Abnormal Liver Blood Tests (LFTs) Algorithm

Safety

Red Flags — Exclude Acute Liver Failure & Serious Pathology

Done

Screen immediately for life-threatening causes before any further workup. Scope: this pathway is for adults. Children, adolescents, pregnancy and the post-partum period require separate interpretation and specialist/local pathways — do not apply adult FIB-4, NFS, ELF thresholds or adult referral criteria automatically to children or pregnancy. Pregnancy-related cholestasis, pre-eclampsia/HELLP and acute fatty liver of pregnancy are separate urgent conditions → same-day maternity assessment.

Encephalopathy / Confusion Reduced consciousness, drowsiness, confusion or personality change; asterixis supports encephalopathy but is not required for the diagnosis → 999 (suspected hepatic encephalopathy / acute liver failure)

Jaundice + Fever + RUQ Pain Suggests acute cholangitis → same-day hospital assessment; 999 if hypotension, confusion, severe sepsis, hypoxia or instability

Suspected acute liver failure Acute liver injury in a person without established cirrhosis, with coagulopathy (typically INR ≥1.5) and new hepatic encephalopathy. Hypoglycaemia, metabolic acidosis, renal failure, jaundice or rapid clinical deterioration indicate severe disease → urgent specialist (hepatology/toxicology) discussion and transfer; 999 if deteriorating. An isolated raised INR is not diagnostic: consider warfarin or another anticoagulant, vitamin K deficiency, malabsorption, disseminated intravascular coagulation and chronic liver disease. No single INR value (e.g. >2.0) is a universal emergency threshold — the clinical picture and trajectory matter more

Haematemesis / Melaena Vomiting blood or significant melaena → 999 (variceal or other upper GI bleed)

Shock / severe sepsis Haemodynamic instability or severe sepsis with abnormal liver blood tests → 999

Jaundice at 40 or over Suspected cancer Suspected cancer pathway referral for pancreatic cancer, with or without weight loss (NICE NG12) — not an automatic 999/emergency transfer unless other emergency features are present. 60+ with weight loss plus diarrhoea, back/abdominal pain, nausea, vomiting, constipation or new-onset diabetes → urgent direct-access CT (USS if CT unavailable)

New ascites Particularly with abdominal pain, fever, renal dysfunction, encephalopathy or hypotension → same-day hospital assessment ± diagnostic paracentesis (decompensated cirrhosis, malignancy, cardiac, pancreatitis, infection)

Drug-induced (DILI) Any prescribed, over-the-counter, recreational, bodybuilding or herbal product started or stopped in the preceding 6 months (latency days to months; injury can occur after withdrawal) with jaundice, coagulopathy, symptoms or marked/rising transaminases → stop a suspected non-essential medicine where clinically safe (essential treatment only with advice), same-day review; suspected severe DILI → same-day hospital assessment

Paracetamol overdose Any suspected overdose, staggered or therapeutic-excess ingestion → immediate hospital/toxicology assessment; 999 for severe poisoning, drowsiness or systemic illness (acetylcysteine timing is critical)

Acute liver failure (ALF) carries >50% mortality without transplant. The window for intervention is narrow — encephalopathy signals hepatic decompensation. Charcot's triad has >90% specificity for cholangitis, a surgical emergency. Drug-induced liver injury accounts for ~10% of acute hepatitis; stopping the causative agent is curative if caught early. Paracetamol toxicity is treatable within 24h but fatal if missed.

Diagnose

Characterise the Pattern — Hepatocellular vs Cholestatic vs Isolated

Done

Abnormal liver blood tests (commonly called abnormal LFTs) should be interpreted using previous results, symptoms, medication history, alcohol intake, comorbidity and examination findings. The magnitude of an abnormality does not reliably predict clinical seriousness (BSG 2017). ALT, AST, ALP and GGT are mainly markers of injury or cholestasis; albumin and INR better reflect synthetic function, although both have important non-hepatic causes. First establish whether the predominant abnormality is hepatocellular, cholestatic, mixed, isolated bilirubin, isolated ALP or isolated GGT, interpreted against the laboratory reference range and the clinical context.

