ALCOHOL WITHDRAWAL

Introduction

Alcohol withdrawal symptoms manifest following cessation or substantial reduction in

alcohol consumption among individuals who have developed a sustained dependence on
the substance over an extended period.

AW syndrome varies significantly among alcoholics in both its clinical manifestations and its
severity. These manifestations1 can range from mild insomnia to severe consequences, such
as delirium tremens (DT’s) and even death. The reported mortality rate for patients who
experience delirium tremens is anywhere from 1 to 5%.

Pathophysiology

There are several mechanisms play role in development in alcohol withdrawal. Researchers
first suggest it occur due to nutritional deficiency and complications such as seizures caused
by direct influence from alcohol use or intoxication.

Although alcoholic patients exhibit many metabolic and nutritional disturbances,

overwhelming laboratory and clinical evidence now indicates that the array of signs and
symptoms known as AW is due to disruption of the CNS by chronic exposure to alcohol.

The theory positing that withdrawal phenomena arise from a lack of adequate alcohol
intake or abstinence among individuals with alcohol dependence, rather than stemming
from nutritional deficits, found support in an initial investigation involving male subjects
who were provided substantial daily alcohol doses. These participants, who maintained
satisfactory nutritional status, each consumed nearly 30 standard alcoholic beverages per
day over a period of up to three months. Upon cessation of this habitual alcohol
consumption, they consistently exhibited symptoms of withdrawal. Furthermore, the
severity of alcohol withdrawal symptoms correlated with the magnitude of alcohol
consumption: individuals who ingested larger quantities of alcohol experienced more
pronounced manifestations of withdrawal, including hallucinations, seizures, and delirium
tremens.

Our CNS system has 2 types of neurotransmitters. Exhibitory and inhibitory

neurotransmitters. Normally, these 2 neurotransmitters’ effects are balanced. But regular
alcohol intake affects to this system. As an illustration, scientific investigations have
illustrated that alcohol amplifies the inhibitory influence of gamma-aminobutyric acid
(GABA) on neurons responsible for receiving signals, resulting in the suppression of neuronal
activity. Nonetheless, prolonged exposure to alcohol leads to a diminished responsiveness
of GABA receptors to this neurotransmitter, necessitating higher alcohol concentrations to
achieve comparable levels of neuronal suppression. This phenomenon, observed clinically, is
termed tolerance.

Upon the cessation of alcohol consumption in this adapted neurological system, the GABA
receptors retain their reduced responsiveness, resulting in an imbalance that favors
excitatory neurotransmission. This imbalance is compounded by alcohol-induced

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upregulation of a specific subtype of receptors for the excitatory neurotransmitter,
glutamate. Even after alcohol withdrawal, the abundance of these receptors remains
elevated, perpetuating heightened excitatory neurotransmission. Both of these mechanisms
collectively contribute to the neuronal hyperexcitability characteristic of alcohol withdrawal.

Clinical Features of Alcohol Withdrawal

Alcohol withdrawal can be categorized into three stages:

1.mild 2. Moderate 3. severe.

Mild signs/symptoms may appear within six hours of stopping alcohol consumption. Mild
symptoms are elevated blood pressure, insomnia, tremulousness, hyperreflexia, anxiety,
gastrointestinal upset, headache, palpitations, shaky hands, nausea, vomiting and sweating

Presentation and range of sysmptoms are depend on several factors such as on the patient,
their duration of alcohol dependence, and the volume typically ingested.

If symptoms do not progress to more severe symptoms within 24 to 48 hours, the patient
will likely recover.

Hallucinations and alcohol withdrawal seizures can occur 12 to 24 hours after cessation of
alcohol. These are moderate symptoms and signs. These symptoms can last up to 5–7 days
and require medical attention. There is a 3% incidence of status epilepticus in these
patients. About 50% of patients who have had a withdrawal seizure will progress to delirium
tremens.

Severe signs and symptoms are typically occur within 2–3 days after the last drink. Delirium
tremens is the most severe form of alcohol withdrawal, and its hallmark is that of an altered
sensorium with significant autonomic dysfunction and vital sign abnormalities. It includes
visual hallucinations, tachycardia, hypertension, hyperthermia, agitation, and diaphoresis.
Symptoms of delirium tremens can last up to seven days after alcohol cessation and may
last even longer.

Some features that may increase your suspicion that a patient is susceptible to severe
withdrawal include a previous history of delirium tremens, as well as a history of low
platelets (thrombocytopenia) or low potassium levels (hypokalemia).

Risk Factors

Risk factors can severe withdrawal symptoms; prolonged symptoms; or withdrawal-specific

complications, such as DT’s or seizures. These factors include, more severe alcohol
dependence, including prior development of withdrawal symptoms, higher levels of alcohol
intake, resulting in higher bac’s, longer duration of alcoholism, abnormal liver function, prior
detoxification, past experience of seizures or DT’s, intense craving for alcohol, concomitant
acute illness, older age (greater than 65), use of other drugs in addition to alcohol, more
severe withdrawal symptoms when presenting for treatment, heavy daily alcohol use,
coexisting health conditions, dehydration, electrolyte imbalances, and brain lesions.

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Assessment and Diagnosis

Before start treatment doctor should do assessment and diagnosis about patient’s situation.
We should evaluation of the presence of coexisting medical and psychiatric conditions, the
severity of the withdrawal symptoms, and the risk of withdrawal complications. This done
through an excellent history and performing a thorough physical examination.

