Alcohol use is common in India with a prevalence of around 21%. The document discusses the extent of alcohol use, definitions of alcohol use disorder according to DSM-V criteria, effects of alcohol on the body, signs and symptoms of alcohol intoxication and withdrawal, and treatments for alcohol use disorder and withdrawal. Key treatments discussed include use of benzodiazepines like diazepam and chlordiazepoxide for managing withdrawal symptoms and medications like disulfiram, naltrexone, and acamprosate to support abstinence from alcohol.

1. EXTENT OF THE PROBLEM
•Alcohol use is quite common
•both in rural and urban areas.
•According to National Household survey (NHS), prevalence of
alcohol use is 21.4%.
•

2. •Males>females
•Urban >rural
•Increasing among adolescents
•A/w increased risk of other drugs abuse

3. DEFINITIONS- DSM V

4. DSM-5 diagnostic criteria for alcohol use disorder are
●Recurrent drinking resulting in failure to fulfill role obligations
●Recurrent drinking in hazardous situations
●Continued drinking despite alcohol-related social or interpersonal problems
●Evidence of tolerance
●Evidence of alcohol withdrawal or use of alcohol for relief or avoidance of withdrawal
●Drinking in larger amounts or over longer periods than intended
●Persistent desire or unsuccessful attempts to stop or reduce drinking
●Great deal of time spent obtaining, using, or recovering from alcohol
●Important activities given up or reduced because of drinking
●Continued drinking despite knowledge of physical or psychological problems caused by
alcohol
●Alcohol craving

5. Disorder state — Modifiers for the diagnosis include:
●In early remission – After full criteria for alcohol use disorder were previously
met, none of the criteria for alcohol use disorder have been met (with the
exception of craving) for at least 3 months but less than 12 months.
●In sustained remission – After full criteria for alcohol use disorder were
previously met, none of the criteria for alcohol use disorder have been met
(with the exception of craving) during a period of 12 months or longer.
●In a controlled environment – If the individual is in an environment where
access to alcohol is restricted.
Disorder severity — The severity of alcohol use disorder at the time of diagnosis
can be specified as a subtype based on the number of symptoms present:
●Mild: Two to three symptoms
●Moderate: Four to five symptoms
●Severe: Six or more symptoms

6. Alcoholic Drinks

7. Pharmacokinetics and Dynamics
•Alcohol is rapidly absorbed from upper gastrointestinal tract.
•Peak blood alcohol concentration (BAC) is reached in 30 to 60
minutes
one standard unit of alcohol is 10ml ofabsolute alcohol, i.e. 7.87g
•70 kg man = 1 drink is likely to raise the BAC to approximately
15 to 20 mg/dl.

8. •Metabolism
follows Zero-order kinetics
eliminated from body at a rate of 7-10 gm (1 standard drink) an
hour
•Metabolised in liver by oxidation
•Small amounts of alcohol(2-4% of the total dose) are lost into
the urine and into the alveolar air by diffusion.
•The alcohol in alveolar air is in equilibrium with the alcohol in
the blood passing through the lungs = breath analyzer can
there-fore be used and estimate blood concentration for
medico-legal purposes.

10. PATHOGENESIS — The pathogenesis of alcohol use disorder is not known, but
its development may be the result of a complex interplay of:
●Genetics
●Environmental influences – Environmental influences can be categorized as
intra-familial influences, including prenatal exposure and parenting patterns,
and peer influences
●Specific personality traits – Personality phenotypes implicated in association
with alcohol use disorder includes neuroticism, impulsivity, and extroversion
●Cognitive functioning – Disorders of cognition, especially cognitive
dysfunction, may be associated with the development of alcohol use disorder

11. NEUROBIOLOGY OF ALCOHOL USE
Recent studies show that different epigenetic modifications can
occur in response to both acute and chronic alcohol exposure.
These changes can affect gene expression and ultimately brain
circuitry

12. NEUROANATOMICAL STRUCTURES IN
ALCOHOL USE
Nucleus Accumbens and Central Nucleus of the Amygdala — Forebrain
structures involved in the rewarding effects of drugs of abuse and drives the
binge intoxication. Contains key reward neurotransmitters: dopamine and
opioid peptides
Extended Amygdala — Composed of central nucleus of the amygdala, bed
nucleus of the stria terminalis, and a transition zone in the medial part of the
nucleus accumbens. Contains “brain stress” neurotransmitter, corticotropin
releasing factor that controls hormonal, sympathetic, and behavioral responses
to stressors, and is involved in the anti-reward effects of drug dependence
Medial Prefrontal Cortex — neurobiological substrate for “executive
function” that is compromised in drug dependence and plays a key role in
facilitating relapse. Contains major glutamatergic projection to nucleus
accumbens and amygdala.

