Case

 36 year old indian gentleman , not known to have any chronic

illness, heavy alcohol consumer for 20 year.
 He use to consume one and half bottle daily for the last 3 years.
 He stopped from the past 6 days.
 Presented to a/e with:
confusion
irrelevant talking
restless,irritable,agetated
visual hallucinations of snakes on floor,
 No loss of consiousness, headache,or blurring of vision.
 No fever or hx of trauma.
 No past medical or surgical history.
 No allergy to any medicine.
 ON examination:
 Vitally stable.
 Fully conscious,oriented,
 easily distracted, Irrelevant talking, no tremors other CNS
examinations were normal.
 Chest was clear.
 CVS:s1+s2 normal
 Abdomen was soft , no organomegally.
 Investigation:
 Fbc result was normal.
 Urea and elect :normal
 LFTS:ALAT 88 (normal>41),bilirubin 2.6, TP:9.6(normal
>8.7),globulin 5(normal 2-3.4).
 Glucose:196(increased).
 Diagnosis was ALCOHOL WITHDRAWAL.
• Alcoholism is such a common condition that virtually every clinician is
confronted with its complications.

• There are an estimated 8 million alcohol-dependent people in uited states,

around 500,000 episodes of withdrawal occur each year and it is severe
enough to require pharmacologic treatment.
• Pathophisiology:
• It is not clearly known why some people suffer from more severe
withdrawal symptoms than others.

• Symptoms of alcohol withdrawal occur because alcohol is a central

nervous system depressant.
• Also altered levels of several neurotransmitters have been noted:

• Gamma-aminobutyric acid:
(GABA) is the major neurotransmitter in the brain.
Its receptor is downregulated and its neuronal activity decreased in alcohol
withdrawal, resulting in hyperarousal.

• Norepinephrine:
elevated levels of norepinephrine are found in the cerebrospinal fluid of
patients withdrawing from alcohol ,and are believed due to a decrease in the
alpha-2-receptor-mediated inhibition of presynaptic norepinephrine
release.this may explain some reported benifets of clonidine as it potentiates
alpha-2 receptor activity in the brain.(but still it is not used in the
management of alcohol withdrawal).

• Serotonin:
Serotonin and its degradation products have been involved in alcohol
tolerance, some of the byproducts of alcohol metabolism such as
acetaldehyde , have shown to increase “appetite” for alcohol and contribute to
their addiction.
• Minor withdrawal symptoms:
• This is due to central nervous system and
sympathetic hyperactivity,they include:
• Insomnia
• Tremulousness
• Mild anxiety
• Gastrointestinal upset
• Headache
• Diaphoresis
• Palpitations
• Anorexia
• Symptoms usually are present within six hours of
the cessation of drinking ,and they resolve within 24
to 48 hours.
• Withdrawal seizures:

• Withdrawal associated seizures are generalized tonic-clonic

convulsions, that usually occur within 48 hours after the last
drink, and may occur after two hours of abstinence.

• Approximately 3% of chronic alcoholics have withdrawal –

associated seizures and of those patients 3% develop status
epilepticus.

• It usually occurs in patients with along history of chronic

alcoholism .

• Recurrent or prolonged seizures should prompt an

investigation into possible structural or infectious etiologies
for seizures ,generally by C.T scan or lumbar puncture.
• Alcoholic hallucinosis:

• Alcoholic hallucinosis refers to

hallucinations that develop within 12 to 24
hours of abstinence and resolve within 24
to 48 hours.

• They are usually visual, although auditory

and tactile phenomena may also occur.
• Delirium tremens:
• 5% of patients who undergo withdrawal from alcohol
suffer from delirium tremens.
• It is a syndrome characterized by :
• Hallucinations
• Disorientation
• Tachycardia
• Hypertension
• Low grade fever
• Agitation
• Diaphoresis
• Dts typically begin between 48 and 96 hours after the last
drink and last one to five days.
• Risk factors for the development of DTs :
A history of sustained drinking
A history of previous DTs
Age greater than 30
The presence of concurrent illness
A greater number of days since last drink( for
example patient who present more than two days after their
last drink for treatment of alcohol withdrawal are more likely
to experience DTs than those who present within two days).
• The condition is associated with mortality
rate of up to5 %.

• Death is usually due to arrhythmias or

complicating illness such as pneumonia,
older age and high body temp (more than
104f) are associated with high risk of
mortality.

• Patients with DTs have significantly

elevated cardiac indices, oxygen delivary,
and oxygen consumption.

• Arterial PH rises due to hyperventilation,

which may be a rebound effect related to
the respiratory depressant properties of
alcohol.
• Hyperventilation and consequent respiratory alkalosis in
this setting result in a significant decrease in cerebral blood
flow .

• Withdrawal may also have an important impact on fluid and

electrolyte status:
• Almost all patients in acute withdrawal are dehydrated as a
result of diaphoresis, hyperthermia, vomiting, and
tachypnea.
• Hypokalemia is common due to renal and extra-renal losses,
alterations in aldosterone levels, and changes in potassium
distribution across the cell membrane.

• Hypomagnesemia occurs frequently with DTs and may

predispose to withdrawal seizures

• Hypophosphatemia may occur due to malnutrition, may be

symptomatic, and if severe, may contribute to cardiac failure
and rhabdomyolysis.
• Management :

• Withdrawal is a diagnosis of exclusion, infection, trauma, metabolic

derangements, drug overdose, hepatic failure, or gastrointestinal bleeding
can occur alone or together with withdrawal symptoms.

• Volume deficits can be calculated and replaced accordingly or, if there

are no contraindications, isotonic intravenous fluid can be infused rapidly
until patients are clinically euvolemic.

• Thiamine 100 mg IV or IM, should be administered prior to any glucose-

containing solutions in order to decrease the risk of precipitating
Wernicke's encephalopathy (WE) or Korsakoff's syndrome (KS).

• Multivitamins containing or supplemented with folate should be given

routinely, and deficiencies of potassium, magnesium, glucose, and
phosphate should be corrected as needed.

• Patients considered at high risk for complications should be monitored in

an intensive care unit
• Benzodiazepines:

Benzodiazepines are used to treat the psychomotor agitation most patients

experience during withdrawal and to prevent progression from minor
withdrawal symptoms to major one.
• Diazepam (valium) and chlordiazepoxide (Librium) are used most
frequently to treat or prevent alcohol withdrawal, but other
benzodiazepine agents also can be used.

• lorazepam (Ativan) and oxazepam (serax) may be useful in the

treatment of patients with advanced cirrhosis because of their shorter
half-life, which may prevent prolonged effects.

• Agents that are available in parenteral form (eg, lorazepam, diazepam)

may be necessary in patients who cannot receive oral medications.
• Route of administration

• Oral formulations are preferred in most settings, but parenteral

therapy is appropriate for patients with seizures or DTs
because rapid therapy is needed and patients may be unable
to swallow pills.

• Intravenous diazepam, 5 to 10 mg IV every five minutes until

the patient is calm but awake, is recommended for most
patients. In general, intramuscular administration should be
avoided because of variable drug absorption.

• If there is no safe alternative route, intramuscular

administration lorazepam can be used .