The symptoms of withdrawal are not specific and easily can be confused with other medical
conditions. Patients with suspicion for alcohol withdrawal should be evaluated for other
underlying disease processes such as dehydration, infection (pneumonia and meningitis),
cardiac issues, electrolyte abnormalities, gastrointestinal bleeding, subdural hematoma, and
traumatic injury. Similarly, during the initial assessment, it's essential to differentiate
seizures and delirium tremens (DTs) from other potential medical conditions. For instance,
DTs, characterized by acute confusion, can resemble delirium stemming from diverse
medical origins like encephalitis, meningitis, medication side effects, or Wernicke's
encephalopathy. Likewise, seizures associated with alcohol withdrawal must be discerned
from seizures caused by alternate factors such as mineral imbalances, electrolyte
disturbances, strokes, brain tumors, epilepsy, or subdural hematoma. Therefore, diagnosing
DTs and alcohol withdrawal seizures should only occur following the exclusion of other
plausible explanations for these complications.

The Clinical Institute for Withdrawal Assessment for alcohol revised scale (CIWA-Ar) is a tool
used to assess the severity of alcohol withdrawal symptoms. The tool allows clinicians to
monitor for the signs and symptoms of withdrawal and determine who needs medical
therapy. The features that are used for the CIWA-Ar scale include the presence of:

 Nausea and vomiting

 Headache
 Auditory disturbances
 Agitation
 Paroxysmal sweating
 Visual disturbances
 Tremor
 Clouding of sensorium
 Orientation
 Anxiety

Complications

A comprehensive evaluation should anticipate the common health issues that often arise in
individuals undergoing alcohol withdrawal. These complications might encompass, gastritis,
gastrointestinal bleeding, liver disease,cardiomyopathy, pancreatitis, disturbances in the
electrolyte balance (e.g., alcohol ketoacidosis and abnormally low levels of magnesium in
the blood), deficiency of the vitamin folate, which can cause lower-than-normal numbers of
blood cells and deficiency of the vitamin thiamine, which can lead to serious neurological
problems, such as wernicke’s encephalopathy.

Treatment

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Based on the patient’s score on the CIWA–Ar, the physician determines the appropriate
treatment.
In monitoring phase, monitor the patient by administering the CIWA–Ar1 test every 4 to 8
hours until the score has been lower than 8 to 10 points for 24 hours and use additional
assessments as needed.
Use symptom-triggered regimens. Perform the CIWA–Ar every hour to assess the patient’s
need for medication and administer one of the following medications every hour when the
CIWA–Ar score is at least 8 to 10 points:
—Chlordiazepoxide (50–100 milligrams [mg])
—Diazepam (10–20 mg)
—Lorazepam (2–4 mg)
Fixed-schedule regimens : Administer one of the following medications every 6 hours:
—Chlordiazepoxide (4 doses of 50 mg, then 8 doses of 25 mg)
—Diazepam (4 doses of 10 mg, then 8 doses of 5 mg)
—Lorazepam (4 doses of 2 mg, then 8 doses of 1 mg)
Provide additional medication if these regimens do not control the symptoms (i.e., the
CIWA–Ar score remains at least 8 to 10 points)

Patients should be kept sedated in a controlled environment to try to minimize the risk of
mild symptoms progressing to hallucinations. With mild to moderate symptoms, patients
should receive supportive care such as intravenous rehydration, correction of electrolyte
abnormalities. Patients with mild withdrawal symptoms (i.e., CIWA–Ar scores of 8 or less)
and no increased risk for seizures can be managed without specific pharmacotherapy.

Patients who experience more severe withdrawal (i.e., who have CIWA-Ar scores of 8 to 15
or greater) should receive pharmacotherapy to treat their symptoms and reduce their risk of
seizures and DT’s. The medications with the best efficacy and safety are the
benzodiazepines. Like alcohol, these agents enhance the effect of the neurotransmitter
GABA on the brain. Because of their similar effects, benzodiazepines and alcohol are cross-
tolerant—in other words, a person who is tolerant to alcohol also is tolerant to
benzodiazepines. Cross-tolerance also implies that when a person experiences a deficiency
of one agent (e.g., alcohol during withdrawal), the other agent (e.g., a benzodiazepine) can
serve as a substitute, thereby easing the withdrawal symptoms.

Patients need to understand that successful treatment of alcohol withdrawal syndrome is

only the initial step that must lead to long-term abstinence to be successful. Abstinence is
not likely unless the patient enrolls in a long-term treatment program. These programs can
include individual counseling, group meetings, and long-term medications to reduce the risk
of relapse.

Patients with a history of alcohol dependence may have confounding social or underlying
psychiatric issues that one should also be aware of once they are stabilized. They will likely
require a multidisciplinary approach before discharge.

Reference

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1. American Psychiatric Association. (2013). Diagnostic and statistical manual of
mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing
2. “Alcohol Withdrawal.” Cleveland Clinic,
my.clevelandclinic.org/health/diseases/alcohol-withdrawal.
3. “Alcohol Withdrawal: MedlinePlus Medical Encyclopedia.” Medlineplus.gov,
2018, medlineplus.gov/ency/article/000764.htm.
4. Egholm, Julie WM, et al. “Perioperative Alcohol Cessation Intervention for
Postoperative Complications.” Cochrane Database of Systematic Reviews, vol. 11,
no. 11, 8 Nov. 2018, https://doi.org/10.1002/14651858.cd008343.pub3.
5. Mary Jo DiLonardo. “What Is Alcohol Withdrawal?” WebMD, WebMD, 6 Oct.
2010, www.webmd.com/mental-health/addiction/alcohol-withdrawal-symptoms-
treatments.
6. Newman, Richard K., et al. “Alcohol Withdrawal.” PubMed, StatPearls
Publishing, 2023,
www.ncbi.nlm.nih.gov/books/NBK441882/#:~:text=Withdrawal%20has%20a
%20broad%20range.