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Guided learning

Nursing assessment of alcohol-related brain damage in young people

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An outline of nursing assessment and management of Wernicke’s encephalopathy and Korsakoff’s syndrome

 

Authors

Joe Brown, MSc, BSc, RMN, RNT,RGN, is lecturer, University of the West of Scotland; Robert McColm, BA, RMN, is psychological nurse therapist, psychology department, Nithbank Hospital, Dumfries; Jackie Aindow, BSc, RGN, is alcohol liaison nurse, Cameron House Drug and Alcohol Unit, Dumfries; Judith Anderson, MSc, BSc, is senior librarian, University of the West of Scotland.

Abstract

Brown, J. et al (2009) Nursing assessment of alcohol-related brain damage in young people. Nursing Times; 105: 41, early online publication.

The long-term consequences of chronic alcohol misuse are increasingly affecting young people. This one-part unit outlines the main signs and symptoms of Wernicke’s encephalopathy and Korsakoff’s syndrome. It details nursing assessment and management of these conditions, as well as regimens for safe detoxification.

Keywords: Alcohol withdrawal, Wernicke’s encephalopathy, Korsakoff’s syndrome

  • This article has been double-blind peer reviewed

 

Learning objectives

1. Know the main signs and symptoms of Wernicke’s encephalopathy and Korsakoff’s syndrome.

2. Understand the main elements of nursing assessment and management of these conditions.

 

Introduction

Acute effects of alcohol on young people include violence, aggression, accidents, unprotected sexual experiences, alcohol poisoning and suicide. The features of alcohol are set out in Box 1.

The increase in alcohol consumption, fuelled by young people’s substantial disposable income, reduction in cost, cultural acceptance and being easily accessible, is associated with a rise in heavy and chronic alcohol misuse at a young age.

As the consequences of chronic misuse affect younger people, nurses need to be aware of the problems associated with it, specifically alcohol-related brain damage such as Wernicke’s encephalopathy and Korsakoff’s syndrome. Once the domain of chronic, middle-aged male drinkers, these are now both real issues for younger people who use alcohol (Scottish Government, 2009).

The introduction of alcopops, specifically targeted at young people, has made alcohol more palatable to this age group. In addition, alcohol is heavily marketed at sporting events through advertisement and sponsorship.

It is widely acknowledged that the past decade has seen increased use and misuse of alcohol among young people aged 13-25. The average age of children first using alcohol is 11, despite the fact that they are legally unable to buy it until they are 18 (with the exception of 16 and 17-year-olds in Scotland, who can buy beer, wine or cider to consume with a meal). They are also generally prohibited from consuming alcohol in public until they are 18, although 16 and 17-year olds in Britain can drink beer, wine or cider with a meal if it is bought by an adult and they are accompanied by an adult.

All these factors may lead to young people being heavy and chronic users of alcohol in their teens or twenties. As a result, they are susceptible to all the possible short- and long-term effects (Drink Aware, 2009).

Box 1. Features of alcohol

  • Psychoactive substance which affects coordination, judgement, cognitive ability and reduces inhibitions, also affecting spatial awareness and orientation.
  • Central nervous system depressant.
  • Acts on gamma-aminobutyric acid (GABA) in the brain, enhancing the effect of this neurotransmitter.
  • Toxic in large amounts leading to death with a blood alcohol content of 800mg/mmol.
  • Affects women more than men because they are smaller, have a higher proportion of adipose tissue and lower levels of alcohol dehydrogenase, the enzyme that breaks down alcohol in the liver.
  • Women may show signs of excessive alcohol use around 10 years earlier than men.
  • Crosses the placenta and can affect the foetus causing foetal alcohol syndrome, which can cause permanent learning difficulties and physical abnormalities in children.
  • Easily available.
  • Cheap to buy.
  • Socially acceptable, culturally encouraged and legal.

 

Wernicke’s encephalopathy

Wernicke’s encephalopathy, named after German neurologist Karl Wernicke (1848-1905), has signs and symptoms strikingly similar to those of alcohol inebriation. It is caused by inadequate intake of thiamine (vitamin B1) (Box 2) or as a result of its malabsorption over a prolonged period. However, the actual length of time the brain needs to be deficient in thiamine before signs and symptoms develop is uncertain and wholly individual (Thomson et al, 2002).

