Surgery in the Patient With Liver Disease and Postoperative Jaundice

Overview

• 1.

  Surgical procedures, whether performed using general or local (i.e., spinal or epidural) anesthesia, are often followed by changes in liver biochemical test results.

• 2.

  Postoperative elevations of serum aminotransferase, alkaline phosphatase, or bilirubin levels are generally minor and transient, and in patients without underlying cirrhosis, these changes are not clinically important.

• 3.

  Clinically significant hepatic dysfunction can occur in patients with preexisting acute liver disease or cirrhosis and is more common in patients with compromised hepatic synthetic function.

Effects of Anesthetic Agents on the Cirrhotic Liver

• 1.

  At baseline, hepatic arterial and venous perfusion of the cirrhotic liver is decreased because of the following:

  • ▪

    Portal hypertension that decreases portal blood flow

  • ▪

    Impaired autoregulation that decreases arterial blood flow

  • ▪

    Arteriovenous shunting around the liver

  • ▪

    Reduced splanchnic inflow

• 2.

  Decreased hepatic perfusion at baseline makes the cirrhotic liver more susceptible to hypoxemia and hypotension in the operating room; induction causes a reduction in hepatic blood flow by 30% to 50%.

Other Intraoperative Factors

Intraoperative factors that may decrease hepatic oxygenation by further decreasing hepatic blood flow or increasing splanchnic vascular resistance are as follows:

• ▪

  Hypotension caused by hepatorenal syndrome or shock

• ▪

  Hemorrhage

• ▪

  Hypoxemia caused by ascites, hepatic hydrothorax, hepatopulmonary syndrome, portopulmonary hypertension, or aspiration

• ▪

  Hypercapnia

• ▪

  Heart failure

• ▪

  Vasoactive drugs

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  Intermittent positive pressure ventilation

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  Pneumoperitoneum during laparoscopic surgery

• ▪

  Traction on abdominal viscera with reflex dilatation of splanchnic capacitance vessels

Hepatic Metabolism of Anesthetic Agents

• 1.

  Inhalational anesthetic agents are lipid-soluble compounds that require hepatic transformation to more water-soluble compounds for biliary excretion.

• 2.

  Consequences of hepatic metabolism

  • a.

    Prolonged anesthetic action in patients with liver disease (also caused by hypoalbuminemia and impaired biliary excretion)

  • b.

    Formation of toxic intermediates or reactive oxygen species, especially in the presence of hypoxia or reduced hepatic blood flow

    • ▪

      Halothane → hepatitis (uncommon)

    • ▪

      Enflurane → hepatitis (even less common)

• 3.

  Isoflurane, desflurane, sevoflurane, and nitrous oxide are preferable in patients with liver disease because these agents undergo the least hepatic metabolism and hepatic arterial blood flow alterations, and resulting hepatitis is rare.

• 4.

  Propofol is an excellent anesthetic choice in patients with liver disease; although it is metabolized by hepatic glucuronidation, its serum half-life remains short even in patients with cirrhosis, it increases hepatic blood flow, and it does not precipitate hepatic encephalopathy.

• 5.

  Of the induction agents, etomidate and thiopental decrease hepatic blood flow, but ketamine does not.

Other Agents in Liver Disease

• 1.

  Narcotics and sedatives are generally well tolerated in patients with compensated liver disease.

  • a.

    These drugs have a prolonged duration of action in decompensated liver disease.

    • ▪

      Narcotics have high first-pass extraction by the liver.

      • –

        Blood levels increase as hepatic blood flow decreases.

      • –

        Bioavailability is increased because of portosystemic shunting.

      • –

        Preferred agents are fentanyl and sufentanil , which have similar durations of action in healthy persons and in patients with cirrhosis.

    • ▪

      Benzodiazepines have low first-pass extraction by the liver.

      • –

        Those eliminated by glucuronidation ( oxazepam, lorazepam ) are not affected by liver disease.

      • –

        Those not glucuronidated (diazepam, chlordiazepoxide) have enhanced sedative effects in liver disease and should be avoided.

  • b.

    They may precipitate hepatic encephalopathy in patients with severe liver disease.

  • c.

    Smaller than standard doses are indicated for those drugs whose metabolism is affected by liver disease.

• 2.

  Muscle relaxants

  • a.

    Succinylcholine should be avoided. Resistance occurs in patients with liver disease in part because of decreased hepatic pseudocholinesterase production. The large doses required in patients with liver disease may cause difficulty in reversing their effect postoperatively.

  • b.

    The volume of distribution for nondepolarizing muscle relaxants is increased, and larger doses than usual may be required. Atracurium and cisatracurium are preferred because neither the liver nor the kidney is required for elimination.

Effect of Surgery

• 1.

  The nature and extent of surgery may be more important determinants of postoperative hepatic dysfunction than anesthesia.

• 2.

  Perioperative risk is increased with biliary tract and open abdominal surgery and is greatest with cardiac surgery and liver resection.

  • a.

    In patients with cholecystitis, laparoscopic cholecystectomy is permissible in patients in Child-Pugh class A and selected patients in Child-Pugh class B without portal hypertension; however, in patients with more advanced cirrhosis with portal hypertension, cholecystostomy is preferable.

  • b.

    Risk factors for hepatic decompensation after cardiac surgery include total time on cardiopulmonary bypass, use of pulsatile as opposed to nonpulsatile bypass, and need for perioperative vasopressor support; cardiopulmonary bypass may exacerbate coagulopathy.

  • c.

    Less invasive cardiovascular procedures (e.g., angioplasty, valvuloplasty, endovascular aneurysm repair) are preferred to open surgery in patients with advanced cirrhosis. Occasionally, however, major cardiac surgery (including heart transplantation) may be performed at the same time as liver transplantation in selected cases.

Problems in Estimating Operative Risk

• ▪

  Large prospective studies and randomized controlled trials are lacking.

• ▪

  Data on acute and chronic hepatitis are limited.

• ▪

  The effects of comorbid conditions on surgical risk are difficult to quantitate.

Acute Hepatitis (see Chapter 3 , Chapter 4 , Chapter 5 )

• 1.

  Acute hepatitis of any cause increases operative risk.

• 2.

  Elective surgery should be avoided in patients with acute hepatitis. In the past, exploratory laparotomy was often performed to differentiate viral hepatitis from cholestatic disorders. Currently, such a distinction is made by a combination of serologic testing, radiologic imaging, cholangiography, and/or percutaneous liver biopsy.

• 3.

  Acute hepatitis is almost always self-limited or treatable. It is best to postpone elective surgery until liver dysfunction is investigated and the course of the disease is observed. Surgery can be undertaken after the patient improves.