13. Neurobiology of addiction

14. Alcohol Intoxication
•Evidence of recent ingestion of ethanol, maladaptive behaviour
developing during or shortly after alcohol intake and atleast one
of the following physiological correlates of intoxication that are
not due to a medical condition or mental disorder.
Slurred speech
Dizziness
Incoordination
Unsteady gait
Nystagmus
Impairment in attention and memory
Stupor or coma
Double vision

15. IMPAIRMENT AT DIFFERENT
BLOOD ALCOHOL
CONCENTRATIONS
20-30mg/dl Euphoria, feeling of relaxation and talking freely
30-80mg/dl Decreased alertness, clumsy movements of hands and feet
80-200mg/dl
Increases in incoordination and judgement errors, impaired driving
ability.
Mood lability
Deterioration in cognition
200-300mg/dl Nystagmus, marked slurring of speech and alcoholic blackouts
>300mg/dl Impaired vital signs and possible death

16. Other manifestations
•Injury
•Acute Pancreatitis/Hepatitis/gastritis
•Hypoglycemia
•Atrial fibrillation
•Lactic Acidosis
•Electrolyte imbalance
•Congestive heart failure
•Pulmonary edema
•Cardiovascular collapse

17. EVALUATION
•History
•Physical examination
•Investigations
• Additional investigations should be considered depending on
the clinical features of the patient, to evaluate potentially harmful
alcohol-related and non-alcohol related diseases.

19. Treatment

20. •Once a patient has become stabilized and both the acute alcohol
intoxication symptoms and the related clinical complications
have been treated, the patient should be monitored for 72 h
following a BAC of 0 mg/dl (0mmol/l).
•He should be clinically assessed for chronic effects of alcohol
use and alcohol dependence.
•Patients who abuse or who are dependent on alcohol may
experience an alcohol withdrawal syndrome following
detoxification.
•Such a syndrome, in its severe form, may be life-threatening and
present with delirium tremens and seizures.

21. Adjunctive supplements
•Due to chronic malnutrition and gastric malabsorption that
followa chronic alcohol abuse, multivitamin supplements in
parenteral form should be administered for initial 3-5 days.
•Thiamine 250mg once a day for the first 3-5 days.Contuniued
for 2 weeks.
•500mg/day for suspected Wernicke’s encephalopathy.

22. Medico-legal aspects
•S 185 of the. Motor Vehicle Act prescribes a maximum
permissible BAC of 30 mg%, "in a test by a breath analyzer",
while driving in India.
•S. 34 Police Act empowers a police person to arrest such a
person without a warrant and the punishment under the Act is
imprisonment up to 8 days

23. Summary of effects of alcohol on
organ systems

24. SCREENING
•CAGE Questionnaire
•AUDIT(Alcohol Use Disorders Identification
test)
•MAST(Michigan Alcoholism Screening Test)

25. Biochemical markers

26. ALCOHOL WITHDRAWAL

27. •Normally excitatory (glutamate) and inhibitory (GABA) neurotransmitters
are in a state of homeostasis
•Chronic alcohol use causes decrease in the number of GABA receptors
(down regulation)
•This results in the requirement of increasingly larger doses of ethanol to
achieve the same euphoric effect, a phenomenon known as tolerance
• Alcohol acts as an NMDA antagonist, thereby reducing the CNS excitatory
tone
•Chronic use of alcohol leads to an increase in the number of NMDA
receptors (up regulation) and production of more glutamate to maintain CNS
homeostasis
(Mainerova,et al 2015)

28. •With sudden cessation of alcohol in chronic user, alcohol
mediated CNS inhibition is reduced and the glutamate mediated
CNS excitation is left unopposed, resulting in a net CNS
excitation
•
•Form of
○ autonomic over activity such as tachycardia, tremors,
sweating
○ neuropsychiatric complications such as delirium and
seizures
(Mainerova,et al 2015)

30. DIAGNOSIS
•The alcohol withdrawal syndrome is diagnosed when the
following two conditions are met
•A clear evidence of recent cessation or reduction of alcohol after
repeated and usually prolonged and/or high-dose use.
•The patient shows symptoms of alcohol withdrawal that are not
accounted for by a medical disorder or by another mental or
behavioral disorder.

