Key facts:
Authors: Natalie Acors and Andrew Stein
Top Tip: Think laterally: patient can have AWS, subdural, hypoglycaemia and also be drunk
Key Differential Diagnoses
- Other causes acute confusion, incl post-ictal
- Sepsis
- Subdural haematoma
- Hypoglycaemia
- Drunk
.. or combination of above (and AWS)
Key Investigations
- FBC, ESR, CRP
- U+E, LFT/GGT, Bone, Magnesium, Glucose
- INR
- ECG, CXR
Key Treatment
- IV PABRINEX 2 vials tds
- PO CHLORDIAZEPOXIDE 20-40 mg qds + PRN doses
Key Management Decision
- Chlordiazepoxide
- ITU
Background
Suspect AWS, if patient becomes confused 2-4d after admission, and there is no other obvious cause. Severe AMS may require ITU
Introduction
- Alcohol (ethanol) is a CNS depressant. Large amounts consumed rapidly can cause respiratory depression, coma, and death. Large amounts chronically consumed damage the liver, brain, heart and other organs
- Alcohol withdrawal manifests as a continuum, ranging from tremor to seizures, hallucinations, and life-threatening autonomic instability in severe withdrawal (delirium tremens). You need to protect the patient from themselves
- Diagnosis is clinical. Blood alcohol is of no value
- 5% have 'delirium tremens' = severe alcohol withdrawal syndrome (AWS). This typically presents after 2-4d of abstinence from alcohol, and can persist for up to 2 wks; it is characterised by hallucinations and has a high mortality (10%)
- In severe withdrawal (and excess) symptoms may resemble those of head injury or cerebral infection, so CT and LP may be needed
- Mild AWS can be managed as an outpatient. Few hospitals have an alcohol detoxication unit ('detox'). So patients may refer themselves to your hospital for detox and then develop alcohol withdrawal
- Psychiatric symptoms, incl hallucinations (requirement for diagnosis of DTs)
Definition
-
A set of symptoms that develop in alcohol-dependent individuals within 6-24h after their last drink
Terminology
-
Try to avoid phrases like 'alcoholic' and 'alcoholism'; they are judgemental
-
It is better to talk about alcohol dependence syndrome; or 'this patient has a high alcohol consumption' or 'alcohol use'
Risk factors
- Male 2x risk
- Occupation: catering, brewing, doctors, services, demolition workers
- Homelessness
- British Afro-Caribbeans and South Asians, have lower rates (though Sikh men may be exception, especially with spirits)
- 20% Oriental people cannot drink alcohol due to inherited lack of acetaldehyde dehydrogenase
- Previous delerium tremens
- Alcohol-related epilepsy
- Benzodiazepine use
- Depression
- Admission for a concurrent acute medical illness
-
Family history: alcohol, mental illness
Symptoms
- Tremor
- Weakness
- Sweating
- GI symptoms
Key questions
- "When did you last have a drink?" (RECORD THIS FACT)
- "What is the most that you drink?"
Note: if you are still in doubt, ask about the CAGE questionnaire:
Cage Questionnaire
(Alcohol dependence is likely if 2 or more positive answers)
- Have you ever felt you should Cut down on your drinking?
- Have people Annoyed you by criticising your drinking?
- Have you ever felt bad or Guilty about your drinking?
- Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (Eye-opener)?
Signs
- Signs of chronic liver disease
- Pyrexia, tachycardia
- Tremor
- Hyper-reflexia
- May smell of alcohol
- Seizures, confusion, psychosis: hallucinations are typically visual, including seeing spiders on the wall
Note: confusion, fitting, reduced LoC, focal neurology are all serious signs
Investigation
In severe AWS (and excess) symptoms may resemble those of head injury or cerebral infection, so CT and LP may be needed
Blood
- FBC (leucocytosis), CRP
- U+E (hyponatraemia?), LFT/GGT: [Ref]
Note: bilirubin; albumin (reflects liver function); raised AST/ALT may suggest alcoholic hepatitis (but an AST/ALT more than 400 IU/L is not consistent with alcoholic hepatitis) - Bone, Magnesium, Glucose (low?)
- INR (liver function?)
