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The most commonly performed liver tests are nei-ther sensitive nor specific. No one test evaluates overall hepatic function, reflecting instead one aspect of hepatic function that must be interpreted in conjunction with other tests and clinical assess-ment of the patient.
Many “liver function” tests, such as serum transaminase measurements, reflect hepato-
cellular integrity more than hepatic function. Liver tests that measure hepatic synthetic function include
serum albumin, prothrombin time (PT, or inter-national normalized ratio [INR]), cholesterol, and pseudocholinesterase. Moreover, because of the liver’s large functional reserve, substantial cirrhosis may be present with few or no laboratory abnormalities.
Liver abnormalities can often be divided into either parenchymal disorders or obstructive dis-orders based on laboratory tests (Table 32–4). Obstructive disorders primarily affect biliary excre-tion of substances, whereas parenchymal disorders result in generalized hepatocellular dysfunction.
The normal total bilirubin concentration, composed of conjugated (direct), water-soluble and uncon-jugated (indirect), lipid-soluble forms, is less than 1.5 mg/dL (<25 mmol/L) and reflects the balance between bilirubin production and excretion. Jaundice is usually clinically obvious when total bilirubin exceeds 3 mg/dL. A predominantly conjugated hyper-bilirubinemia (>50%) is associated with increased urinary urobilinogen and may reflect hepatocellular dysfunction, congenital (Dubin–Johnson or Rotor syndrome) or acquired intrahepatic cholestasis, or extrahepatic biliary obstruction. Hyperbilirubinemia that is primarily unconjugated may be seen with hemolysis or with congenital (Gilbert or Crigler– Najjar syndrome) or acquired defects in bilirubin conjugation. Unconjugated bilirubin is neurotoxic, and high levels may produce encephalopathy.
These enzymes are released into the circulation as a result of hepatocellular injury or death. Two aminotransferases are most commonly measured: aspartate aminotransferase (AST), also known as serum glutamic-oxaloacetic transaminase (SGOT), and alanine aminotransferase (ALT), also known as serum glutamic pyruvic-transferase (SGPT).
Alkaline phosphatase is produced by the liver, bone, small bowel, kidneys, and placenta and is excreted into bile. Normal serum alkaline phosphatase activ-ity is generally 25–85 IU/L; children and adolescents have much higher levels, reflecting active growth. Most of the circulating enzyme is normally derived from bone; however, with biliary obstruction, more hepatic alkaline phosphatase is synthesized and released into the circulation.
The normal serum albumin concentration is 3.5– 5.5 g/dL. Because its half-life is about 2–3 weeks, albumin concentration may initially be normalwith acute liver disease. Albumin values less than 2.5 g/dL are generally indicative ofchronic liver disease, acute stress, or severe malnu-trition. Increased losses of albumin in the urine (nephrotic syndrome) or the gastrointestinal tract (protein-losing enteropathy) can also produce hypoalbuminemia.
Significant elevations of blood ammonia levels usually reflect disruption of hepatic urea syn-thesis. Normal whole blood ammonia levels are 47–65 mmol/L (80–110 mg/dL). Marked elevations usually reflect severe hepatocellular damage and may cause encephalopathy.
The PT, which normally ranges between 11–14 sec, depending on the control value,measures the activity of fibrinogen, prothrom-bin, and factors V, VII, and X. The relatively short half-life of factor VII (4–6 h) makes the PT useful in evaluating hepatic synthetic function of patients with acute or chronic liver disease. Prolongations of the PT greater than 3–4 sec from the control are considered significant and usually correspond to an INR 1.5. Because only 20% to 30% of normal factor activity is required for normal coagulation, prolon-gation of the PT usually reflects either severe liver disease or vitamin K deficiency. (See Table 32–5 for a list of coagulation test abnormalities.)
This technology provides a “real time” assessment of the coagulation status and utilizes thromboelas-tography (TEG ®), rotation thromboelastometry (ROTEM®), or Sonoclot® analysis to assess global coagulation via the viscoelastic properties of whole blood (Figure 32–7). A clear picture is provided of the global effect of imbalances between the proco-agulant and anticoagulant systems and the profibri-nolytic and antifibrinolytic systems and the resultant
clot tensile strength, allowing precise management of hemostatic therapy. The rate of clot formation, the strength of the clot, and the impact of any lysis can be observed. The presence of disseminated intravas-cular coagulation can be evaluated, as can the effect of heparin or heparinoid activity. In addition, plate-let function can be assessed, including the effects of platelet inhibition.
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