Hepatocellular

ALT / AST predominantly elevated (disproportionate to ALP/GGT; no single ULN multiple defines it) → hepatitis, MASLD, alcohol, drugs, autoimmune, Wilson's

Cholestatic

ALP + GGT elevated (disproportionate to ALT) — confirm ALP is hepatobiliary using GGT or an appropriate laboratory method, and interpret with bilirubin and symptoms → biliary obstruction, PBC, PSC, drugs, pregnancy

Mixed

All markers elevated → consider drugs, sepsis, infiltrative disease (sarcoid, lymphoma)

Isolated ALP ↑

If GGT normal → investigate non-hepatic causes: bone disease (Paget's, metastases, puberty), vitamin D deficiency/osteomalacia and pregnancy-related causes where relevant — bone profile, vitamin D ± isoenzymes

Isolated GGT ↑

Review alcohol, obesity/metabolic risk (MASLD), smoking, medication and enzyme-inducing drugs (phenytoin, rifampicin). Often non-specific, but do not simply dismiss it; a persistent unexplained rise needs aetiology assessment or specialist discussion

AST:ALT ratio

Supportive only: >2 can occur in advanced alcohol-related liver disease but is not diagnostic; never use the ratio alone to separate alcohol, MASLD or viral hepatitis

Bilirubin

Unconjugated ↑ with normal ALT, ALP, GGT and haemoglobin → consider Gilbert's (harmless, fasting-related) once haemolysis is excluded (FBC, reticulocytes, LDH, haptoglobin ± blood film); do not diagnose Gilbert's from a single bilirubin result. Conjugated ↑ → investigate hepatic or cholestatic disease. Jaundice with systemic illness, pain or cholestasis → urgent assessment

Albumin / INR

Low albumin and prolonged INR may mean impaired synthetic function — interpret with drugs (warfarin), nutrition, inflammation, renal disease and vitamin K status; platelets, bilirubin and imaging help assess advanced disease

Pattern recognition prevents unnecessary investigation. A mildly raised isolated GGT may be alcohol-, drug- or metabolic-related, but persists unexplained → aetiology assessment, while a cholestatic pattern with ALP 3× ULN needs urgent ultrasound and hepatology input. The AST:ALT (De Ritis) ratio is supportive at best and never diagnostic on its own. Gilbert's syndrome affects ~5% of the population and causes benign unconjugated hyperbilirubinaemia — misdiagnosis leads to unnecessary anxiety and investigation.

Diagnose

Targeted History — Systematic Cause Identification

Done

Use a structured history to cover the five main aetiological categories.

Alcohol

AUDIT-C score. Units/week (1 unit = 10ml pure alcohol). Binge pattern. Duration of heavy use. Lower-risk limit (not a "safe" limit): no more than 14 units/week, spread over 3 or more days with several alcohol-free days. Harmful drinking — men >50 units/week, women >35 units/week for several months → offer fibrosis assessment (NICE NG50). Assess dependence and withdrawal risk

Drugs / Supplements

ALL prescription drugs (statins, methotrexate, amiodarone, antifungals). OTC, herbal (kava, green tea extract), recreational and bodybuilding products. Anything started or stopped in the preceding 6 months? Anticoagulants and antiplatelets

Metabolic risk

BMI, T2DM, dyslipidaemia, HTN, PCOS → MASLD screen. Rapid weight loss → acute fatty change

Viral exposure

IV drug use, tattoos, body piercing, blood transfusion (pre-1992), sexual history, household/sexual contact with hepatitis B, ethnicity/country of birth, travel to endemic regions (HEV); previous blood-borne virus results and immunosuppression

Autoimmune history

Other autoimmune conditions (thyroid, IBD, coeliac), family history of liver disease, female sex → autoimmune hepatitis

Biliary symptoms

RUQ pain, fat intolerance, pale stools, dark urine, pruritus → cholestatic disease

