The risk of surgery cannot be separated from the risk of anesthesia. Sedatives, narcotics, and intravenous induction agents are generally well tolerated in patients with compensated liver disease but must be used with caution in patients with decompensated hepatic dysfunction, because they may cause prolonged depression of consciousness and precipitate hepatic encephalopathy.
Blood levels of narcotics that undergo high first-pass extraction by the liver, increase as hepatic blood flow decreases. Elimination of benzodiazepines that undergo glucuronidation (e.g
., oxazepam, lorazepam) is unaffected by liver disease, whereas the elimination of those that do not undergo glucuronidation (e.g
., diazepam, chlordiazepoxide) is prolonged in liver disease. Long acting narcotics and sedatives should (therefore) be avoided in cirrhotic patients. However, the use of various narcotics like Fentanyl, Sufentanil and sedatives like Oxazepam, Lorazepam, in conjunction with anesthetics is recommended, because their actions are less prolonged in patients with liver disease[36
Anesthesia can affect the liver functions by reducing its blood flow. In healthy volunteers, hepatic blood flow decreases by 35%-42% in the first 30 min of induction of anesthesia[37
]. Studies in animals have shown that under the conditions of stress, hepatic blood flow increases to compensate for the reduced portal blood flow but patients with liver disease, especially cirrhosis under the influence of anesthesia cannot compensate for the reduced portal blood flow, which may cause hepatic dysfunction[38
]. The anesthetic agents Halothane and Enflurane reduce hepatic arterial blood flow. These effects are minimal with Isoflurane.
Acute hepatitis associated with the administration of halothane is believed to be caused by immune sensitization to trifluoroacetylated liver proteins formed by oxidative metabolism of halothane by cytochrome P450 2E1 in genetically predisposed persons[39
]. With this notable exception, few data suggest that either the choice of anesthetic agent or mode of administration (inhaled or spinal) influences surgical outcome in patients with liver disease[40
Inhalational agents Isoflurane, Desflurane and Sevoflurane undergo hepatic metabolism, extent of which is 0.2% for isoflurane, 2%-4% for Enflurane, and 20% for Halothane[41
] presumably, this leads to a lesser incidence of drug-induced hepatitis. Therefore, Isoflurane has become the inhalation agent of choice in patients with liver disease.
Propofol is an excellent anesthetic agent of choice in patients with liver disease, because it retains a short half-life even in patients with decompensated cirrhosis[42
The volume of distribution of non-depolarizing muscle relaxants is increased in patients with liver disease, and therefore larger doses may be required initially to achieve adequate neuromuscular blockade. The actions of neuromuscular blocking agents may be prolonged in patients with liver disease because of reduced pseudocholinesterase activity, decreased biliary excretion, and larger volume of distribution. Atracurium and cisatracurium are the preferred muscle relaxants in patients with liver disease because neither the liver nor the kidney is required for their elimination. Doxacurium is the preferred muscle relaxant in longer procedures such as liver transplantation, as it is metabolized by the kidney.
No correlation could however be established in patients with cirrhosis undergoing cardiac surgery and hepatic decompensation or mortality between the use of Enflurane, Isoflurane, Fentanyl, Sufentanil, Midazolam or Morphine[28
]. The type of anesthetic management either general anesthesia, regional anesthesia, or monitored anesthesia care did not affect the mortality in one of the largest reported series of 733 patients[4