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KEY CONCEPTS
Because of increased perioperative risk, patients with acute hepatitis should have any elective surgery postponed until the acute hepatitis has resolved, as indicated by the normalization of liver tests.
Isoflurane and sevoflurane are the volatile agents of choice for patients with significant liver disease because they preserve hepatic blood flow and oxygen delivery. Factors known to reduce hepatic blood flow, such as hypotension, excessive sympathetic activation, and high mean airway pressures during controlled ventilation, should be avoided.
In evaluating patients for chronic hepatitis, laboratory test results may show only a mild elevation in serum aminotransferase activity and often correlate poorly with disease severity.
Liver cirrhosis refers to the damaging effects to the liver of inflammation, hepatocellular injury, and the resulting fibrosis and regeneration of hepatocytes.
Liver cirrhosis leads to portal hypertension, varices, and widespread endothelial damage from toxins not cleared by the liver that may cause multiorgan dysfunction.
Massive bleeding from gastroesophageal varices is a major cause of morbidity and mortality in patients with liver disease, and, in addition to the cardiovascular effects of acute blood loss, the absorbed nitrogen load from the breakdown of blood in the gastrointestinal tract can precipitate hepatic encephalopathy.
Cardiovascular changes observed in cirrhotic patients are usually those of hyperdynamic circulation, although clinically significant cirrhotic cardiomyopathy is often present and not recognized.
The effects of hepatic cirrhosis on pulmonary arterioles may result in vasodilation, causing shunts and chronic hypoxemia, or conversely lead to pulmonary vasoconstriction and medial hyperplasia, causing an increase in vascular resistance and pulmonary hypertension.
Hepatorenal syndrome is a functional renal defect in patients with cirrhosis that usually follows gastrointestinal bleeding, aggressive diuresis, sepsis, or major surgery. It is characterized by progressive oliguria with avid sodium retention, azotemia, intractable ascites, and a very high mortality rate.
Factors known to precipitate hepatic encephalopathy in patients with cirrhosis include gastrointestinal bleeding, increased dietary protein intake, hypokalemic alkalosis from vomiting or diuresis, infections, worsening liver function, and drugs with central nervous system depressant activity.
Following the removal of large amounts of ascitic fluid, aggressive intravenous fluid replacement is often necessary to prevent profound hypotension and acute kidney injury or failure.
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The prevalence of liver disease is increasing. Cirrhosis, the terminal pathology of most liver diseases, has a general population incidence as high as 5% in some autopsy series. It is a major cause of death in men in their fourth and fifth decades of life, and mortality rates are increasing. Ten percent of the patients with liver disease undergo operative procedures during the final 2 years of their lives. The liver has remarkable functional reserve, and thus overt manifestations of hepatic disease are often absent until extensive damage has occurred. When patients with little hepatic reserve come to the operating room, effects from anesthesia and the surgical procedure can precipitate hepatic decompensation and frank hepatic failure.
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COAGULATION IN LIVER DISEASE
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The hemostatic changes ...