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Alcohol withdrawal

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
    • Associated with DT
  • 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
Management

a) 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) surgical
  • n/a
Prognosis
  • 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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