Family history

Wilson's disease (<40yo), haemochromatosis, alpha-1 antitrypsin deficiency, PBC

Systemic features

Weight loss, night sweats, lymphadenopathy → infiltrative/malignant cause

Pregnancy status

Pregnant or post-partum → separate obstetric interpretation and same-day maternity pathway where unwell

Decompensation

Ascites, oedema, confusion (encephalopathy), haematemesis/melaena (variceal bleeding), muscle wasting

Previous results

Previous liver blood tests and trend, previous imaging, platelet trend

History identifies the cause in ~70% of cases, before any blood test. MASLD is now the most common cause of incidental LFT derangement in the UK (prevalence ~25% of population). Drugs account for 10% of cases — suspect DILI when the temporal relationship (latency days to months; injury can follow withdrawal), the biochemical pattern and exclusion of competing causes support it. Wilson's disease is rare but treatable and fatal if missed; screen anyone <40 with unexplained hepatitis.

Diagnose

Targeted Examination — Signs of Chronic Liver Disease

Done

Look for signs of established liver disease, portal hypertension, and metabolic risk factors.

Hands / Nails

Leukonychia (hypoalbuminaemia), clubbing (cirrhosis, IBD), palmar erythema, Dupuytren's (supportive of, not diagnostic of, alcohol-related disease), asterixis (a sign of encephalopathy, not required for the diagnosis)

Eyes / Face

Jaundice (scleral icterus), Kayser-Fleischer rings (Wilson's — need specialist slit-lamp assessment; not sensitive enough to exclude Wilson's), xanthelasma (PBC, dyslipidaemia)

Chest / Abdomen

Spider naevi (no reliable standalone count threshold), gynaecomastia (alcohol/cirrhosis), hepatomegaly, splenomegaly (portal HTN), ascites (shifting dullness, fluid thrill)

Skin

Jaundice, scratch marks (pruritus = cholestasis), bruising (coagulopathy), parotid enlargement (supportive of, not diagnostic of, alcohol-related disease)

BMI / Waist

Obesity (BMI >30), central adiposity assessed with current UK guidance (waist-to-height ratio, ethnicity-specific thresholds) → MASLD risk factors

Blood pressure

Hypertension + obesity + abnormal LFTs = metabolic syndrome → MASLD pathway

Neurological

Tremor, dysarthria, personality change → Wilson's disease, hepatic encephalopathy

Signs of chronic liver disease (spider naevi, leukonychia, splenomegaly) indicate established cirrhosis and change management significantly — these patients need hepatology referral, variceal screening, and HCC surveillance. Kayser-Fleischer rings (golden-brown corneal deposits) support Wilson's disease but need slit-lamp assessment, and their absence does not exclude it. Ascites indicates portal hypertension and often requires diuretics and paracentesis — cannot be managed in primary care alone.

Diagnose

Investigations — Systematic Second-Line Bloods & Imaging

Done

Order investigations based on the pattern identified in Step 2. Avoid a 'scattergun' approach.

All cases 1st line

Standard liver aetiology screen (BSG) whatever the level or duration — liver USS, HBsAg, HCV antibody (reflex HCV RNA or core antigen if positive), ferritin + transferrin saturation, AMA, ANA, SMA, immunoglobulins, caeruloplasmin if under 40 (Wilson's) — plus FBC (low platelets = portal HTN), U&E, eGFR, glucose/HbA1c, lipids, INR, albumin. Repeat alone only for a clear transient cause or after stopping a drug/alcohol. Then assess fibrosis via the locally commissioned pathway (see Metabolic/MASLD)

Hepatocellular pattern

Targeted, not routine for every patient — guided by acuity and severity, age, exposure/travel, autoimmune features, suspected inherited disease, immunosuppression and clinical hepatitis syndrome: anti-HBc; hepatitis A, CMV, EBV if acute hepatitis picture; hepatitis E in acute hepatitis and possible DILI, particularly with compatible exposure or unexplained acute presentation; anti-HBs, HBV DNA if HBV; anti-LKM1 if autoimmune hepatitis still possible; urinary copper (suspected Wilson's), alpha-1-antitrypsin where an inherited cause is suspected

