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The anesthesia literature is replete with detailed descriptions regarding the preoperative assessment of cardiac risk for noncardiac surgery.[89] In addition, preoperative renal risk factors have been delineated.[90] Defining preoperative risk factors for the development of postoperative hepatic dysfunction or failure after nonhepatic surgery has not been so clearly elucidated, and as such, anesthesiologists have based decisions regarding the care of patients with preoperative hepatic dysfunction on data derived 4 to 5 decades ago. Unfortunately, prospective studies addressing these issues in the current era of newer anesthetic and surgical techniques are lacking. Assessment of risk factors for postoperative hepatic insufficiency requires consideration of (1) asymptomatic elevations in preoperative liver enzyme test results; (2) acute hepatitis (viral, drug, toxin), steatosis, chronic hepatitis, and cirrhosis; and (3) the types of surgery that potentially predispose to postoperative liver dysfunction.
Unnecessary laboratory test screening may reveal abnormally elevated liver enzyme test results in otherwise healthy patients. Abnormalities in standard liver enzyme tests, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase, occur in 0.1% to 4% of the general population[91] [92] and to as many as 36% of psychiatric patients in whom alcohol and illicit drug abuse is prominent.[93] However, the overall prevalence of clinically significant hepatic dysfunction in asymptomatic patients is less than 1%. Thus, pursuing more extensive evaluation with costly tests such as ultrasonography, radionuclide imaging, or liver biopsy is rarely indicated.
In general, the most appropriate initial approach to a surgical patient with abnormal liver enzyme test results is a detailed history and physical examination. Symptoms of fatigue, anorexia, nausea, vomiting, biliary colic, pruritus, fever, or dark-colored urine warrant further evaluation because they may suggest clinically active hepatobiliary disease and thus potentially preclude elective surgery. If, however, the patient is asymptomatic, the significance of abnormal enzyme test results can be questioned. The patient should be further queried about a history of associated diseases such as chronic hepatitis, a family history of Wilson's disease, hemachromatosis, α1 -antitrypsin deficiency, diabetes mellitus, hyperthyroidism or hypothyroidism, and previous transfusion history. All medications, including vitamins and herbal or other homeopathic remedies, should be reviewed for potential hepatotoxic side effects. The patient should be further questioned regarding alcohol or other illicit drug use, the presence of tattoos, sexual promiscuity, and consumption of raw seafood because they are potential risk factors for infectious hepatitis.
Physical examination may reveal findings consistent with active liver disease, such as icterus, palmar erythema, spider angiomas, gynecomastia, hepatosplenomegaly, ascites, or peripheral edema. Although these findings invariably suggest a diagnosis of cirrhosis, it is reasonable to repeat the test if a complete history and physical examination fail to suggest an etiology of the biochemical abnormality. Minor elevations in liver enzyme test results are considered to be less than twice the normal value [94] and, given a negative history and physical examination, do not warrant additional testing before anesthesia and surgery. Assessment of larger elevations in liver enzyme test results requires an analysis of the specific abnormality.
AST and ALT are sensitive indicators of hepatocyte integrity. AST is present in hepatocyte cytoplasm and mitochondria, but it is also ubiquitous in cardiac and skeletal muscle; kidney, brain, pancreas, and lung tissue; and red and white blood cells. AST is therefore a less specific index of cellular injury than ALT is, which is primarily found in the cytoplasm of hepatocytes. Both enzymes are released when the hepatic cell membrane is injured, although there appears to be a correlation between the degree of injury and serum aminotransferase levels. The AST/ALT ratio may also be helpful in distinguishing between alcohol-induced hepatitis and viral hepatitis. Alcohol tends to preferentially damage hepatocyte mitochondria, thereby causing an elevation in AST usually greater than twice the ALT.[95] In addition, ALT activity is diminished in patients with alcohol-induced liver disease because these individuals tend to have deficiencies of pyridoxal 5-phosphate, a vitamin necessary for ALT function. In contrast, a decrease in the AST/ALT ratio is more consistent with a diagnosis of viral hepatitis. Aminotransferases also increase in choledocholithiasis, cholangitis, and ischemic hepatitis. Ischemic hepatitis may not uncommonly produce levels greater than 10,000 IU/L.
Similar to AST, alkaline phosphatase is present in many tissues, including bone, intestine, kidney, and placenta, as well as in leukocytes. The enzyme catalyzes the hydrolysis of orthophosphate from ester substrates at an alkaline pH. In hepatocytes, alkaline phosphatase is synthesized by biliary epithelial cells and released in relation to the degree of bile duct obstruction. Measuring serum γ-glutamyl-transferase (GGT), an enzyme found predominantly in hepatocytes and biliary epithelial cells, may aid in distinguishing between hepatic and bone etiologies of increased alkaline phosphatase. Although GGT is a very sensitive indicator of the presence or absence of hepatobiliary disease, by itself it lacks specificity because it is also increased in patients with myocardial infarction, renal disease, diabetes mellitus, and chronic obstructive pulmonary disease. If both alkaline phosphatase and GGT are elevated, the abnormality probably reflects hepatobiliary disease. Increased levels of alkaline phosphatase and GGT usually occur with extrahepatic bile duct obstruction and intrahepatic cholestasis from infiltrative diseases such as sarcoidosis, from mass lesions such as primary or metastatic carcinoma, or from drug-induced cholestasis.
Although liver enzyme elevation is an indication of active disease, synthetic hepatic function is best measured by serum bilirubin, albumin, and the prothrombin time. The bilirubin concentration in plasma varies in accordance with its production and inversely with hepatic clearance. Hepatic microsomal enzymes convert unconjugated bilirubin to the more water-soluble form, thereby permitting excretion in bile and preventing central nervous system toxicity. Total bilirubin levels represent both conjugated (direct bilirubin) and unconjugated (indirect bilirubin) forms. Unconjugated hyperbilirubinemia suggests hemolysis or an inherited disorder of bilirubin metabolism such as Gilbert's syndrome. If more than 50% of the total serum bilirubin is conjugated, cholestasis or hepatocellular dysfunction is implied. Albumin is synthesized solely in the liver and, in healthy adults, has a half-life of approximately 21 days. The normal level of 3.5 g/dL usually decreases in long-standing and severe liver disease but is also influenced by overall nutritional status.
Finally, hepatobiliary dysfunction can cause an abnormal prothrombin time by impairing synthesis of the essential clotting factors II (prothrombin), VII, IX, and X. Hepatic synthesis of these factors is dependent on vitamin K, a fat-soluble vitamin found in certain foods and produced by intestinal bacteria, so abnormalities in prothrombin activity (as expressed by the international normalized ratio [INR]) may also occur in patients with malnutrition or malabsorption syndromes. The plasma half-time of these vitamin K-dependent factors is very short (less than 24 hours), and hence the INR responds rapidly to changes in synthetic function, which makes this test a more sensitive index of hepatic function than albumin is.
Although no prospective, randomized, controlled studies have been designed to assess the perioperative risk of anesthesia or surgery in asymptomatic patients with elevated liver enzyme test results, a suggested approach to these patients is outlined in Figure 55-5 . Abnormal liver enzyme test results in an otherwise healthy patient reflect either a subclinical acute process such as viral or toxin-mediated hepatitis or a chronic disorder such as chronic hepatitis.
Figure 55-5
Approach to asymptomatic patients with abnormal liver
test results presenting for surgery.
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