Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Alcohol-related liver disease and alcoholic hepatitis
Gastroenterology and hepatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
!
Time-critical presentation
Confusion, gastrointestinal bleeding, sepsis, hypotension, acute kidney injury, severe jaundice, hypoglycaemia or dangerous alcohol withdrawal requires hospital assessment. Use the current BSG–BASL decompensated-cirrhosis bundle and local withdrawal pathway, with early hepatology, critical-care and alcohol-care-team involvement.
Overview
Detect alcohol-related liver disease without stigma, manage withdrawal and decompensation safely, and recognise severe acute alcohol-related hepatitis requiring specialist treatment.
Alcohol causes oxidative injury, steatosis, inflammation and progressive fibrosis, but susceptibility varies with dose pattern, sex, obesity, diabetes, genetics, nutrition and coexisting viral or metabolic disease. Patients may have substantial portal hypertension before symptoms appear.
Acute alcohol-related hepatitis usually presents with relatively recent jaundice, malaise, anorexia, tender hepatomegaly and inflammatory features in a person with sustained harmful exposure. It can coexist with cirrhosis and carries high short-term mortality when severe.
The central decisions are whether the patient is withdrawing, whether the liver is decompensated or acutely inflamed, and whether specialist treatment or transplant assessment is appropriate. Language should describe alcohol exposure and disease, not define the person.
Key points
Alcohol-related liver disease spans steatosis, steatohepatitis, fibrosis and cirrhosis; normal aminotransferases
Practice
Two practice questions
Your practice draft is saved in this browser.
Question 1 of 2
0 correct
Gastroenterology and hepatologyOriginal SBA
Jaundice with suspected alcohol-related hepatitis
A patient with sustained harmful alcohol use develops jaundice, fever and tender hepatomegaly. INR and bilirubin are raised, and ascites is present. What is the most appropriate first principle before considering corticosteroid?
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Ask about alcohol neutrally using beverage type, volume, strength, frequency, alcohol-free days and recent change, then convert to UK units and screen for dependence.
A dependent patient can develop seizures or delirium tremens if alcohol stops abruptly; plan monitored withdrawal rather than simply advising immediate unsupported cessation.
Acute alcohol-related hepatitis is a clinical syndrome of recent jaundice and systemic inflammation after sustained harmful drinking, not merely an AST higher than ALT.
Exclude infection, biliary obstruction, viral hepatitis, drug injury, gastrointestinal bleeding and acute-on-chronic decompensation before attributing jaundice to alcohol-related hepatitis.
Obtain a diagnostic ascitic tap promptly in anyone admitted with cirrhosis and ascites, including those without abdominal pain or fever.
Nutrition and thiamine are active treatments: assess refeeding risk, provide dietitian-led energy and protein support, and use parenteral thiamine when Wernicke risk or features demand it.
Corticosteroids are considered only for specialist-confirmed severe acute alcohol-related hepatitis after contraindications are addressed and benefit is reviewed early with a validated response score.
Long-term outcome depends on integrated treatment of both liver disease and alcohol dependence, with relapse-prevention, mental-health, social and transplant pathways offered equitably.
Aetiology
01
Sustained alcohol exposure
Cumulative alcohol intake and repeated heavy exposure drive risk, but individual susceptibility varies and history should be obtained neutrally in UK units.
02
Metabolic and host susceptibility
Obesity, diabetes, sex, genetic variation and coexisting steatotic or viral liver disease modify progression at similar reported alcohol exposure.
03
Nutrition and smoking
Malnutrition, micronutrient deficiency and smoking commonly coexist, worsening frailty and broader health risk even though they do not alone establish alcohol-related causation.
Pathophysiology
1
Steatosis and oxidative stress
Alcohol metabolism alters hepatic redox balance, promotes triglyceride accumulation and generates toxic metabolites and oxidative cellular injury.
2
Inflammation and hepatocyte death
Gut-derived inflammatory signals, acetaldehyde and immune activation cause steatohepatitis, ballooning injury and, in severe episodes, acute jaundice and systemic inflammation.
3
Fibrosis and portal hypertension
Repeated injury activates stellate cells and collagen deposition, distorting architecture into cirrhosis with portal hypertension and reduced synthetic reserve.