Cholestatic pattern

AMA → PBC (with a cholestatic ALP pattern, after excluding obstruction). PSC is suspected clinically (cholestasis, especially with IBD) and needs MRCP via specialist — ANCA is not diagnostic. No CA 19-9/CEA: urgent USS/CT and HPB route if malignancy suspected. Isolated ALP: repeat with GGT; GGT normal → bone profile, vitamin D ± isoenzymes; persistent >1.5× ULN needs investigation

Metabolic/MASLD

Fasting glucose, HbA1c, lipids, TSH, ferritin, transferrin saturation. Fibrosis: use the locally commissioned pathway. NICE NG49 supports ELF testing — ELF ≥10.51 indicates advanced fibrosis → hepatology referral. Some UK pathways (and the BSG guideline) use FIB-4 (or NFS) as initial triage, followed by ELF or elastography. Do not combine thresholds from different pathways without identifying which pathway is being used. FIB-4 = (age × AST) ÷ (platelets × √ALT): <1.3 generally low risk in adults under 65; ≥1.3 → second-line assessment or local pathway review; higher age-adjusted thresholds are commonly used over 65; less reliable in younger adults and during acute illness. A low FIB-4 reduces the likelihood of advanced fibrosis but does not exclude it

Alcohol related

GGT (sensitive but non-specific), MCV (macrocytosis), CDT (carbohydrate-deficient transferrin) if occupational/forensic relevance

Genetic / rare

Ferritin + transferrin saturation (haemochromatosis — TS >45%), serum caeruloplasmin if under 40 (Wilson's), alpha-1 antitrypsin phenotype

Isolated unconjugated bilirubin

FBC, reticulocyte count, LDH, haptoglobin, blood film if indicated — before labelling Gilbert's

Imaging All

Liver ultrasound: structural causes (gallstones, biliary obstruction, fatty infiltration, masses, cirrhotic texture, splenomegaly)

When NOT to investigate

A clear transient explanation (recent acute illness, stopped drug) — repeat promptly. Placental ALP in pregnancy can be physiological, but a markedly raised or symptomatic cholestatic result is not dismissed. An unexplained isolated GGT still needs the history and risk review

The BSG abnormal liver blood tests guideline (Gut, October 2017) recommends a standard aetiology screen plus targeted tests. Liver ultrasound is the first-line imaging modality (sensitivity 80-90% for hepatic steatosis, >95% for biliary dilation). FibroScan (transient elastography) quantifies liver stiffness non-invasively — thresholds are aetiology-, device- and pathway-specific (inflammation, alcohol, obesity and fasting alter them), so no single kPa cut-off classifies everyone; NICE NG49 uses ELF ≥10.51 for advanced fibrosis. HCV serology is mandated as it is now curable in >95% of cases. Haemochromatosis (transferrin saturation >45%) affects 1:200 Northern Europeans.

Refer

Referral Criteria — When to Escalate to Secondary Care

Done

Most mildly abnormal LFTs resolve in primary care; these criteria require specialist input.

999

Reduced consciousness or suspected hepatic encephalopathy, haematemesis or significant melaena, shock/haemodynamic instability, severe sepsis, suspected acute liver failure with deterioration (acute liver injury without established cirrhosis, INR typically ≥1.5 plus new encephalopathy — not INR alone), severe paracetamol poisoning or suspected toxic ingestion needing immediate toxicology assessment

Same-day

Escalate on the whole picture — bilirubin, INR, albumin, glucose, renal function, symptoms, trend and cause — not an ALT multiple alone: marked or rapidly rising transaminases, new jaundice, coagulopathy, encephalopathy, hypoglycaemia, systemic illness; jaundice + fever + RUQ pain; new ascites (particularly with pain, fever, renal dysfunction, encephalopathy or hypotension); rapidly worsening jaundice or liver blood tests with raised INR, hypoglycaemia, renal dysfunction or systemic illness; suspected severe DILI; acute hepatitis with clinical deterioration

Suspected cancer

Jaundice at 40 or over → pancreatic suspected cancer pathway (NICE NG12); 60+ with weight loss + qualifying symptom → urgent direct-access CT. Liver mass or concerning imaging → urgent route. Jaundice at 40+ alone is a suspected cancer referral, not an automatic 999 transfer.