Wernicke’s encephalopathy is as likely to develop in young people as it is in older adults (Alcohol Concern, 2007; Alzheimer Scotland, 2004). It usually has a fast onset of 1-4 days and even in younger people can be fatal if left untreated. It is characterised by the following symptoms:

  • Unsteady gait;
  • Incoherent speech;
  • Confusion (sometimes leading to hallucinations, disorientation and aggressive behaviours);
  • Ophthalmoplegia (Salen, 2009; Thomson et al, 2002).

Its symptoms mean that Wernicke’s encephalopathy is often undiagnosed due to assumptions that patients are inebriated and also because they are unlikely to present to services (Thomson et al, 2002). Although it usually results from chronic alcohol misuse, anyone with poor nutritional intake can be susceptible, such as patients with haemodialysis, malignancy, Aids, hyperemesis gravidarum and eating disorders such as anorexia and bulimia (Patient UK, 2008; Alexander et al, 2006).

Around 13% of all chronic alcohol users show the classic signs and symptoms of Wernicke’s encephalopathy (Alcohol Concern, 2007), with 75-85% of those who show symptoms going on to develop some degree of Korsakoff’s syndrome, possibly due to missed diagnosis (Agabio, 2004). Given that Wernicke’s encephalopathy is thought to have a 17-20% mortality rate (Cook et al, 1998), and that it can be quickly and easily reversed by giving patients B vitamins, it is vital it is properly diagnosed and quickly treated. This particularly applies to younger people, where the condition is not routinely observed and assessed because they are not seen as a high-risk group.

Box 2. Vitamin B

  • Thiamine or vitamin B1 is needed for a healthy neurological system, to maintain strong heart muscles, to help in absorbing other vitamins and in breaking down carbohydrates into energy (Guyton and Hall, 1996).
  • Thiamine can only be obtained through diet if taken regularly from sources such as green vegetables, nuts, pork and beef, so depletion is a real possibility (Thurnham, 2000).
  • The vitamin is not stored by the body; instead, it stays for only short periods before being broken down and excreted through urine. Since alcohol acts as a diuretic, this also contributes to the excretion of thiamine (Thomson and Marshall, 2005).
  • Thiamine is soluble in water but insoluble in alcohol, meaning the absorption of thiamine in the body is reduced when alcohol has been ingested. This can lead to neurological damage in the brain, notably in the Wernicke’s area, which is associated with speech and language (Thomson and Marshall, 2005).
  • The intake of large amounts of alcohol over a sustained period reduces the amounts of thiamine being ingested, synthesised, stored and transported in the body, which has a significant impact on thiamine levels (Medline Plus, 2008).
  • Typically, people with chronically high alcohol consumption tend to present with poor dietary intake, GI upsets (haemorrhage, ulcers, vomiting), and various physical problems which all result in malabsorption of nutrients (Barclay et al, 2008).

 

Korsakoff’s syndrome

Korsakoff’s syndrome, named after Russian neuro-psychiatrist Sergei Korsakoff (1854-1900), is an irreversible impairment of short-term memory. Those affected cannot form new memories, despite the fact that their immediate recall remains intact and they retain normal cognitive ability (Alcohol Concern, 2007). Although disturbances in orientation and sequencing of events are common, as is confabulation (use of compensatory explanations for poor, inaccurate or bizarre memory) (Alzheimer Scotland, 2004). Peripheral neuropathy and unsteady gait may be present, as well as delirium, paranoia and tactile and olfactory hallucinations (Patient UK, 2008).

Again, Korsakoff’s syndrome is not routinely assessed in the younger age group, mainly because it is not expected to be present.

It is extremely difficult to identify the precise point at which Wernicke’s encephalopathy becomes Korsakoff’s syndrome because there is no defining indication of this happening; it is a seamless transition.

As with Wernicke’s encephalopathy, the presenting signs and symptoms can be mistaken for alcohol intoxication, especially in people who continue to consume alcohol. Deaths from Korsakoff’s syndrome are thought to be at a similar level to those from Wernicke’s encephalopathy but true statistics may never be known (Alzheimer Scotland, 2004).

Nursing assessment

Assessment should eliminate other potential causes of patients’ presentation. This may indicate the need for drug screening, assessment for anaemia, leukaemia and hyper-/hypoglycaemia. Blood tests should include y-glutamyl transpeptidase, serum B1, pyruvate level and index of thiamine status through level of erythrocyte tranketolase activity as these will aid diagnosis (Salen, 2009)

In addition, an EEG to assess seizure activity, CT or MRI scanning to assess brain changes and testing for hypernatraemia are also indicated (Zuccoli et al, 2007). Box 3 outlines the points to cover when assessing younger patients where alcohol is thought to be a factor in their presentation.