Clinical features and red flags
Compensated alcohol-related fibrosis
There may be no symptoms despite thrombocytopenia, splenomegaly, firm liver, raised GGT or abnormal non-invasive fibrosis tests. Normal ALT or a normal ultrasound does not reliably exclude advanced disease.
Acute alcohol-related hepatitisRed flag
New jaundice over days to weeks with anorexia, fever, tender hepatomegaly, leukocytosis and AST typically exceeding ALT after sustained drinking supports the syndrome once infection and obstruction are excluded.
Decompensated cirrhosisRed flag
Ascites, oedema, encephalopathy, variceal bleeding, spontaneous bacterial peritonitis, jaundice or hepatorenal dysfunction marks a major prognostic transition and requires structured acute care.
Alcohol withdrawalRed flag
Tremor, sweats, anxiety, nausea, tachycardia, hypertension and insomnia can progress to hallucinations, seizures or delirium tremens, especially with previous complicated withdrawal or high dependence.
Wernicke encephalopathyRed flag
Confusion, ataxia or eye-movement abnormality may be incomplete and subtle; malnutrition, vomiting or withdrawal increases risk. Treat suspected disease promptly with parenteral thiamine rather than awaiting imaging.
Infection during severe liver diseaseRed flag
Spontaneous bacterial peritonitis, pneumonia, urinary infection and bacteraemia may present without fever or leukocytosis. New kidney injury, encephalopathy or hypotension may be the only clue.
Investigations
01Structured alcohol history and AUDIT assessmentFirst step
Why
Quantify exposure, dependence, harms and withdrawal risk without judgement.
Interpretation and limitations
Document units, pattern, last drink, morning drinking, loss of control, previous seizures or delirium, and periods of abstinence. Biomarkers can support but never replace the history.
02Full blood count, liver panel, INR and renal profile
Why
Assess inflammation, portal hypertension, synthesis, electrolytes and organ dysfunction.
Interpretation and limitations
Macrocytosis, thrombocytopenia, bilirubin rise and prolonged INR support severity but are nonspecific. Creatinine and sodium strongly influence prognosis and require serial review.
03Blood cultures, chest imaging, urine and ascitic studies
Why
Find infection before immunosuppression and in any decompensation.
Interpretation and limitations
Perform diagnostic paracentesis promptly when ascites is present and obtain cell count with differential plus culture using the local method. Treat suspected sepsis before all results return.
04Ultrasound liver with portal Doppler
Why
Assess morphology, portal hypertension, ascites, focal lesions and biliary obstruction.
Interpretation and limitations
Nodularity, splenomegaly or collateral vessels support advanced disease, while duct dilatation suggests another cause of jaundice. Imaging cannot prove
Differential diagnosis
01
Metabolic steatotic liver disease
Cardiometabolic risk and steatosis may indicate MASLD, but metabolic and alcohol-related injury often coexist rather than forming mutually exclusive diagnoses.
02
Viral or autoimmune hepatitis
Compatible serology, immunoglobulins, autoantibodies and exposure history identify treatable alternatives; an AST-predominant pattern alone is not diagnostic of alcohol-related hepatitis.
03
Drug-induced liver injury
A close medicine or supplement timeline, compatible latency and improvement after withdrawal favour DILI after viral, obstructive and immune causes are assessed.
Additional chapter-specific clues
Alternative acute insultRed flag
Very high aminotransferases, severe abdominal pain, shock, paracetamol exposure or biliary dilatation is atypical for alcohol-related hepatitis alone and should redirect the diagnostic work-up.
Management
01AdmissionFirst day of decompensated diseaseFirst stepAscites, encephalopathy, gastrointestinal bleeding, jaundice with organ dysfunction or suspected infection.+
1Use ABCDE and the current BSG–BASL admission bundle: obtain bloods and cultures, review medicines, assess bleeding and encephalopathy, monitor urine and identify the precipitant.
2Perform diagnostic ascitic tap without avoidable delay when ascites is present, start indicated infection or bleeding treatment and involve hepatology early.
3Assess alcohol withdrawal and Wernicke risk on arrival; prescribe the local symptom-triggered withdrawal and thiamine regimen with higher-observation care for previous seizures or severe dependence.