- ABG, if unwell (25% metabolic acidosis on admission)
Other
- ECG
- CXR
Key investigations
- LFT/GGT
- INR
Specialist investigation
- Liver US with Dopplers (to exclude alcoholic hepatitis (bright) and hepatoma)
Differential diagnoses
- Other causes of acute confusion, incl post-ictal
- Sepsis including meningitis and encephalitis
- Subdural haematoma
- Hypoglycaemia
- Drunk
.. or combination of above - Hyponatremia
- Hepatic encephalopathy (these are also likely in patients with alcohol dependence syndrome)
- Acute haemorrhage
- Hypoxia
- CVA
- Drug (prescribed or recreational) toxicity/withdrawal
- Other causes psychosis, eg schizophrenia
Note 1: patients who abuse alcohol are susceptible to acute hepatic failure, severe liver necrosis, and hepatic coma when taking paracetamol; doses as low as 4g have been reported to cause acute hepatic failure. Therefore, the diagnosis of paracetamol overdose should be considered in all alcohol dependent patients with abnormal liver function tests; with prompt administration of N-acetylcysteine
Note 2: There may also be features of acute alcoholic hepatitis (AAH) the management of which is discussed separately
Treatment
Make sure you give the correct dose of Pabrinex
Treatment - first line
Drugs
- Multivitamin preparations to prevent the onset of Wernicke's encephalopathy:
- IV PABRINEX 2 vials tds, for 3-6d; give over 30 mins (resuscitation equipment to hand); before changing to oral treatment (PO THIAMINE 100 mg tds, for one month)
- ± IV GLUCOSE, 20 mls 50%, if BG <4 mmol/L
Note: GLUCOSE increases risk of Wernicke's encephalopathy, so give IV PABRINEX first - Benzodiazepines to prevent a more severe AWS:
- CHLORDIAZEPOXIDE 20-40 mg qds, reducing over 5 days according to patient response
Note: larger doses are used in severe withdrawal - prescribe PRN doses and be prepared to adjust regime according to response - or, PO LORAZEPAM 1-4 mg, reducing course
- ± IV LORAZEPAM 4 mg (can be repeated once, in the event of seizures (note: national shortage of lorazepam at moment; may have to use another benzodiazepine eg DIAZEPAM 10 mg over 2 mins; then repeat after 10 mins, if necessary)
UK/RCP: Guidelines for managing [Ref]Treatment - second line
- IV line
Note: observe for delirium tremens, continuous vomiting (ARF?), or deterioration in mental state, biochemistry (ARF?), LFTs
- CHLORDIAZEPOXIDE 20-40 mg qds, reducing over 5 days according to patient response
Supportive measures
- Physical restraints should be avoided if possible to minimise additional agitation. But patients must not be allowed to leave the hospital, remove IVs, or otherwise endanger themselves, or other people
- Psychiatric help may be required
Key management decisions
- Chlordiazepoxide/not (if you are not giving, why are you admitting?)
- ITU
Stop
-
Alcohol
Treatment - second line
Drugs
- Prednisolone, is suspect AAH
Procedures
- ?Ventilate; if very unwell, or status epilepticus
Note: critically ill patients typically require much higher than normal doses of benzodiazepines to treat AWS, up to 100-fold
Prescribing issues
- Adjust reducing course CHLORDIAZEPOXIDE regime properly;ie don't just write "reducing course"; nurses need clear instructions; don't let patient out of hospital with a large supply of the drug (they may take the lot!); in drug history, ask about sedative drugs as patients often take these as well
Admit?
- Usually
Bed plan
- Medical admission ward, if admission <48h
- Gastroenterology, if admission >48h
- ± ITU
- ± Psychiatry (if suspect another cause of psychosis; or need powers of Mental Health Act)
Referrals
Medical
- Gastroenterology
- ± ITU
- ± Psychiatry (if suspect another cause of psychosis; or need powers of Mental Health Act)
Other
- Community alcohol service
The Rest
Hallucinations are typically visual, including seeing spiders on the wall
Complications
- Mild AWS can develop into DTs
Thiamine deficiency: - Wernicke's encephalopathy = an acute neuropsychiatric disorder characterised by the triad of ataxia, nystagmus and confusion. The classic triad occurs in only 10% of patients. Disease onset can be acute or chronic. For these reasons, diagnosis can be difficult (see references)
- It is caused by lesions in the medial thalamic nuclei, mammillary bodies, periaqueductal and periventricular brainstem nuclei, and superior cerebellar vermis; often resulting from inadequate intake or absorption of thiamine (Vitamin B1), especially in conjunction with carbohydrate ingestion
- Korsakoff's psychosis is a late complication of persistent Wernicke's encephalopathy and results in memory deficits, confusion, and behavioural changes; characterised by antegrade and retrograde amnesia, disorientation, and confabulation. It occurs in 80% of untreated patients with Wernicke's encephalopathy
- Why Korsakoff's psychosis develops in only some patients with Wernicke's encephalopathy is unclear. A severe or repeated attack of DTs can trigger Korsakoff's psychosis whether or not a typical attack of Wernicke's encephalopathy has occurred first
- Many clinicians consider these two diagnoses variants of one syndrome, Wernicke-Korsakoff Syndrome
- Alcohol-related epilepsy is difficult to treat
CT head: Wernicke's Encephalopathy
Follow-up
- Community alcohol service
Prognosis
- DTs: 10% mortality
Risk stratification
(who can be managed as outpatient)
- May be possible to manage as OP, if patient does not have reduced LoC, confusion, focal neurology or fitting
2° Prevention
+ Health promotion
- Encourage attendance at community alcohol service, and Alcoholics Anonymous. To most patients, advise NO aclohol consumption for 6 months, in first instance. If no end-organ damage, then normal 'safe' alcohol limit is advised below. If end-organ damage, patient should remain teetotal
- ACAMPROSATE – helps relieve intense anxiety, cravings and insomnia
- DISULFIRAM – causes unpleasant side effects with alcohol ingestion
Don't forget
- Think about the other causes of cerebral irritability, in someone with high alcohol consumption. Patients can have combination
- Or, the diagnosis is nothing to do with alcohol (eg schizophrenia, or meningitis or encephalitis)
- Diagnosis is clinical. Blood alcohol is of no value
- 5% have 'delirium tremens' = severe alcohol withdrawal syndrome (AWS). This typically presents after 2-4d of abstinence from alcohol, and can persist for up to 2 wks; it is characterised by hallucinations and has a high mortality, and may require ITU
- So, protect the patient from themselves
- In severe withdrawal (and excess) symptoms may resemble those of head injury or cerebral infection, so CT and LP may be needed
- Think about acute alcoholic hepatitis (steroid-responsive)
- Avoid phrases like 'alcoholic'; use ‘alcohol dependence syndrome’ for eg
- Many patients are drinking again in 2 wks; some are not. Make sure all are given information regarding the community alcohol service (CAS)
Red flags
- Reduced conscious level
- Confusion
- Focal neurology
- Fitting
