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.
- Acute jaundice with confusion, hypoglycaemia, coagulopathy, severe systemic illness or rapidly worsening tests requires same-day specialist escalation and an acute liver failure pathway.
- Raised ALP with raised GGT supports hepatobiliary origin; a normal GGT makes bone, placental or other non-hepatic ALP sources more likely but does not replace clinical assessment.
- Do not simply repeat unexplained abnormalities indefinitely. Complete an adult liver aetiology screen and ultrasound, then risk-stratify fibrosis where metabolic or alcohol-related disease is plausible.
- Take a precise history of prescribed, over-the-counter, herbal, recreational and performance-enhancing substances, including start dates, dose changes and dechallenge.
- Normal aminotransferases do not exclude advanced cirrhosis, and low albumin may reflect inflammation, renal loss or malnutrition rather than hepatic failure.
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.
New hepatic injury with coagulopathy and any encephalopathy in a person without known cirrhosis is a time-critical syndrome. Check glucose, paracetamol exposure and acid-base state and contact a transplant-linked liver service urgently.
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.
- Discuss early with gastroenterology or hepatology; any suspected acute liver failure requires urgent contact with a transplant-linked liver unit, not routine referral.
- Trend INR, glucose, lactate, renal function, bilirubin and mental state because aminotransferase movement alone is insufficient.
Stable unexplained abnormal liver tests without emergency features.
- Confirm the dominant biochemical pattern and review alcohol, metabolic risks, medicines, supplements, viral exposure, family history and previous results.
- Complete the standard adult liver aetiology screen and ultrasound rather than repeating the same panel in isolation.
- Apply phenotype-led second-line tests and fibrosis risk stratification; refer cholestatic, autoimmune, viral, iron-overload, focal-lesion or advanced-fibrosis signals appropriately.