Urgent 2/52

HBsAg positive → specialist referral for all adults (NICE CG165): send HBeAg/anti-HBe, HBV DNA, anti-HBc IgM, anti-HCV and anti-HDV where appropriate, FBC, liver blood tests, albumin and coagulation; assess fibrosis; consider HIV testing; urgent if decompensated · HCV antibody → HCV RNA; RNA positive → treatment pathway · suspected autoimmune hepatitis · any cirrhosis → hepatology (NG50) · significant/confirmed iron overload · Wilson's suspected (<40y) · persistent unexplained abnormality after appropriate investigation. A positive autoantibody alone is interpreted with pattern, IgG and imaging

Routine

Advanced fibrosis without cirrhosis or decompensation — e.g. MASLD with high-risk FIB-4/NFS, ELF ≥10.51 or high-risk elastography (local thresholds), suspected PBC (cholestatic pattern + AMA), suspected PSC (cholestasis ± IBD, for MRCP), unexplained persistent derangement after a negative screen

Primary care manage

Explained isolated GGT with a reviewed history — alcohol advice, recheck. Low-risk MASLD (low FIB-4/NFS or ELF <10.51, no features of advanced disease). Gilbert's syndrome (harmless, reassure)

The ALT level does not reliably predict severity — chronic disease can have a normal ALT while acute viral or toxic injury can exceed 1000 U/L without liver failure — so bilirubin, INR, glucose and the clinical state decide urgency. Autoimmune hepatitis is treatable (prednisolone + azathioprine) but if missed leads to cirrhosis. Pancreatic cancer has a 5-year survival of <5%, making an early suspected cancer pathway referral critical. MASLD without advanced fibrosis is largely managed in primary care with lifestyle modification.

Treat

Treatment — Cause-Specific Management Pathway

Done

Treatment depends on the underlying cause. Most causes managed in primary care have lifestyle as the cornerstone.

MASLD (formerly NAFLD; most common)

Lifestyle first First-line

Gradual, sustained weight loss — around 7–10% can improve steatosis and inflammation; greater loss more likely to improve fibrosis. Manage diabetes, BP, lipids and CV risk. Drugs only for their diabetes/obesity indications per formulary; pioglitazone or vitamin E for advanced fibrosis only in secondary care (NG49).

Alcoholic Liver Disease

Abstinence + support Core

Abstinence goal with alcohol-service involvement; assess withdrawal risk — no abrupt cessation in dependence without withdrawal planning. After successful withdrawal, NICE CG115 recommends acamprosate or oral naltrexone with a psychological intervention and appropriate medical assessment. In advanced liver disease: avoid disulfiram; avoid naltrexone in acute hepatitis, liver failure and generally in advanced alcohol-related liver disease; acamprosate is not hepatically metabolised but needs renal assessment and is unsuitable in severe renal impairment; baclofen should generally be specialist-led (sedation and encephalopathy risk). Follow the UK clinical guidelines for alcohol treatment, current SPC and local formulary. Thiamine where indicated.

Hepatitis C

DAA therapy Curative

Positive HCV antibody → confirmatory HCV RNA or core-antigen testing and referral to the local hepatitis treatment pathway. Direct-acting antiviral regimen and duration depend on cirrhosis, renal function, previous treatment, drug interactions and local commissioning — specialist-selected; do not initiate in primary care. Before DAA treatment, assess for current or previous HBV infection, because HBV reactivation can occur during or after treatment.

