Alcoholic Liver Disease

Question 1

Aetiology of ALD?

Answer 1

Alcohol overuse (reccommened is <14 units a week in M and F)

Alcohol dependence

Genetic component?

Question 2

Pathophsyiology of ALD

Answer 2

There is a stepwise process of progression ofALD:

1. Alcohol related fatty liver

Drinking leads to a build-up of fat in the liver. If drinking stops this process reverses in around 2 weeks.

2. Alcoholic hepatits

Drinking alcohol over a long period causes inflammation in the liver sites. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence.

3. Cirrhosis (scarring)

This is where the liver is made up of scar tissue rather than healthy liver tissue. This is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.

fatty -> hepatitis -> scarring

Question 3

Clinical presentation of ALD?

Answer 3

Signs of liver disesease:

• jaundice
• hepatomegaly
• spider naevi (face, neck, legs)
• palmar erythema
• gynaecomastia
• bruising → due to abnormal clotting
• ascites
• caput medusae → engorged superficial epigastric veins
• Asterixis → “flapping tremor” in decompensated liver disease

Question 4

Selected investigation findings?

Answer 4

gamma-GT is characteristically elevated

the ratio of AST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis

Question 5

Blood results in alcoholic liver disease?

Answer 5

FBC – raised MCV (mean corpuscular volume → average size of erythrocytes)

LFTs – elevated ALT and AST (transaminases) and particularly raised gamma-GT. ALP will be elevated later in the disease. Low albumin due to reduced “synthetic function” of the liver. Elevated bilirubin in cirrhosis.

Clotting – elevated prothrombin time due to reduced “synthetic function” of the liver

U+Es may be deranged inhepatorenal syndrome.

Question 6

Ultrasound in alcoholic liver disease?

Answer 6

An ultrasound of the liver may show fatty changes early on described as “increased echogenicity”. It can also demonstrate changes related to cirrhosis if present.

“FibroScan” can be used to check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis.

Question 7

CT and MRI in alcoholic liver disease

Answer 7

CT and MRI can be used to look for fatty infiltration of the liver, hepatocellular carinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites

Question 8

Liver biopsy in alcoholic liver disease

Answer 8

liver biopsy can be used to confirm the diagnosis of alcohol-related hepatitis or cirrhosis. NICE recommend considering a liver biopsy in patient where steroid treatment is being considered

Question 9

Treatment + management of alcoholic liver disease

Answer 9

Stop drinking alcohol permanently

Consider a detoxication regime

Nutritional support with vitamins (particularly thiamine) and a high protein diet

Steroids improve short term outcomes (over 1 month) in severe alcoholic hepatitis but infection and GI bleeding need to be treated first and do not improve outcomes over the long term

Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)

Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral

Question 10

What is a complication of ALD?

Answer 10

Delerium tremens

Question 11

Explain delerium tremens

Answer 11

Symptoms occur at different times after alcohol consumption ceases:

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours:hallucinations
24-48 hours:seizures
24-72 hours: “delirium tremens”

medical emergency associated with alcohol withdrawa lwith a mortality of 35% if left untreated. Alcohol stimulatesGABA receptors in the brain. GABA receptors have a “relaxing” effect on the rest of the brain. Alcohol also inhibits glutamate receptors (also known as NMDA receptors) having a further inhibitory effect on the electrical activity of the brain.

When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excessadrenergic activity. This presents as:

Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias

Question 12

Selected management notes for alcoholic hepatitis:

Answer 12

glucocorticoids(e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis

• Maddrey’s discriminant function (DF)is often used during acute episodes to determine who would benefit from glucocorticoid therapy
• it is calculated by a formula using prothrombin time and bilirubin concentration

pentoxyphylline is also sometimes used
- the STOPAH study (see reference) compared the two common treatments for alcoholic hepatitis,
pentoxyphylline and prednisolone. It showed that prednisolone improved survival at 28 days and that pentoxyphylline did not improve outcomes