Box 3. Nursing assessment

Assessment of younger people where alcohol is believed to be involved should consider:

  • Baseline observations;
  • Reasons for initial admission/referral, such as falls, burns or mental health problems;
  • Drink history;
  • Last time they drank;
  • Past medical/psychiatric history;
  • Current social situation;
  • Diet and hydration;
  • Vomiting/nausea;
  • Medication (prescribed or not);
  • Mobility;
  • Tremor;
  • Headaches;
  • Abdominal pain (ascites);
  • Current level of intoxication;
  • Liver function tests;
  • Pallor;
  • Neuropathy;
  • Speech;
  • Eye movements;
  • Level of consciousness;
  • Epilepsy/blackouts;
  • Hallucinations/delusions;
  • Impaired judgement;
  • Physical appearance;
  • Mood/personality changes;
  • Self-harm/suicidal ideation;
  • Weight;
  • Current levels of orientation/confusion;
  • Delirium tremens;
  • Use of scales such as the Selective Severity Assessment Scale;
  • Police involvement;
  • Problems or changes at school/home.

Source: McDougall, 2006; Rutter and Taylor, 2005; McCrady and Epstein, 1999.

 

Nursing management

A presumptive diagnosis of Wernicke’s/Korsakoff’s should always be considered, regardless of age, if patients present with the signs and symptoms outlined, although they are not always obvious (Smith and Hillman, 1999). If other medical conditions are ruled out, a drinking history should be obtained if this has not already been done.

If Wernicke’s encephalopathy or Korsakoff’s syndrome is diagnosed, first-line treatment should be high-dose injection, preferably intravenous, of thiamine (Pabrinex) with a maximum dose of 300mg for severe deficiency (Thomson and Marshall, 2005). This gives the body a much needed boost of essential vitamin B1 and can prevent brain damage or death (Jacobson, 2000); patients should be re-assessed after this treatment. There is a low risk of allergic reaction to high doses of thiamine and it is important that nurses monitor this and are appropriately prepared in case of anaphylaxis (British National Formulary, 2009).

Electrolyte levels should be checked and monitored daily for 7-10 days (Dewar, 2000) and both food and fluid intake and output monitored. Parenteral nutrition should be incorporated in the treatment plan because patients can find it difficult to metabolise and absorb essential vitamins and minerals due to damage caused by prolonged alcohol consumption.

Care should be taken to avoid “re-feeding” syndrome, where patients have a sudden increase of high protein calories beyond their normal tolerance levels, which can result in cardiac failure (Mehanna et al, 2008).

Glucose infusion before thiamine administration should be avoided because of the likelihood of unstable electrolyte and fluid levels and the potential for a rise in insulin levels caused by the sudden increase of food (Xiong et al, 2008).

 

Alcohol withdrawal

Stopping drinking abruptly can result in life-threatening changes to the body and brain, even where there are no signs of Wernicke’s encephalopathy or Korsakoff’s syndrome. Nurses therefore need to be aware of signs and symptoms of acute alcohol withdrawal (delirium tremens) (see Box 4).

Withdrawal symptoms usually start within 48-72 hours after stopping drinking, although they may start within 6–8 hours. They can last for 3–5 days, or longer if there are underlying physical conditions (Yim and Wiener, 2007).

 

Box 4. Signs and symptoms of acute alcohol withdrawal

  • Profuse sweating
  • Restlessness/agitation (shakes)
  • Abdominal cramps
  • Frequent micturition/diarrhoea
  • Tachycardia
  • Increased blood pressure, pulse, temperature and respirations
  • Vomiting and nausea
  • Hallucination (tactile, olfactory or visual)
  • Seizures/blackouts
  • Nightmares
  • Anxiety
  • Skin having poor turgor
  • Fluctuation in levels of consciousness
  • Aggression and violence
  • Craving for alcohol

Source: Yim and Wiener (2007)

 

Safe detoxification

Observations should be charted every 15 minutes until stable and then hourly for 4–8 hours with doctors’ advice followed after that. Rest should be encouraged and, if possible, patients should be in a single room with minimal noise or distraction (Varcarolis, 2000). Staff may be required to support or complete hygiene tasks for them until independence is regained (Yim and Wiener, 2007). Due to potential memory problems and patients forgetting why they are in hospital, staff need to eliminate potential risks from the room such as cigarettes, lighters and sharp instruments which may pose a risk to themselves or others.

