Alcohol Withdrawal Syndrome (AWS)
Alcohol withdrawal syndrome is intermediated by a mixed bag of
mechanisms. The mind maintains neurochemical symmetry through
repressive and excitant neurotransmitters. The principal
inhibitory neurotransmitter is gamma-aminobutyric acid (GABA),
that works through the GABA-alpha (GABA-A) neuroreceptor. One of
the major excitant neurotransmitters is glutamate, which behaves
through the N-methyl-D-aspartate (NMDA) neuroreceptor.
Alcohol raises the outcome of GABA on GABA-A neuroreceptors,
resulting in diminished total brain excitability. Habitual
exposure to alcohol results in a compensative decrease of GABA-A
neuroreceptor response to GABA, proved by increasing tolerance
of the outcomes of alcohol.
Alcohol subdues NMDA neuroreceptors, and Habitual alcohol
exposure results in up regulating of these receptors. Sharp
cessation of alcohol exposure results in head hyperexcitability,
because receptors previously subdued by alcohol are no longer
suppressed. brain hyperexcitability demonstrates clinically as
anxiousness, surliness, agitation, and tremors. Terrible
materializations include alcohol withdrawal seizures and
delirium tremens.
An crucial conception in both alcohol craving and alcohol
withdrawal is the kindling phenomenon; the term refers to
long-term changes that happen in neurons following duplicated
detoxifications. Recurrent detoxifications are postulated to
step-up obsessional thoughts or alcohol craving. Kindling
explicates the observance that subsequent installments of
alcohol withdrawal tend to progressively worsen.
Although the implication of kindling in alcohol withdrawal is
deliberated, this phenomenon may be significant in the selection
of medicines to address withdrawal. If certain medications
reduction the kindling result, they might become preferable
agents
Differential Diagnosis
Alcohol withdrawal syndrome can be confused with other
conditions. Thyrotoxicosis, anticholinergic drug poisoning, and
amphetamine or cocaine use can result in signs of increased
sympathetic activity and altered mental status. Central nervous
system infection or hemorrhage can cause seizures and mental
status changes. Withdrawal from other sedative-hypnotic agents
causes symptoms similar to those occurring in alcohol withdrawal
syndrome.
Goals of Treatment
The American Society of Addiction Medicine lists three immediate
goals for detoxification of alcohol and other substances: (1)
"to provide a safe withdrawal from the drug(s) of dependence and
enable the patient to become drug-free"; (2) "to provide a
withdrawal that is humane and thus protects the patient's
dignity"; and (3) "to prepare the patient for ongoing treatment
of his or her dependence on alcohol or other drugs."6
General Care
Abnormalities in fluid levels, electrolyte levels, or nutrition
should be corrected. Intravenous fluids may be necessary in
patients with severe withdrawal because of excessive fluid loss
through hyperthermia, sweating, and vomiting. Intravenous fluids
should not be administered routinely in patients with less
severe withdrawal, because these patients may become
overhydrated.
Routine administration of magnesium sulfate has not been shown
to improve withdrawal symptoms,9 but supplementation is
appropriate if a patient is hypomagnesemic. Multivitamins and
thiamine (100 mg per day) should be provided during treatment
for alcohol withdrawal. If intravenous fluids are administered,
thiamine (100 mg intravenously) should be given before glucose
is administered, to prevent precipitation of Wernicke's
encephalopathy.
Medication Regimens
Medication can be administered using fixed-schedule or
symptom-triggered regimens (Table 3).10 With a fixed-schedule
regimen, doses of a benzodiazepine are administered at specific
intervals, and additional doses of the medication are given as
needed based on the severity of the withdrawal symptoms. In a
symptom-triggered regimen, medication is given only when the
CIWA-Ar score is higher than 8 points.
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