Alcohol Withdrawal Syndrome

Key Differential Diagnoses

Causes acute confusion, coma, collapse and epilepsy
Sepsis
Subdural haematoma
Hypoglycaemia
Drunk
  .. or combination of above

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

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

Definitions

A set of symptoms that develop in alcohol-dependent individuals within 6-24h after their last drink

Epidemiology

(For excess alcohol use)
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

Risk factors

(For AWS)
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
Hallucinations (requirement for diagnosis of DTs)

Key questions

"When did you last have a drink?" (RECORD THIS FACT)
"What is the most that you drink?"
If you are still in doubt, ask the:
CAGE questionnaire:
Alcohol dependence is likely if 2 or more positive answers to:
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

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

Causes acute confusion, coma, collapse and epilepsy
Sepsis including meningitis and encephalitis
Subdural haematoma
Hypoglycaemia
Drunk
  .. or combination of above

Hyponatraemia
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 (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]  

[Ref]
IV line
Note: observe for delirium tremens, continuous vomiting (ARF?), or deterioration in mental state, biochemistry (ARF?), LFTs

Key management decisions

Chlordiazepoxide/not (if you are not giving, why are you admitting?)

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

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

Complications

Mild AWS can develop into DTs
Thiamine deficiency:
• Wernicke's encephalopathy = an acute neuropsychiatric disorder characterised by ataxia, nystagmus  and confusion. The classic triad of symptoms 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

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
• 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