Definition: inflammation of hepatocytes
» Multiple causes, including viral infection, toxin, fatty liver infiltration of pregnancy, sepsis, congestive heart failure.
» Symptoms in order of incidence: dark urine, fatigue, anorexia, nausea, fever, emesis, headache, abdominal discomfort, light-colored stool, pruritus.
» Hepatitis A
Fecal-oral transmission; blood transmission is rare.
Chronic disease or carrier state does not exist.
» Hepatitis B
Parenteral, oral-oral, sexual transmission.
HBsAg indicates infectivity.
HBcAg indicates high infectivity.
HBsAg presence for >6 mo suggests a chronic carrier state (1-10% become chronic).
Chronic active disease often progresses to cirrhosis.
» Hepatitis C
Causes most posttransfusion hepatitis.
Chronic liver disease develops in 80% of infected pts & 20% of these will develop cirrhosis.
Sexual & casual household contact w/ saliva is inefficient means of transmission.
» Hepatitis D
Requires the presence of hepatitis B for its expression.
Hepatitis B vaccination prevents hepatitis D.
» Epstein-Barr virus (EBV): usually produces mild hepatitis associated w/ infectious mononucleosis
» Cytomegalovirus (CMV): CMV is present in most adults; liver disease is mild & nonchronic
» Toxins: alcohol, carbon tetrachloride, vinyl chloride
» Therapeutic drugs most frequently implicated: isoniazid, methyldopa, rifampin, acetylsalicylic acid, nonsteroidal anti-inflammatory drugs (NSAIDs)
» Halothane produces two types of hepatotoxicity:
Mild self-limited postop toxicity due to changes in hepatic blood flow that affect hepatic oxygenation
Halothane hepatitis, a life-threatening immune-mediated response after repeat exposure to halothane via trifluoroacetyl metabolite (less likely in pediatric pts)
» Isoflurane/enflurane/desflurane/sevoflurane, like halothane, can produce mild self-limited postop toxicity due to changes in hepatic blood flow. However, they all maintain blood flow similarly & better than halothane
These compounds, w/ exception of sevoflurane, may be capable of producing a more severe immune-mediated hepatitis but undergo less extensive metabolism than halothane
Elective surgery should be postponed for pts w/ acute hepatocellular injury due to increased morbidity & mortality.
» One study found a 31% mortality rate for pts undergoing exploratory laparotomy w/ unsuspected parenchymal liver disease.
» Another study noted a 9.5% mortality rate for pts w/ acute viral hepatitis undergoing laparotomy.
Severely jaundiced pts (>8 mg/dL) are more likely to develop postop renal failure & sepsis.
Decreased perfusion of the liver, which occurs during all anesthetics, neuraxial & general, may be responsible for poor outcomes in pts w/ parenchymal liver disease.
Liver perfusion is affected most greatly by procedures anatomically adjacent (eg, cholecystectomy).What To Do
Rule out acute liver failure (as opposed to merely acute hepatitis).
» Findings in acute liver failure can include encephalopathy, cerebral edema, coagulopathy, renal failure, infection, hypoglycemia, etc.
» See also Coexisting Disease chapter "Acute Liver Failure."
Blood glucose may be low w/ severe liver injury & should be corrected.
Thrombocytopenia should be corrected if present.
Evaluate LFTs & viral serology if appropriate.
» Prothrombin time: assesses current liver synthetic function
May be prolonged by vitamin K deficiency; consider vitamin K administration if this is suspected
» Aspartate aminotransferase (AST), alanine aminotransferase (ALT):
Found in large quantity in the liver.
Levels >500 U/L occur w/ acute hepatocellular injury.
Modest injury <300 U/L occurs in a variety of conditions (eg, acute or chronic hepatocellular injury, infiltrative disease, biliary obstruction).
ALT is generally more sensitive than AST for viral hepatitis.
AST is elevated twofold in excess of ALT in alcoholic liver disease.
If transaminase levels are >3 times normal, nonelective procedures requiring general or regional anesthetic should be postponed & a gastroenterologist consulted.
Lower elevations require repeat evaluation to assess for worsening levels, stable levels, or improvement in levels as well as viral hepatitis serologies.
Surgery may proceed if moderately elevated transaminase levels are stable or trending down & viral serologies are negative; otherwise, seek gastroenterology consult.
Synthesized by liver
Half-life of 14-21 days, so is not beneficial for evaluation of acute disease
» Alkaline phosphatase (AP): present in bone, intestine, liver. AP is elevated in biliary obstruction, cholestasis, space-occupying lesions, infiltrative diseases.
» Gamma-glutamyl transpeptidase (GGT)
Increases in GGT & AP tend to occur in similar diseases.
GGT is elevated in pts ingesting certain agents (eg, alcohol, barbiturates, phenytoin).
» Lactate dehydrogenase (LDH): abundant in the liver but may arise from many sources, including red blood cells, as during hemolysis
» Total bilirubin (a byproduct of heme degradation) is either conjugated (direct-acting, water-soluble, renally excreted) or unconjugated (indirect-acting, protein-bound).
Jaundice is apparent when levels exceed 3-4 mg/dL.
Indirect bilirubin increases w/ hemolysis, Gilbert's or Crigler-Najjar syndrome, heart failure, or portosystemic shunting.
Direct bilirubin increases w/ hepatocellular dysfunction or biliary tract obstruction.
Drug disposition may be difficult to predict.
» Isoflurane, desflurane, sevoflurane may be best for maintenance of hepatic blood flow; consider supplementation w/ nitrous oxide & IV agents (which may have delayed clearance).
» Pseudocholinesterase deficiency is rare such that succinylcholine & mivacurium action should not be prolonged.
» Atracurium & cis-atracurium are cleared independent of liver function.
» Vecuronium & rocuronium are unlikely to be prolonged unless large doses are used.
To optimize liver perfusion & prevent secondary ischemic injury, minimize hypotension & hypoxia & maintain normocarbia.
Administer fresh-frozen plasma for coagulopathy.
Consider monitoring of blood glucose, acid-base status, coagulation profile, urine output.
Be alert to worsening liver function after surgical stress.
Severe postop jaundice may be related to hypotension, hypoxia, multiple transfusions.
"Shock liver" is a condition caused by marked or prolonged hypotension.
» Typical findings include
Tenfold increase in transaminase levels
Possibly liver failure
» A milder form can be seen in pts after cardiopulmonary bypass.
Reversible, minor abnormalities in LFTs can be detected in up to 50% of all patients postop.
Postop jaundice is present in 20% of all patients after major surgery.
Causes of postop jaundice (can be distinguished by LFT evaluation).
» Increased bilirubin
Hemolysis of transfused blood
Resorption of hematoma
» Hepatic damage
Common bile duct stone
Bile duct injury
Gilbert's disease (7-10% of patients) exacerbated by fasting state, cholecystitis
Joseph Cotten, MD, PhD
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