Alcohol abuse is widespread in Western Society, and is a common presenting complaint in Emergency Departments, both with and without clinical manifestations.
The recommended weekly intake of alcohol is:
- 14 Units for all individuals (regardless of gender)
Bottle of wine
Glass of wine (large – 250ml)
Bottle of spirits
Pint of beer
Strong pint of beer
Bottle of cheap cider
Susceptibility to alcoholic disease varies widely. 1/3 of serious alcoholics will get cirrhosis. Some may drink 500 units a week for years, and never have any liver problems, but some might drink 100 a week for a year and already start to show serious signs of damage.
- City Workers
- Barmen (drink 7x greater than average)
- Chefs (5x)
- Publicans (10x)
- Architects and accountants drink the least
- Doctors drink just very slightly above the average. Psychiatrists are significantly higher than other specialities.
- Eastern Europe
- Britain (above average, but not as high as those mentioned above)
Consequences due to drunkenness
- Vomiting – this can lead to aspiration, which if light, is likely to cause pneumonia, but if serious could lead to death as the patient is unable to breathe.
- Radial nerve palsy – if you fall asleep with your arm in an unusual position (e.g. over the back of a chair) then your radial nerve can get stuck in the radial groove and compressed. This can lead to nerve damage. The typical sign of this damage is a drooping wrist. Sometimes it is permanent, but in some cases it may only last a couple of weeks.
- Risk taking behaviours – e.g. climbing trees, swimming across rivers etc.
- Vasodilatation – this is not necessarily very dangerous, unless you combine it with being in a cold place for a long time – e.g. sleeping in the park after a drunken night out. In this case it may lead to hypothermia.
- 50% of weekend hospital admissions in some cities (Manchester included) are due to alcohol.
Consequences of Withdrawal
- Alcohol is a GABA agonist; GABA neurones are inhibitory. Therefore, alcohol suppresses brain activity.
- Withdrawal therefore is related to overactivity of the nervous system.
- Hallucinations – these are almost always persecutory; e.g. imagining spiders and snakes crawling all over them.
- Tremens – this is due to overactivity of the peripheral nervous system. The patient will be very sweaty (possibly sweating up to 10L of fluid a day!) and will shake.
- Epilepsy – this is usually unilateral and will often result in a tonic-clonic seizure.
- Cardiac problems – arrhythmias
- Loss of appetite
- The drugs used to treat the withdrawal symptoms are benzodiazepines. The one most commonly used to treat alcohol withdrawal is librium (chlordiazepoxide). Patients will generally be on one of these for several, with a gradually reducing dose. The doses are often very large in comparison to doses of these drugs for other indications. Check you hospital policy for more details.
- Other examples of benzodiazapines include diazepam (aka valium) which is often used to treat anxiety, and lorazepam. These drugs nearly always end in –epam.
- If you consciously decide to stop drinking alcohol and pro-actively seek help to do it then you have a 10% chance of success. If, on the other hand you stop ‘opportunistically’ i.e. you come into hospital for something else, and see that you can get help to stop, then you only have a 5% chance of success.
- Complications of withdrawal are treated in their own right.
- Frequent ‘detoxing’ increases the risk of epilepsy. For this reason, and its lower success rate, opportunistic cessation of drinking is not normally encouraged by practitioners.
Consequences of long-term alcohol abuse
- Fatty liver – this is the first sign. It can either be steatohepatits, or steatohepatosis.
- Alcoholic hepatitis – this leads to fibrosis, then micronodular cirrhosis of the liver.
- Clotting factors no longer produced – the liver normally produces factors 2, 7, 9 & 10. Without these the patients may easily bruise, and bleeding is not easily stopped.
- Reduced albumin production – albumin is the thing that holds all the bloods contents in the blood – it provides osmotic pressure. Without it, products normally contained in the blood easily escape into peripheral tissue, causing peripheral oedema.
- Asterixis – this is a shaking of the hands caused by encephalopathy. Secondary to build up of toxic metabolites in the brain which can no longer be properly metabolised by the liver.
- Jaundice – the liver is essential for removing bilirubin from the body. It conjugates it so it is soluble and can be excreted in the bile. Some of this is metabolised by bacteria in the gut and re-absorbed, and it is then excreted in the urine. Without proper liver function, this will not happen.
- You can probably survive with about ¼ of a normal liver. There is a sudden cut off point at which your liver can no longer survive. This varies slightly from person to person, and there is no way to determine where this cut-off point is. When it occurs though, many of these symptoms will start abruptly.
- Varices – if the liver is damaged, then intra-hepatic pressure increases causing portal hypertension. This then leads to oesophageal and rectal varices, as the blood tries to find another way to bypass the liver back to the systemic circulation. These varices can burst and bleed, and they are a common cause of death. GI bleeding is a common emergency presentation in patients with alcoholic liver damage.
- Acute pancreatitis – acute causes can be listed with the acronym – GET SMASHED! Plugs form in the ducts of the pancreas due to ingestion of too much alcohol. These plugs block the pancreas’ own digestive products from reaching the intestine, and instead they begin to digest the pancreas. This also leads to massive inflammation.
