Definition - Condition that occurs in alcohol abusers as a result of decrease or cessation of alcohol drinking
- Results in blood alcohol levels below the level to which the drinker has become habituated
- Begins about 4 to 12 hours after the last drink and may progress to delirium tremens with seizures, hallucinations, coma, and death
Risk Factors - Abrupt withdrawal of alcohol
- The severity of symptoms is proportional to the previous duration and level of alcohol consumed
Differential diagnosis Epidemiology - On a worldwide basis, alcohol misuse is responsible for 1.8 million deaths and 58.3 million disability-adjusted life years
- In 2003, the prevalence of disorders related to alcohol use was 1.7% in developed countries
- In England, 52,270 hospital admissions in 2005/2006 were directly related to alcohol abuse and there were 6,570 alcohol-related deaths
- The reporting rate for alcohol-related deaths in the UK is rising, from 6.9 cases per 100,000 in 1991 to 13.4 per 100,000 in 2006
Aetiology - Aetiology is not known
- Chronic alcohol use is associated with:
- an up-regulation of postsynaptic glutamate receptors
- or a down-regulation of postsynaptic gamma-amino butyric acid (GABA) receptors
- Alcohol-related seizures are likely the result of a combination of brain pathology, irritability related to alcohol withdrawal, or trauma related to alcoholism
- Alcoholic hallucinosis does not have a definitive aetiology; it is known to be related to the severity of dependence and frequency of major withdrawal
Clinical features - Alcohol use
- Structured approach to drinking habits includes asking about alcohol use in the past year and using the CAGE questionnaire to assess whether the patient needs a referral
- Patients are at risk for major withdrawals if they:
- drink more than 2 litres of wine or equivalent quantity of hard liquor
- have a history of heavy alcohol use for more than 5 years
- usually drink throughout the day
- have a prior history of withdrawal
- Change in mental status
- Patient has severe memory disturbances, remains disoriented to time, place, and person, and has waxing and waning in the level of consciousness
- Seizures
- Occurs in 1% to 3% of patients with alcohol withdrawal syndrome
- Usually happens in the early phase of withdrawal (up to 2 days)
- Most patients have one seizure that is usually tonic-clonic in nature
- Focal onset and status epilepticus are rare
- Hallucinations
- Examples of visual hallucinations include insects crawling on self or animals circling the bed
- Tactile hallucinations include sensation of pins or electric shocks all over the body and insects crawling on the skin
- Associated with delirium tremens (DT), which occurs in 5% of patients hospitalised for alcohol withdrawal
- Delusions
- Tremor
- Associated with minor withdrawal
- Also a feature of delirium tremens
- Nausea and vomiting
- Associated with minor withdrawal
- Hypertension
- Associated with minor withdrawal
- Tachycardia
- Associated with withdrawal of any severity
- Fever
- Associated with major withdrawal and DT
Pathophysiology - Prolonged exposure causes adaptive changes in the brain receptors and neurotransmitters
- Responsible for various effects such as addiction, tolerance, and withdrawal
- Frequent withdrawal episodes are associated with irreversible brain damage from cell death
- This phenomenon has been demonstrated in animal studies
- There are multiple neurotransmitters in the brain that play a role in alcohol withdrawal
- Their effects are interactive, and some of the neurotransmitters involved include glutamate, GABA, opioid receptors, dopamine, and serotonin receptors
- One of the excitatory neurotransmitters is glutamate, which acts through the fast-channel NMDA (N-methyl D-aspartate)
- Alcohol inhibits glutamate, resulting in an increase in the NMDA receptors
- When an individual stops drinking alcohol, inhibitory effects of alcohol on glutamate stop, and excitatory effects manifest clinically
- One of the inhibitory chemical substances in the brain is GABA, which acts through the GABA-A receptor
- It has been shown that increasing the concentration of GABA in the brain produces similar effects to alcohol intoxication
- It has also been noted in studies that repeated exposure to alcohol can reduce GABA hyperpolarisation and neuronal inhibition, resulting in development of tolerance
- Dopamine release has been noted in the brain when alcohol is ingested, and alcohol withdrawal is associated with inhibition of dopamine
- Alcohol use is also associated with an increase in endorphins, and chronic use is associated with lower levels of endorphins
- Studies show that an increase in serotonin has been noted with alcohol consumption
- Has shown to be responsible for development of tolerance, intoxication, withdrawal, and regulation of alcohol consumption
- Increased craving for alcohol after repeated detoxifications is referred to as kindling
- This occurs as a result of long-term changes in neurons, and explains the progression of withdrawal
Investigations- Serum urea and creatinine
- Elevated, normal, or reduced
- Dehydration may occur in a delirious patient and may lead to impaired renal function
- Uraemic encephalopathy can mimic alcohol withdrawal delirium because of change in mental status
- LFTs
- All parameters may be elevated
- May suggest additional diagnoses such as alcoholic hepatitis
- Toxicology screen
- May be positive for other drugs of abuse
- May be used to determine other causes for altered mental status or abnormal vital signs
- Serum and urine drug testing (both quantitative and qualitative) should be based on clinical suspicion at time of decision making
- Electrolyte panel
- Metabolic acidosis
- Lactic acidosis may be related to alcoholic seizures, ketoacidosis, or ingestion of other alcohols
- CT head
- To exclude other causes of the clinical presentation if indicated
Managementa) conservative- Supportive care
- Vitamin supplementation
- Thiamine supplementation is given if Wernicke’s encephalopathy is suspected
- Other water-soluble vitamins that may need to be supplemented during hospital or emergency department course include folic acid and magnesium
b) medical - benzodiazepine or clomethiazole
- chlordiazepoxide
- 25-100 mg orally/intravenously/intramuscularly every 4-6 hours, reduce dose as symptoms abate, maximum 300 mg/day
- diazepam
- 5-10 mg orally/intravenously/intramuscularly every 6-8 hours
- lorazepam
- 1-4 mg orally/intravenously/intramuscularly every 6-8 hours
- magnesium
- Severe hypomagnesaemia (<1 mg/dL) and symptomatic patients in the
emergency setting may need up to 2 g of magnesium sulphate given by
intravenous infusion
c) surgicalPrognosis- Patients may complain of persistent insomnia and autonomic symptoms for a
few months after acute withdrawal phase
- These symptoms usually last
about 6 months
- About 50% of patients remain abstinent for a year
- Relapse prevention can be achieved by counselling strategies, self-help
groups (e.g., Alcoholics Anonymous), and pharmacotherapy
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