The use of alcohol comes with several problems. Alcohol causes damage to various tissues in the body and can also lead to alcohol dependence syndrome. Here we will cover alcoholic liver disease and alcohol dependence and touch on some of the other harmful effects of alcohol consumption.
Alcoholic liver disease results from the effects of the long term excessive consumption of alcohol on the liver. The onset and progression of alcoholic liver disease varies between people, suggesting that there may be a genetic predisposition to having harmful effects of alcohol on the liver.
There is a stepwise process of progression of alcoholic liver disease:
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 hepatitis
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.
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.
Recommended Alcohol Consumption
That latest recommendations (Department of Health, 2016) are to not regularly drink more than 14 units per week for both men and women. If drinking 14 units in a week, this should be spread evenly over 3 or more days and not more than 5 units in a day.
The government guidelines also state that any level of alcohol consumption increases the risk of cancers, particularly breast, mouth and throat.
Pregnant women should avoid alcohol completely.
The CAGE question can be used to quickly screen for harmful alcohol use:
- C – CUT DOWN? Ever thought you should?
- A – ANNOYED? Do you get annoyed at others commenting on your drinking?
- G – GUILTY? Ever feel guilty about drinking?
- E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?
The Alcohol Use Disorders Identification Test (AUDIT) was developed by the World Health Organisation to screen people for harmful alcohol use. It involves 10 questions with multiple choice answers and gives a score. A score of 8 or more gives an indication of harmful use.
Complications of Alcohol
- Alcoholic Liver Disease
- Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
- Alcohol Dependence and Withdrawal
- Wernicke-Korsakoff Syndrome (WKS)
- Alcoholic Cardiomyopathy
Signs of Liver Disease
- Spider Naevi
- Palmar Erythema
- Bruising – due to abnormal clotting
- Caput Medusae – engorged superficial epigastric veins
- Asterixis – “flapping tremor” in decompensated liver disease
- FBC – raised MCV
- 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 in hepatorenal syndrome.
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.
Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected.
CT and MRI scans
CT and MRI can be used to look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.
Liver biopsy can be used to confirm the diagnosis of alcohol-related hepatitis or cirrhosis. NICE recommend considering a liver biopsy in patients where steroid treatment is being considered.
- 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
When someone is alcohol dependent there is a risk of them developing withdrawal symptoms when they stop drinking. These can range from mild and uncomfortable to delirium tremens, which is life-threatening. 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”
Delirium tremens is a medical emergency associated with alcohol withdrawal with a mortality of 35% if left untreated. Alcohol stimulates GABA 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.
Chronic alcohol use results in the GABA system becoming down-regulated and the glutamate system becoming up-regulated to balance the effects of alcohol. When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excess adrenergic activity. This presents as:
- Acute confusion
- Severe agitation
- Delusions and hallucinations
- Ataxia (difficulties with coordinated movements)
Managing Alcohol Withdrawal
The CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised) tool can be used to score the patient on their withdrawal symptoms and guide treatment.
Chlordiazepoxide (“Librium”) is a benzodiazepine used to combat the effects of alcohol withdrawal. Diazepam is a less commonly used alternative. It is given orally as a reducing regime titrated to the required dose based on the local alcohol withdrawal protocol (e.g. 10 – 40 mg every 1 – 4 hours). This is continued for 5-7 days.
Intravenous high-dose B vitamins (pabrinex). This should be followed by regular lower dose oral thiamine.
Wernicke-Korsakoff Syndrome (WKS)
Alcohol excess leads to thiamine (vitamin B1) deficiency. Thiamine is poorly absorbed in the presence of alcohol and alcoholics tend to have poor diets and rely on the alcohol for their calories. Wernicke’s encephalopathy comes before Korsakoffs syndrome. These result from thiamine deficiency.
Features of Wernicke’s encephalopathy
- Oculomotor disturbances (disturbances of eye movements)
- Ataxia (difficulties with coordinated movements)
Features of Korsakoffs syndrome
- Memory impairment (retrograde and anterograde)
- Behavioural changes
Wernicke’s encephalopathy is a medical emergency and has a high mortality rate if untreated. Korsakoffs syndrome is often irreversible and results in patients requiring full time institutional care. Prevention and treatment involve thiamine supplementation and abstaining from alcohol.
Last updated January 2019