Anesthesia for patients with hepatocellular disease

Published on 07/02/2015 by admin

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Anesthesia for patients with hepatocellular disease

Joseph J. Sandor, MD

Knowledge of the varied physiologic functions of the liver (Box 177-1) allows the anesthesia provider to anticipate potential problems when patients with hepatocellular disease present for surgery.

Box 177-1   Critical Processes Performed by the Liver

Patients with hepatocellular disease may have altered perioperative coagulation disorders and hypoglycemia. The pharmacokinetics and pharmacodynamics of anesthetic drugs may be altered by alcohol-induced microsomal enzyme induction, which can accelerate the metabolism of drugs and alter the amount of anesthetic drug necessary to achieve a specific anesthetic depth. Hypoalbuminemia increases the pharmacologically active fraction of several protein-bound drugs, which, combined with decreased degradation, results in an increased sensitivity to many drugs (e.g., opioids) in patients with hepatocellular disease.

Acute hepatic failure

Central nervous system manifestations of acute hepatic failure include encephalopathy, altered levels of consciousness, and hyperventilation from vitamin deficiency and increased serum levels of ammonia and other toxic metabolites. Hypoglycemia may result from impaired gluconeogenesis, depleted glycogen stores, and reduced insulin degradation. Cardiac output is increased from reduced systemic vascular resistance and increased arteriovenous shunting. Intrapulmonary shunting may produce hypoxemia. Patients often have coexisting renal disease and are more susceptible to developing infections. Of the proteins synthesized by the liver, factor VII has one of the shortest half-lives (t1⁄2 approximately 6 h). Accordingly, the prothrombin time provides valuable information as to acute changes in hepatic function.

Surgery should be performed in patients with acute hepatic failure only in an emergency. Fresh frozen plasma and vitamin K can be given preoperatively to correct coagulation abnormalities. Because these patients have decreased rates of drug metabolism, anesthetic requirements are significantly reduced, and the effects of barbiturate and opioidergic agents are prolonged. Because plasma cholinesterase levels may be decreased but are usually adequate (t1⁄2 approximately 14 days), succinylcholine does not significantly prolong apnea and, therefore, may be used. Blood glucose concentrations should be monitored.

These patients are at an increased risk of developing hypoxemia, hypotension, acidosis, hypokalemia, hypocalcemia, and hypomagnesemia. Large-bore intravenous access should be obtained preoperatively; hemodynamic measures should be invasively monitored, as appropriate; and anesthetic drugs should be carefully titrated to effect.

Chronic hepatic disease

Anesthetic management of patients with chronic liver disease is dictated by the number and severity of cirrhosis-induced extrahepatic complications. Cardiovascular abnormalities may include increased cardiac output, increased intravascular volume, decreased blood viscosity, increased severity of arteriovenous shunting, congestive heart failure, and cardiomyopathy (e.g., ethanol-induced dilated cardiomyopathy). Arterial hypoxemia results from intrapulmonary arteriovenous shunting, ventilation/perfusion mismatch (as the result of decreased functional reserve capacity from ascites displacing the diaphragm cephalad), and recurrent pneumonia (related to decreased immunity and increased atelectasis). Hypoglycemia in the perioperative period should be anticipated. Patients with chronic hepatic disease are more likely than the general population to have cholestasis and cholelithiasis, either of which increases their susceptibility to developing cholecystitis and pancreatitis. Peptic ulcer disease occurs twice as often in people with liver disease, as compared with people without liver disease. These patients also may have gastroesophageal reflux and intestinal hypomotility.

Portal hypertension (causing varices and splenomegaly) and impaired coagulation from thrombocytopenia, factor deficiencies, disseminated intravascular coagulation, and fibrinolysis place these patients at risk for developing sudden massive bleeding. Renal disease may coexist with chronic liver disease; however, hepatorenal syndrome occurs as a manifestation of end-stage liver disease. Hepatic encephalopathy and peripheral neuropathy from nutritional deficiencies may arise.

Anesthesia considerations

The preoperative history and physical examination of patients with hepatocellular disease should focus on identifying extrahepatic manifestations of chronic liver failure. The laboratory evaluation comprises arterial blood gas concentration, complete blood count, coagulation studies, and a chemistry panel that includes albumin and glucose concentrations. If the patient has no coagulopathy, a regional anesthetic technique may be used.

Benzodiazepine and opioidergic agents should be used cautiously. Some anesthesia providers advocate the use of H2 antagonists, nonparticulate antacids, or proton pump inhibitors prior to induction of anesthesia to reduce these patients’ risk of aspirating gastric contents.

The placement of an intraarterial catheter should be considered to facilitate perioperative monitoring of blood pressure and blood withdrawal to measure arterial blood gases; electrolyte, hemoglobin, and glucose concentrations; and coagulation status. Monitoring central venous pressure and, occasionally, pulmonary artery pressure aids in perioperative fluid management. If surgery is likely to be associated with massive blood loss, a rapid-infusion pump should be readily available. A peripheral nerve stimulator should be used to avoid administering excess amounts of neuromuscular blocking agents.

Rapid-sequence induction or awake intubation facilitates airway protection from aspiration. Doses of induction agents (etomidate, propofol) should be reduced because of the likelihood of patients having an increased sensitivity to the neurologic and cardiovascular effects of these drugs. In patients with liver disease, the hepatic arteries contribute a much greater proportion of blood to total hepatic blood flow; thus, decreases in mean arterial pressure should be avoided to prevent hepatocellular hypoxia. Avoiding light anesthesia, hypoxia, hypercarbia, and excessive positive-pressure ventilation prevents increased splanchnic vascular resistance; using halogenated inhalation agents without N2O allows for delivery of a higher fraction of inspired O2. Postoperative analgesic requirements are usually reduced in patients with hepatocellular disease.

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Anesthesia for patients with hepatocellular disease

Joseph J. Sandor, MD

Knowledge of the varied physiologic functions of the liver (Box 177-1) allows the anesthesia provider to anticipate potential problems when patients with hepatocellular disease present for surgery.

Box 177-1   Critical Processes Performed by the Liver

Patients with hepatocellular disease may have altered perioperative coagulation disorders and hypoglycemia. The pharmacokinetics and pharmacodynamics of anesthetic drugs may be altered by alcohol-induced microsomal enzyme induction, which can accelerate the metabolism of drugs and alter the amount of anesthetic drug necessary to achieve a specific anesthetic depth. Hypoalbuminemia increases the pharmacologically active fraction of several protein-bound drugs, which, combined with decreased degradation, results in an increased sensitivity to many drugs (e.g., opioids) in patients with hepatocellular disease.

Acute hepatic failure

Central nervous system manifestations of acute hepatic failure include encephalopathy, altered levels of consciousness, and hyperventilation from vitamin deficiency and increased serum levels of ammonia and other toxic metabolites. Hypoglycemia may result from impaired gluconeogenesis, depleted glycogen stores, and reduced insulin degradation. Cardiac output is increased from reduced systemic vascular resistance and increased arteriovenous shunting. Intrapulmonary shunting may produce hypoxemia. Patients often have coexisting renal disease and are more susceptible to developing infections. Of the proteins synthesized by the liver, factor VII has one of the shortest half-lives (t1⁄2

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