4EscalationAddress nutrition, refeeding electrolytes, thrombosis and gastrointestinal prophylaxis individually, and review transplant suitability or ceilings of care rather than assuming alcohol exposure excludes escalation.
Complications
01
Decompensated cirrhosis
Progressive fibrosis can lead to ascites, variceal bleeding, encephalopathy, infection and hepatorenal dysfunction even when aminotransferases are modest.
02
Severe alcohol-related hepatitis
An acute inflammatory episode may cause rapidly worsening jaundice, coagulopathy, infection susceptibility, kidney injury and a high short-term mortality risk.
03
Withdrawal and malignancy risk
Abrupt unsupported cessation in dependence can provoke seizures or delirium, while established cirrhosis increases hepatocellular carcinoma risk and requires surveillance assessment.
Monitoring and follow-up
During acute admission, trend early-warning score, cognition, withdrawal score, glucose, fluid balance, urine output, renal function, electrolytes, INR and bilirubin with the care bundle.
Repeat infection screening when physiology, encephalopathy or kidney function worsens, even after initially negative cultures, because severe alcohol-related hepatitis is infection prone.
If corticosteroid is used, monitor infection, gastrointestinal bleeding, glucose and the defined early response score; document the continue-or-stop decision.
During nutritional rehabilitation, monitor phosphate, magnesium, potassium, glucose and fluid status for refeeding syndrome and adjust with dietetic support.
Long term, monitor alcohol outcomes, mental health, social stability, fibrosis or cirrhosis complications, nutrition, sarcopenia and engagement using coordinated liver and alcohol services.
Special situations
Normal enzymes do not reassure
Advanced cirrhosis may have modest or normal aminotransferases because little active inflammation remains. Platelets, synthetic function, examination and fibrosis assessment are more informative.
Withdrawal and encephalopathy overlap
Agitation and confusion may be attributed incorrectly to withdrawal, while benzodiazepines worsen hepatic encephalopathy. Timing, autonomic signs, asterixis, precipitants and serial review separate them.
Tap ascites early
Spontaneous bacterial peritonitis can be painless and afebrile. New encephalopathy or kidney injury may be its only presentation, so diagnostic paracentesis should not wait.
Nutrition is not protein restriction
Routine protein restriction worsens sarcopenia and is not standard encephalopathy care. Dietitians should deliver adequate protein and energy while managing refeeding risk.
Steroids require an exit
Prednisolone is not a default for every jaundiced drinker. Diagnosis, severity, infection status and an early response score determine whether exposure remains justified.
Stigma causes clinical error
Assuming non-adherence, denying analgesia or delaying transplant referral because alcohol contributed to disease undermines accurate history, safety and equitable specialist care.
Common pitfalls
01
Advising a dependent patient to stop abruptly without assessing withdrawal risk.
02
Diagnosing acute alcohol-related hepatitis solely from an AST-to-ALT ratio.
03
Starting corticosteroid before excluding infection and gastrointestinal bleeding.
04
Missing spontaneous bacterial peritonitis because ascites is not painful.
05
Restricting protein routinely in encephalopathy and worsening sarcopenia.
06
Withholding transplant referral based on an informal fixed abstinence rule.
acute alcohol-related hepatitis
.
05Viral, autoimmune and metabolic liver screen
Why
Identify coexisting or alternative liver disease.
Interpretation and limitations
Use the BSG aetiology screen and adapt to age and context; iron indices can be distorted by inflammation and alcohol, so specialist confirmation may be needed.
06Validated alcohol-hepatitis severity score
Why
Estimate short-term risk and determine whether specialist corticosteroid assessment is warranted.
Interpretation and limitations
Use the currently adopted local score, often discriminant function or MELD, after accurate baseline values. A threshold is a decision aid, not a diagnosis or automatic prescription.
07Early treatment-response score
Why
Identify non-response after corticosteroid initiation.
Interpretation and limitations
Calculate the current validated Lille or locally mandated response measure at the specified day. Stop ineffective corticosteroid treatment through specialist review rather than completing a fixed course regardless.
08Transient elastography or other fibrosis test
Why
Risk-stratify stable patients after acute inflammation and abstinence planning.
