure from either ischemic or drug-induced stresses.
  • “Shock liver” – acute ischemic hypoperfusion and subsequent reperfusion injury – is a severe condition reflecting massive damage to hepatocytes from ischemia. It leads to a large increase in the level of tissue transaminases along with a similar rise in the international normalized ratio, reflecting a deterioration in the synthetic functions of the liver. Exposure to a variety of hepatotoxic drugs can cause a similar picture, often developing in the days after surgery and improving after cessation of the offending drug (e.g., acetaminophen, inhaled volatile agents, amoxicillin/clavulanate, amiodarone).
• Posthepatic jaundice is usually secondary to the surgery itself (where damage to the biliary system often requires endoscopic intervention to aid resolution).
  • This presents with an obstructive jaundice picture (conjugated hyperbilirubinemia with mildly elevated transaminases and alkaline phosphatase).
  • A common example would be bile duct stenosis following liver transplantation.
• Postoperative jaundice is often multifactorial in origin (Figure 1, Table 1).

Prevention and Management

• Patients should be properly assessed and investigated before selection.
• The most appropriate anesthetic technique considering the patient’s pre-existing condition is important.
• Management of POLD should focus on treating the underlying cause.
• Frequent monitoring of blood tests may be necessary.
• Find alternatives for any potentially hepatotoxic drugs
• Seek specialized advice for potential surgical problems
• Supportive care is often the only option until the liver is able to self-repair.