Hepatitis B

Specialist antiviral (e.g. tenofovir / entecavir)

Refer all HBsAg-positive adults (NICE CG165). Treatment choice depends on HBV DNA, ALT, fibrosis/cirrhosis, pregnancy, renal function and comorbidity — a specialist decision, not selected in primary care. Send HBeAg/anti-HBe, HBV DNA, anti-HBc IgM, anti-HCV and anti-HDV where appropriate; consider HIV testing. HCC surveillance per CG165 (see Step 9).

DILI (Drug-Induced)

Stop causative drug Urgent

Stop the suspected drug where safe (essential medicines only with advice); document timing and all supplements; check bilirubin, INR, albumin, glucose, renal function and trend. Urgent referral for jaundice, coagulopathy, encephalopathy or rapid worsening. Steroids only via hepatology if an autoimmune phenotype is suspected.

PBC (cholestatic ALP + AMA)

Ursodeoxycholic acid

AMA alone does not establish PBC — needs a cholestatic pattern after excluding obstruction. UDCA is specialist-directed; second-line agents are specialist-only with safety and commissioning restrictions.

Statin LFTsDo not withhold statins solely because of stable MASLD or transaminases <3× ULN (NG238). Monitoring: baseline transaminases; repeat transaminases (with lipids) within 3 months of starting or changing treatment and at 12 months, then only if clinically indicated. Persistent unexplained transaminases >3× ULN → investigate; usually do not start, or withhold if already taking, pending review — not automatic permanent discontinuation; consider cautious reintroduction once resolved

HaemochromatosisConfirm iron overload, genotype and secondary causes; venesection targets and frequency set by the specialist service. Advise avoiding iron supplements and excess alcohol; manage coexisting liver disease (no routine red-meat restriction)

Gilbert's syndromeNo treatment required. Explain benign nature. Bilirubin rises with fasting, illness, or exercise. Not associated with liver disease. Reassure and discharge.

Next steps: see Fatty liver (MASLD) · Harmful drinking and alcohol dependence · Gilbert's syndrome · Cholecystitis and gallstones · Hepatitis A · HIV

MASLD is common — gradual, sustained weight loss (around 7–10%) can improve steatosis and inflammation, with greater loss more likely to improve fibrosis (NICE NG49). Statins are frequently (and wrongly) stopped due to abnormal LFTs — the BSG/BASL 2017 abnormal liver blood tests guideline confirms statins do not cause clinically significant liver disease and are safe in MASLD, and NICE NG238 (2023) advises not excluding people from statins because transaminases are raised but below 3 times the upper limit of normal. HCV is now curable — every positive HCV Ab should trigger HCV RNA testing and hepatology referral. Venesection in haemochromatosis, if started before cirrhosis, achieves normal life expectancy.

Lifestyle

Non-Pharmacological — The Foundation of Liver Health

Done

Lifestyle modification is the primary treatment for MASLD and alcohol-related disease — more effective than most drug interventions.

Weight loss (MASLD) Target 7-10% body weight reduction. Reduces steatosis, inflammation, and fibrosis. Gradual, sustained loss.

Alcohol reduction Lower-risk limit: no more than 14 units/week, spread over 3 or more days with several alcohol-free days. Complete abstinence if alcohol-related liver disease, and in established cirrhosis whatever the cause (NG50). Smoking cessation.

Exercise 150 min/week moderate aerobic activity. Resistance exercise reduces hepatic fat independently of weight loss. Benefits seen even without weight loss.

Mediterranean diet Reduce refined carbohydrates, saturated fat, processed foods. Increase vegetables, legumes, fish, olive oil.

Stop hepatotoxic drugs Review all OTC supplements (herbal teas, bodybuilding supplements, kava). Check for unnecessary medications. RCGP medication review tool.

Vaccinations HAV and HBV vaccination in patients with chronic liver disease or at risk (PWID, MSM, travel). Influenza annually. Pneumococcal vaccination in chronic liver disease (check current eligibility in the UKHSA Green Book and local schedule).

Coffee May be discussed as an optional dietary habit — not prescribed or presented as treatment.