Interpretation and limitations
Recent heavy drinking and acute hepatitis can transiently increase stiffness. Repeat under the commissioned pathway when inflammatory confounding has settled rather than over-staging from one acute value.
02HepatitisSevere acute alcohol-related hepatitisRecent jaundice and inflammatory liver dysfunction after sustained harmful alcohol use.+
1Confirm the clinical syndrome and timing, exclude sepsis, obstruction, viral or drug injury and uncontrolled gastrointestinal bleeding, and calculate a locally approved severity score with hepatology.
2Provide alcohol-withdrawal prevention, parenteral thiamine when indicated, dietitian-led high-energy and adequate-protein support, fluid and electrolyte care, and prompt treatment of infection or kidney injury.
3If severe and suitable, discuss prednisolone under NICE and specialist protocol after contraindication review; do not start corticosteroid because the AST-to-ALT ratio alone appears typical.
4Reassess early using the approved response score and adverse-event review, stopping ineffective treatment and considering transplant-centre or palliative-care discussion according to trajectory and patient wishes.
03WithdrawalPrevent complicated alcohol withdrawalDependence, previous withdrawal complication or symptoms after reduction in intake.+
1Estimate timing and severity, check glucose, magnesium and other electrolytes, identify head injury, sepsis or hepatic encephalopathy that could masquerade as withdrawal, and choose an appropriate monitored setting.
2EscalationUse the local symptom-triggered benzodiazepine protocol with a liver-appropriate agent and trained observations, escalating seizures, hallucinations or delirium to senior and critical-care teams.
3Give prophylactic or treatment-dose thiamine according to Wernicke risk; suspected Wernicke encephalopathy requires parenteral therapy, and emergency glucose must never be withheld from hypoglycaemia.
4Before discharge, link the patient directly with an alcohol care team for relapse-prevention medication, psychological treatment, safeguarding and community follow-up rather than giving advice alone.
04RecoveryLong-term integrated liver and alcohol careStabilisation after admission or identification of compensated alcohol-related liver disease.+
1Agree a supported abstinence or harm-reduction plan matched to dependence and readiness, with relapse framed as a signal to intensify care rather than a reason for discharge.
2Stage fibrosis after acute confounders settle and enrol cirrhosis into variceal, hepatocellular carcinoma, vaccination, nutrition and osteoporosis pathways under current guidance.
3Consider acamprosate or another relapse-prevention medicine through addiction and liver specialists, accounting for renal function, hepatic impairment, opioids and patient goals.
4Refer appropriate advanced disease for transplant assessment using UK criteria and a multidisciplinary addiction evaluation; fixed unsupported abstinence rules should not replace an individualised referral.
Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
Prevents or treats thiamine-deficiency neurological injury during withdrawal, malnutrition and refeeding.
Parenteral thiamine
Use the local prophylaxis or treatment regimen matched to Wernicke risk.
Suspected Wernicke encephalopathy needs prompt high-potency parenteral treatment in a monitored setting. Rare anaphylaxis can occur; emergency glucose for hypoglycaemia must not be delayed.
Prevents seizures and delirium while controlling autonomic alcohol-withdrawal symptoms.
Symptom-triggered benzodiazepine
Titrate through the authorised withdrawal scale and local liver-impairment protocol.
Hepatic encephalopathy, sepsis and head injury can mimic withdrawal. Oversedation and respiratory depression are dangerous; severe liver dysfunction affects agent choice and requires experienced review.
May improve short-term survival in selected severe acute alcohol-related hepatitis.
Prednisolone for selected severe hepatitis
Use only the specialist protocol after severity scoring and contraindication assessment.
Exclude or control infection and assess gastrointestinal bleeding, renal dysfunction and diagnostic uncertainty. Review early response with the mandated score and stop when benefit is unlikely.
Supports maintenance of abstinence alongside psychosocial treatment in suitable patients.
Acamprosate
Initiate and adjust through the alcohol-dependence pathway after withdrawal is complete.
Renal function governs suitability and dose; adherence requires multiple daily dosing. It does not treat withdrawal, and medicine choice in advanced liver disease should be coordinated with addiction specialists.