- Gatrointestinal Tract
- Mouth – alcoholics often have poor dental care. They will have bad teeth, and often will have scurvy due to lack of vitamin C. Scurvy causes inflammation and recession of the gums.
- Reflux oesophagitis due to alcohol’s relaxation effect – the lower oesophageal sphincter becomes dilated, as does the stomach
- Mallory-Weiss tear
- Increased risk of ulcers
- Malnourishment; due to:
- Not much food eaten
- Low nutritional quality of food eaten
- Pancreatitis means food might not be properly digested
- Liver damage means food is not metabolised properly
- Increased risk of atherosclerosis
- Increased size of red blood cells, which leads to increased mean cell volume (MCV)
- Folic acid and vitamin B12 deficiency
- Bone marrow damage – this can lead to reduced platelet production, which along with the liver damage can severely hamper clotting ability
- Alcoholic cardiomyopathy – this is the 3rd most common type of myopathy. Another common cause is coronary artery disease. It causes thickening of the heart muscle, which will produced enlarged ECG traces. The most common complication of this is atrial fibrillation, although ventricular fibrillation is not unheard of can be deadly.
- Nervous system
- Korsakoff’s syndrome – this is caused by a lack of thiamine (vitamin B1) in the brain. In this condition, consolidation of new memories is not possible, but usually, old memories are not forgotten. These patients may hold a conversation with you in which they totally make up what they are talking about; e.g. ‘Oh I saw you down in the café getting a snack’ – ‘oh yes – I had a jacket potato too’ – when in actual fact they have been in bed all day! Often alcoholics present just before their deficiencies are low enough for this syndrome to occur, so every alcoholic coming into hospital is put on a thiamine drip within an hour of admission!
- General thiamine deficiency – It causes irreversible cerebellar nerve damage and thus will affect gait and eye movement.
- Peripheral neuropathy – like that seen in diabetes – it affects the extremities of the body – hands, feet and toes.. However, unlike diabetes, it is very painful.
- Endocrine system
- Problems with metabolism of oestrogen to testosterone – this causes feminisation of many patients – they will lose their body hair, their testicles will atrophy etc.
- Diabetes due to liver cirrhosis.
Managing The Alcoholic Patient
- Give IV vitamin B12 + thiamine (pabrinex : vitamin B1) + other B vitamins – Patients are likely to be deficient as a result of diet, due to the fact they are drinking so much – they are unlikely to eat properly for various reasons (Alcohol is appetite suppressant, maybe not able to afford food etc). there is often coexistant macrocytic anaemia. these also protect against Wernicke encephelopathy and the longer term Korskoff’s Syndrome
- Drain the ascites and test the fluid (infection, blood, transudate / exudate)
- Give librium (chlordiazepoxide). Typical dose of 10-50mg/Kg every 6 hours for the first three days. then wean over the following 7-14 days. reduces hallucinations. diazepam is an alternative
- Provide Adequate nutrition – 35Kcal/Kg/day in non-protein energy, PLUS 1.5g/Kg/day of protein. This has been shown to reduce sepsis, mortality and enecephalopathy.
- Consider the use of Steroids – calculate the Maddrey Discriminant Factor. a score of >32 indicates severe disease, and should be treated with 40mg/day for 5 days, with a tapering dose of the subsequent 3 weeks. Mortality correlated with the Maddrey Discriminant Factor Score.
- Severe disease mortality – 50% in the first 30 days
- Mild disease mortality – 5% in the first 30 days
- 1 year mortality regardless of severity – 40%
- Give tramadol and laxatives. Tramadol is an opiod used commonly to relieve neuralgia. You should give the laxatives to avoid constipation. Constipation can be dangerous as it can allow excess production of bacterial toxins, which the liver is unable to remove..
- Give potassium sparing diuretics (e.g. spironolactone). Loop diuretics are more effective at diuresis in normal patients, but are contraindicated in alcoholics:
- Alcoholic patients have a low blood volume due to hypoalbuminaemia. The synthetic function of the liver is damaged, and so alcoholic patients have a low blood albumin level. Their renin-angiotensin system is already activated to a much larger extent than usual due to their low blood volume. This system causes retention of sodium to retain fluid in the body. However in patients with liver failure, the sodium doesn’t stay in the blood, and instead dissipates to the peripheral tissues causing oedema and ascites. So, you must block this system, to allow proper fluid excretion..
- Patients should be weighed every day to see if they are losing fluid. Ideally they should lose 0.5-1kg a day (i.e. 0.5-1L of fluid) for the first few days, until the noticeable oedema is gone. After this, they should lose no more than 0.5L per day. To ensure this is achieved, you have to restrict the patient’s fluid intake. Losing more weight per day than this can cause dangerous fluid shifts.
- Huge doses are often required! (e.g. 200-300mg spironolactone)
- Many patients will also be on furosemide
- Managing Encephelopathy
- Patients will often present and re-present with encephelopathy. For many, this is an acute exacerbation, caused by either constipation or infection. Therefore it is very important that patients with alcoholic liver disease receive regular laxatives to avoid encephelopathy. Patients should open their bowels at least 3x/day when on regular laxatives.