In this section : Liver Disease
Metabolic Syndrome Associated Fatty Liver Disease (MAFLD)
Decompensated Liver Disease
Acute Liver Failure
Asymptomatic Raised Transaminases (ALT & AST)
Ascites in Cirrhosis
Alcohol Related Liver Disease
Hepatitis C
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Alcohol Related Liver Disease
Last updated 10th October 2022
Disease Spectrum and Risk
- Disease spectrum ranges from fatty liver through varying degrees of inflammation (hepatitis such as alcoholic hepatitis which is an acute immune reaction to alcohol) to a varying degree of fibrosis including cirrhosis with or without complication.
- The amount of alcohol ingested is the most important risk factor rather than the type of alcohol.
- Any alcohol consumption increases the risk of liver disease with appropriate co-factors.
- Women are more likely than men to develop cirrhosis for a given alcohol intake
- To keep health risks from alcohol to a low level if you drink most weeks:
- According to Government guidelines, people should not drink more than 14 units of alcohol each week, people should have drink free days and not binge.
- Risk factors suggestive of the metabolic syndrome are risk factors for more advanced liver disease obesity, high blood pressure, dyslipidaemia or hyperglycaemia (and increase the cardiovascular risk).
Alcoholic Hepatitis
- Develops in 10-35% heavy drinkers, usually against a background of chronic liver disease including cirrhosis.
- Symptoms – usually acutely unwell with fever, malaise, anorexia, though abdominal pain uncommon.
- Signs – jaundice, spider naevi (as sign of excessive alcohol consumption and liver disease), tender hepatomegaly, may also have decompensation with ascites and / or encephalopathy.
- AST >400 IU/L or ALT >200 IU/L are uncommonly seen with alcoholic hepatitis and would suggest another aetiology. If higher consider viral (HBV) or ischaemic hepatitis or paracetamol. But always check for other aetiologies.
- Bilirubin, serum albumin and INR can all be abnormal. Leucocytosis and thrombocytopenia are both common.
- A significant proportion of those who do not already have cirrhosis will progress to cirrhosis.
Alcoholic Cirrhosis
- Develops in around 10% heavy drinkers.
- Symptoms – In most cases asymptomatic until the patient decompensated. Common late presentations are anorexia, malaise, fatigue, weight loss.
- Signs – stigmata of chronic liver disease, liver not usually palpable but splenomegaly, ascites and encephalopathy are common.
- Typically AST > ALT but both less than 5 x ULN but then patients are usually cirrhotic.
- Bilirubin, serum albumin and INR can all be abnormal as sign of decreased function in cirrhosis.
Management of Alcoholic Liver Disease
- Abstinence is the most important predictor of prognosis – refer to alcohol liaison team in inpatients. Support groups, medication treatment such as naltrexone or acamprosate, Nalmefene or baclofen should be considered.
- Like in all patients admitted for / with liver disease follow the BASL / BSG liver bundle.
- Treatment of alcohol withdrawal – with vitamins (i.v. Pabrinex) and sedatives.
- Nutrition – nutritional supplements, consider NG feeding if malnourished.
- Corticosteroids – for severe acute alcoholic hepatitis with Glasgow Alcoholic Hepatitis Score >9 and early presentation consider treatment with Prednisolone 40 mg/day. Calculate Lille score at day 7 (https://www.mdcalc.com/calc/2024/lille-model-alcoholic-hepatitis). Stop if no improvement.
- Standard treatment for decompensated features – hypoglycaemia, ascites (see ascites in cirrhosis), varices (see acute variceal upper gi bleed), infection (see spontaneous bacterial peritonitis), encephalopathy (see decompensated liver disease), renal failure (see hepatorenal syndrome), coagulopathy.
- Liver transplantation – onsider if discharged and abstinence can be verified for at least 3 months.
Glasgow Alcoholic Hepatitis Score
Score Given | 1 | 2 | 3 |
---|---|---|---|
Age | <50 | ≥50 | |
WCC | <15,000 | ≥15,000 | |
Urea (mmol/L) | ≥5.0 | ||
INR | <1.5 | 1.5 - 2.0 | >2.0 |
Bilirubin | <125 | 125 - 250 | >250 |
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Content by Dr Mathis Heydtmann & Dr Moawad Mahgoub