31. SIGNS SYMPTOMS
Elevated Blood Pressure Anxiety
Tachycardia Insomnia
Sweating/Tremulousness Illusions
Dilated pupils Hallucinations
Disorientation Paranoid ideas
Hyperarousal Nausea
Seizures Irritability

32. Assessment of the severity of Alcohol
withdrawal- CIWA-Ar (clinical institiute
withdrawal assesment score) scale
•The scale includes 10 common signs and symptoms of alcohol
withdrawal.
• It can be administered bedside in about 5 min.
•0-9 indicate absent to minimal withdrawal,
•10-19 indicate mild to moderate withdrawal (marked autonomic
arousal)
•20 or more indicate severe withdrawal (impending DT).

33. CIWA-Ar

34. CIWA-Ar(contd…)

35. Minor withdrawal
•Starts about 6h after cessation or decrease in intake, lasts upto
24-48h.
•Features include tremors, sweating, tachycardia, GI upset,
headache, anxiety and intact orientation.
•Usually corresponds to CIWA-Ar<10.

36. Alcoholic hallucinosis
•Hallucinations(visual/tactile/auditory) and illusions in a clear
sensorium and stable vitals.
•Lasts for 24h- 6 days and rarely beyond one month but
definitely <6 months.

37. Alcohol withdrawal seizure
•Begins within 6-48h after the last drink.
•Multiple seizures(upto 6) can occur, within a span of 6h.
•There is a high risk of progression to Delirium tremens.

38. Delirium Tremens
•Characterized by tremors, sweating, tachycardia, anxiety,
hallucinations/illusions, disorientation, agitation secondary to
previous symptoms.
•Begins 48-72 h after the last drink and may last upto two weeks.
•Usually CIWA-Ar >20.

39. MANAGEMENT
General supportive care.
•Quiet room with low lightning and minimal stimulation.
•i.v. access
•Adequate sedation
•Correction of fluid and electrolyte imbalances
•Adequate nutrition

40. Medications
•Chlordiazepoxide is far better in preventing seizures and DT in
patients with alcohol withdrawal compared to
chlorpromazine,hydroxyzine,thiamine or placebo.(Kaim et al,
1969)
•Anticonvulsants have not been proven to be better than
benzodiazepines.
•Dose of BZD is calculated according to average daily alcohol
intake.
•Alcohol(in g) = Volume of liquor(in ml) x 0.008 x % ethanol
content in the liquor(w/v).

41. Treatment regimens
Fixed dose regimen
•Fixed daily dose of benzodiazepine is administered in four
divided doses.
•Dose needs to be based on severity of withdrawals and time
since last drink.
•After 2-3 days of stabilisation of withdrawal syndrome, the
benzodiazepine is gradually tapered off over a period of 7-10
days.

43. Loading dose regimen
•Oral loading dose of 20mg of diazepam given every 2h.
•The withdrawal severity CIWA-Ar and the clinical condition
should be monitored before each dose.
•This regimen reduces the risk of complications, total dose of
BZD needed and duration of withdrawal symptoms.
•Loading dose strategies use long acting BZD as they provide a
self-tapering effect due to their pharmacokinetic properties.

44. Symptom Triggered treatment
•Chlordiazepoxide(25-100mg) is given when CIWA-Ar ratings
are 8 or more.
•Requires close monitoring as in-patient.
•Not safe in patients with a past history of withdrawal seizures.

45. Withdrawal seizures
•Regardless of the CIWA-Ar score, the occurrence of seizures during the
alcohol withdrawal period is indicative of severe alcohol withdrawal.
•Seizure prophylaxis with lorazepam 2 mg intravenously must be given to all
patients with seizures
•
May require repeated doses
•This strategy helps to prevent the development of DT.

