Synopsis
Interpret abnormal liver blood tests by biochemical pattern, severity, synthetic function and clinical context; identify acute liver failure or obstruction promptly; and complete a proportionate aetiology and fibrosis assessment rather than repeatedly sampling without a plan.
- Liver enzymes describe injury or cholestasis, not liver function: bilirubin, albumin, INR and the clinical state provide different information about excretion and synthetic reserve.
- Classify the dominant pattern as hepatocellular, cholestatic, isolated bilirubin or mixed, then compare with the patient's baseline and the timing of symptoms, medicines and exposures.
- The size of an abnormality does not reliably predict significance: mild persistent tests can mark advanced fibrosis, while very high aminotransferases narrow the acute differential.
Key red flags
ALP and GGT predominate, often with conjugated bilirubin, pruritus, pale stool or dark urine. Pain, fever and jaundice suggest infected obstruction and need urgent biliary assessment.
Investigation priorities
Confirm the pattern with bilirubin, ALT, ALP, GGT, albumin, FBC and INR when synthetic dysfunction or acute illness is possible; add AST, creatine kinase or fractionated bilirubin selectively.
Use an age-aware first-line score such as FIB-4 followed by transient elastography or ELF according to the local metabolic or alcohol-related liver pathway.
Management branches
New jaundice, very abnormal enzymes, coagulopathy, hypoglycaemia, confusion or systemic instability.
- Use ABCDE, bedside glucose, sepsis assessment and a complete medication and overdose history; send urgent liver, renal, coagulation, gas, lactate and paracetamol tests.
- Stop plausible hepatotoxins where safe, start time-critical antidotal or sepsis treatment under the relevant protocol, and image promptly for obstruction or vascular disease.
Stable unexplained abnormal liver tests without emergency features.