A careful sequence of investigations is mandatory in patients with jaundice ( Fig 1). Interpretation of patterns of liver blood test abnormality is problematic as such tests carry low sensitivity and specificity. Nevertheless, they are of use in certain specific diagnoses.
Fig. 1 Investigations of jaundice in the critically ill patient: TPN, total parenteral nutrition.
A diagnostic strategy to exclude hemolysis is considered elsewhere but, in any patient with jaundice, the conjugated and unconjugated bilirubin fraction should be identified, in addition to a reticulocyte count and haptoglobin level. The latter is less discriminatory during critical illness because changes in haptoglobin synthesis may occur in this situation. Furthermore, the finding of an unconjugated hyperbilirubinemia does not confirm hemolysis as it may be a reflection of Gilbert's syndrome, a hereditary disorder due to abnormal gene expression of bilirubin-conjugating enzymes in which bilirubin levels may rise up to 70 pmol/l during stressed states.
On confirmation of a conjugated hyperbilirubinemia, the most important discriminatory test is an ultrasound scan of the liver, bile ducts, pancreas, and spleen, and Doppler interrogation of the hepatic vasculature. In experienced hands considerable additional information can be obtained from assessing liver texture.
Dilated bile ducts involving intra- or extrahepatic ducts require further delineation with abdominal CT scanning or endoscopic retrograde cholangiopancreatography (ERCP). In the presence of non-dilated ducts, evidence of portal hypertension suggests underlying chronic liver disease or Budd-Chiari syndrome, whereas heterogeneity of liver texture with abdominal or other lymphadenopathy and splenomegaly raises the possibility of disseminated malignancy or lymphoma ( Fig 1).
Occasionally, dramatic elevations of alkaline phosphatase and g-glutamyl transpeptidase herald underlying malignant infiltrations or hepatosplenic candidiasis.
Ischemic hepatitis, resulting from a profound fall in hepatic oxygen delivery, is associated with a rapid rise in transaminases, returning towards normal within 2 to 3 days, and a prothrombin time that may not be significantly prolonged. Both viral hepatitis and drug hepatotoxicity may mimic this pattern, but a rapidly rising prothrombin time (INR) with evidence of hepatocellular damage always points towards acute liver failure.
Biochemical cholestasis can have a number of causes, including bacterial cholangitis, acute pancreatitis, drug hepatotoxicity, and parenteral nutrition, and it is also a common pattern with hepatic infiltrations and hepatosplenic candidiasis in the immunosuppressed. Similarly, in patients with multiple systems organ failure, the liver dysfunction is often just a conjugated hyperbilirubinemia with transaminases or alkaline phosphatase twice the upper limit of normal.
Supplementary radiology will depend on the clinical context, but ERCP may be necessary to confirm (and treat) cholelithiasis and nuclear medicine white cell scans may be important in identifying intra-abdominal or other septic foci. Intra-abdominal fluid collections, subphrenic abscesses, and pancreatic pathology can be detected by ultrasonography, but CT scanning is often a better radiological modality for the latter.
Occasionally, liver histology is important, as in the diagnosis of some causes of acute liver failure and of opportunistic infections in immunocompromised patients. In those with a significant coagulopathy this will need to be done by the transjugular route. In contrast, liver histology is usually not diagnostic in those cases with jaundice associated with sepsis, multiple systems organ failure, and cholestatic drug hepatotoxicity.
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