46. Delirium Tremens
•The goal is to achieve a calm, but awake state or light
somnolence defined as a sleep from which the patient is easily
aroused.
•An initial dose of 10 mg diazepam is given intravenously.
Further doses of 10 mg can be repeated every 5-20 min interval.
•Once the goal of light somnolence is achieved, the patient is
shifted to a SML dose regimen.

47. Refractory DT
•High dose IV diazepam
•
• phenobarbital 100-200 mg/h
•
•Haloperidol given in doses of 0.5-5 mg by intramuscular route
every 30-60 min or 2-20 mg/h
•Newer antipsychotics like risperidone (1-5 mg/day) or
olanzapine (5-10 mg/day)
•
•propofol infusion (0.3-1.25 mg/kg/h) in an intensive care setting
has been used in a few cases.

48. Alcoholic hallucinosis
•It is one of the conditions that may cause apparent failure of the
loading dose regimen
• A fixed dose strategy to cover the period of alcoholic
hallucinosis is recommended.
•The patient may be given low doses of antipsychotics like
chlorpromazine 100-200 mg/day or risperidone 1-3 mg/day

49. DE-ADDICTION
•Pharmacological
•Non-pharmacological

50. MANAGEMENT
Pharmacological treatment –
•Deterrant agents
➢ Disulfiram
•Anti-craving agents
➢ Naltrexone
➢Acamprosate

51. DISULFIRAM
•It is an aversive treatment that enhances that enhances
motivation for continued abstinence by making the “high”
unavailable.
•The cognitive awareness of occurrence of Disulfiram-ethanol
reaction prevents a drinking response when exposed to alcohol
use related cues.
•Unpleasant physical effects are due to accumulation of
acetaldhehyde.
•Should always be given after taking informed consent and
supervised therapy is beneficial.

52. Administration
•Before initiation of treatment, the patient should be abstinent
from alcohol for atleast 24 hours.
•Disulfiram alcohol reaction may occur as long as 1-2 weeks
after the last dose of disulfiram.
•Dose- 800mg for the first dose, reducing to 100-200mg daily for
maintenance.
•Contraindications- Cardiac failure, CAD, hypertension, h/o
cerebrovascular disease, liver disease, peripheral neuropathy and
severe mental illness.

53. Adverse drug reactions-
•Drowsiness and gastric irritation.
•Hepatotoxicity
•Skin reactions
•Psychosis

54. Treatment of DER
•Mainly supportive
•For controlling fall in blood pressure- Inotropes may be
required.
•Anti-histaminics
•4-methylpyrazole blocks formation of acetaldehyde

55. NALTREXONE
•Opioid receptor blockade prevents increased dopaminergic
activity after the consumption of alcohol, thus reducing its
rewarding effects.
•Naltrexone can be started when patients are still drinking or
during medically-assisted withdrawal.
•50mg/day is administered for 6 months.
•ADR include nausea, headache, abdominal pain, reduced
appetite and fatigueability, hepatotoxicity at high doses.

56. •Absolute contraindications to naltrexone include-
➢Acute liver failure
➢Current dependence on opiate or opiate withdrawal
➢Need for opiate medications

57. Acamprosate
•Functional glutaminergic NMDA antagonist and increases
GABA ergic function.
•666mg thrice daily for 6 months.
•ADR include diarrhoea, abdominal pain, nausea, vomiting and
pruritis.
•Contraindicated in severe renal or hepatic impairment.

58. Other drugs
•Baclofen
•Topiramate
•Ondansetron
•Gabapentin
•Pregabalin

59. Psychosocial intervention
•Brief Interventions- FRAMES
➢Feedback
➢Personal responsibility
➢Advice
➢Menu
➢Empathy
➢Self-efficacy

60. •Extended interventions
•Relapse prevention
➢Identification and management of specific relapse precipitant
situations/events
➢Maintaining abstinence
➢Correction of psychosocial and physical consequences of drug use
➢Sociooccupational
➢Rehabilitation/reintegration
➢Modifying or reverting underlying neuroadaptive process/changes

61. •Cognitive and Behaviour therapy
•Group therapy
•Family therapy
•Self-help approach- Alcoholic Anonymous