Analgesia in liver disease Paracetamol is often preferred to NSAIDs for analgesia in cirrhosis, but dose should be individualised according to body weight, nutrition, alcohol use, frailty, renal function, severity of liver disease and total intake from all combination products. In advanced or decompensated liver disease, use a reduced maximum dose in accordance with local or specialist advice. Avoid duplicate paracetamol-containing products. Generally avoid NSAIDs in decompensated cirrhosis with ascites, renal dysfunction or portal hypertension (renal injury, sodium retention, bleeding risk); uncomplicated MASLD alone is not a reason to avoid NSAIDs.

Gradual weight loss, regular aerobic and resistance exercise, a Mediterranean-style diet and smoking cessation improve liver fat and cardiometabolic risk, which is what drives outcomes in MASLD. In established cirrhosis complete alcohol abstinence is advised whatever the original cause (NG50). Vaccination eligibility follows the current UKHSA Green Book.

Safety

Follow-Up & Monitoring — Structured Review Plan

Done

Monitoring intervals depend on severity and cause. Document a clear follow-up plan.

4-6 weeks

Recheck after stopping an implicated drug or alcohol, or after a transient illness — alongside, not instead of, the aetiology screen

3–6 months

MASLD on lifestyle programme — review weight, metabolic risk, alcohol intake and lifestyle progress at approximately 3–6 months. Repeat liver blood tests if clinically useful or if the abnormality persists, worsens or is being used to monitor a suspected reversible cause. Fibrosis assessment if not yet done, via the local pathway

6 months

Alcohol-related — LFTs, FBC, GGT trend. Assess engagement with alcohol services. AUDIT re-score.

MASLD (risk-based)

Low risk: metabolic and CV review; reassess fibrosis about every 2–3 years per local pathway (NICE NG49: adults with ELF <10.51 → reassess every 3 years, no interim fibrosis tests required). Advanced fibrosis or cirrhosis: specialist-led follow-up

HCC surveillance

People with cirrhosis: refer to hepatology and offer 6-monthly ultrasound ± AFP according to aetiology and local specialist protocol (NG50). Chronic HBV: ultrasound and AFP for significant fibrosis or cirrhosis, and selected non-cirrhotic patients by age, family history and HBV DNA (CG165). Not routinely indicated in advanced fibrosis without cirrhosis. Not for end-of-life care or those unfit for HCC treatment. AFP alone is not adequate surveillance.

Safety-net 999

Vomiting blood or black stools, confusion or marked drowsiness, hypoglycaemia, rapid deterioration with jaundice → call 999 immediately

Safety-net same-day

New jaundice, fever with jaundice or RUQ pain, rapidly increasing abdominal distension or new ascites, significant bruising or bleeding, severe vomiting, any new neurological symptoms → same-day GP/ED

Discharge criteria

Discharge only when the cause is assessed, serious liver disease and advanced fibrosis are excluded, the abnormality is resolved or explained, and a monitoring plan is documented. Normal LFTs alone do not exclude chronic liver disease, HBV or HCV

Repeat non-invasive fibrosis testing at the interval set in NICE NG49 (the 2016 version advised ELF every 3 years in adults without advanced fibrosis). HCC surveillance (6-monthly USS ± AFP) reduces HCC mortality by 37% in cirrhotic patients (RCT evidence) — but is not cost-effective in non-cirrhotic patients. GGT has a half-life of ~26 days — normalisation with abstinence is useful to confirm alcohol as cause. LFTs that remain elevated after 6 months of lifestyle modification and alcohol reduction warrant re-investigation and hepatology input — a cause has likely been missed.

🧪 Abnormal Liver Blood Tests (LFTs)

Red Flags — Exclude Acute Liver Failure & Serious Pathology

Characterise the Pattern — Hepatocellular vs Cholestatic vs Isolated

Targeted History — Systematic Cause Identification

Targeted Examination — Signs of Chronic Liver Disease

Investigations — Systematic Second-Line Bloods & Imaging

Referral Criteria — When to Escalate to Secondary Care

Treatment — Cause-Specific Management Pathway

Non-Pharmacological — The Foundation of Liver Health

Follow-Up & Monitoring — Structured Review Plan