Communication should be clear and concise, with the tone reflecting calm and reassurance (Evans et al, 2004). Instructions should be simple but precise, and it is important to exhibit understanding and patience even when patients need regular repetition.

Staff should also attempt to orientate patients to time, place and person to help reassure them they are safe. Again, repetition and patience with these instructions are essential.

Alcohol withdrawal is treated by benzodiazepines (Box 5) in conjunction with vitamins as part of a pre-planned detoxification programme or due to acute alcohol withdrawal. A benzodiazepine regimen should be started to prevent the onset of withdrawal symptoms and the potentially life-threatening changes that can occur from alcohol withdrawal.

The benzodiazepine chlordiazepoxide can be given over a 24 hour period, usually four times daily from 10-50mg (BNF, 2009) and should be titrated to meet individual needs. It is administered in a decreasing dose, reducing by 10-20mg per day over a period of 7-14 days (Chick, 2004). This is a proven and standard method of reducing withdrawal symptoms but should not be given where alcohol consumption continues.

Input from specialist alcohol misuse services or community psychiatric nurses may be needed if patients opt for withdrawal in the community.

Box 5. Withdrawal medication

  • Chlordiazepoxide – has low potential for addiction and a high margin of safety if alcohol is still present.
  • Diazepam – has a long half-life and is seen by many as the drug of choice in detoxification. However, care should be taken as diazepam is more rapidly absorbed than chlordiazepoxide, making it potentially more addictive.
  • Lorazepam – short-acting half-life, it is prescribed off-licence for agitation caused by alcohol withdrawal.
  • As all three drugs have several cautions and contraindications, doctors’ or expert prescribing advice should be sought before use.

Source: BNF (2009).

 

Rehabilitation and future treatment

Due to the potentially long-term, irreversible cognitive deficits caused by Korsakoff’s syndrome, future treatments need to be tailored to each individual’s needs.

At times, patients are placed inappropriately – for example in medical or acute psychiatric admission wards – because there is no space on specialist units. Return to the community should never be ruled out, regardless of whether patients are going to live independently or in supported accommodation (Alzheimer Scotland, 2004).

There is a real need to establish specialist units to accommodate people with Korsakoff’s syndrome and to help with ongoing rehabilitation, which can take many years but can result in minor improvements in cognitive abilities (Alzheimer Scotland, 2004).

Best practice involves a multidisciplinary approach. Occupational therapy assessment helps maintain and develop structured activity that is both therapeutic and purposeful, while support packages via social work and voluntary organisations can help with structured activity, household tasks and avoiding alcohol. Family support is also important, as is follow-up by CPNs and neuropsychologists (Alcohol Concern, 2007).

Young people under 18 benefit from input from child and adolescent mental health services, which incorporates both psychological interventions and family therapy.

The following simple yet effective interventions have been shown to help people with Korsakoff’s syndrome:

  • Reality orientation;
  • Diaries;
  • Whiteboards for reminders;
  • Mind-maps;
  • Keeping lists with patients and ticking off tasks achieved;
  • Useful numbers beside the phone (reconsider this if the person calls people inappropriately);
  • Continuing support from family, friends and professionals to help fill in any gaps in memory through use of life stories (Baddeley et al, 2002).

Where no residual evidence of Korsakoff’s syndrome is noted, those who have gone through alcohol detoxification will need follow-up and support either to maintain abstinence or control their drinking. This can be provided by groups such as Alcoholics Anonymous, local NHS alcohol services, GPs and families/carers. This will also help to maintain contact with services which can monitor progress and provide support where and when necessary.

Conclusion

It is imperative that all nurses working with young people are aware of the presenting signs and symptoms of both Wernicke’s encephalopathy and Korsakoff’s syndrome, as failing to recognise and manage these conditions has serious implications.

Contemporary social change affecting young people and their attitude to alcohol and drinking means this group will increasingly present to services with alcohol-related problems. Indeed alcohol-related brain damage is affecting young people at an alarming rate. Living with Korsakoff’s syndrome does not reduce life expectancy so people developing it in their teens or twenties could live with the condition for 50 years or more. This has a huge impact on the person, their family and society.

Nurses need to be aware of these potential problems and be able to identify and deal with them quickly and effectively. They also need to raise awareness of the dangers of alcohol among young people to help reduce the incidence of Wernicke’s encephalopathy and Korsakoff’s syndrome.

 

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