Alcohol withdrawal syndrome is a potentially life-threatening condition that can occur in people who have been drinking heavily for weeks, months, or years and then either stop or significantly reduce their alcohol consumptionAlcohol withdrawal symptoms can begin as early as two hours after the last drink, persist for weeks, and range from mild anxiety and shakiness to severe complications, such as seizures and delirium tremens (also called DTs). The death rate from DTs -- which are characterized by confusion, rapid heartbeat, and fever -- is estimated to range from 1% to 5%.Because alcohol withdrawal symptoms can rapidly worsen, it's important to seek medical attention even if symptoms are seemingly mild. Appropriate alcohol withdrawal treatments can reduce the risk of developing withdrawal seizures or DTs.
Alcohol withdrawal syndrome is the set of symptoms seen when an individual reduces or stops alcohol consumption after prolonged periods of excessive alcohol intake. Excessive use of alcohol leads to tolerance, physical dependence, and an alcohol withdrawal syndrome. The withdrawal syndrome is largely due to the central nervous system being in a hyper-excitable state. The withdrawal syndrome can include seizures and delirium tremens and may lead to excito-neurotoxicity.
Pathophysiology
Alcohol withdrawal syndrome is mediated by a variety of mechanisms. The brain maintains neurochemical balance through inhibitory and excitatory neurotransmitters. The main inhibitory neurotransmitter is γ-amino-butyric acid (GABA), which acts through the GABA-alpha (GABA-A) neuroreceptor. One of the major excitatory neurotransmitters is glutamate, which acts through the N-methyl-D-aspartate (NMDA) neuroreceptor.Alcohol enhances the effect of GABA on GABA-A neuroreceptors, resulting in decreased overall brain excitability. Chronic exposure to alcohol results in a compensatory decrease of GABA-A neuroreceptor response to GABA, evidenced by increasing tolerance of the effects of alcohol.Alcohol inhibits NMDA neuroreceptors, and chronic alcohol exposure results in up-regulation of these receptors. Abrupt cessation of alcohol exposure results in brain hyperexcitability, because receptors previously inhibited by alcohol are no longer inhibited. Brain hyperexcitability manifests clinically as anxiety, irritability, agitation, and tremors. Severe manifestations include alcohol withdrawal seizures and delirium tremens.An important concept in both alcohol craving and alcohol withdrawal is the “kindling” phenomenon; the term refers to long-term changes that occur in neurons after repeated detoxifications. Recurrent detoxifications are postulated to increase obsessive thoughts or alcohol craving. Kindling explains the observation that subsequent episodes of alcohol withdrawal tend to progressively worsen.Although the significance of kindling in alcohol withdrawal is debated, this phenomenon may be important in the selection of medications to treat withdrawal. If certain medications decrease the kindling effect, they may become preferred agents.
Signs and symptoms
The severity of the alcohol withdrawal syndrome can vary from mild symptoms such as mild sleep disturbances and mild anxiety to very severe and life threatening including delirium, particularly visual hallucinations in severe cases and convulsions (which may result in death).These symptoms initially appear characteristically on waking, due to the fall in the blood alcohol concentration during sleep. The severity of alcohol withdrawal depends on various factors including age, genetics[citation needed], and, most importantly, degree of alcohol intake and length of time the individual has been using alcohol and number of previous detoxifications.
-Agitation -Alcoholic hallucinosis
-Anorexia -Anxiety and panic attacks
-Catatonia -Confusion
-Delirium tremens -Depersonalization
-Depression -Derealization
-Diaphoresis -Diarrhea
-Euphoria -Fear
-Gastrointestinal upset -Hallucinations
-Headache -Hypertension
-Hyperthermia (fever) -Insomnia
-Irritability -Migraines
-Nausea and vomiting -Palpitations
-Psychosis -Rebound REM sleep
-Restlessness -Seizures and death
-Tachycardia -Tremors
-Weakness
Progression of symptoms
Typically the severity of the symptoms experienced will depend on the amount and duration of prior alcohol consumption, as well as the number and severity of previous withdrawals. Even the most severe of these symptoms can occur in as little as 2 hours after cessation, therefore the overall unpredictability necessitates either pre-planned hospitalization, treatment coordinated with a doctor, or at the very least fast access to medical care and a supporting system of friends or family should be introduced prior to addressing detoxification. In many cases however, symptoms follow a reasonably predictable time frame as exampled below:Six to 12 hours after the ingestion of the last drink, withdrawal symptoms such as shaking, headache, sweating, anxiety, nausea or vomiting occur. Other comparable symptoms may also exist in this period. Twelve to 24 hours after cessation, the condition may progress to such major symptoms as confusion, hallucinations, (with awareness of reality) tremor, agitation, and similar ailments. It's between the 24 and 48 hour period that seizures typically may begin to emerge among the previous symptoms in the period, and this is where the serious risk of mortality begins. Although most often, the condition begins to improve past the 48 hour mark, it can sometimes continue to increase in severity to delirium tremens, characterized by hallucinations that are indistinguishable from reality, severe confusion, more seizures, high blood pressure and fever which can persist anywhere from 4 to 12 days.
Protracted withdrawal
A protracted alcohol withdrawal syndrome occurs in many alcoholics where withdrawal symptoms continue beyond the acute withdrawal stage but usually at a subacute level of intensity and gradually decreasing with severity over time. This syndrome is also sometimes referred to as the post acute withdrawal syndrome. Some withdrawal symptoms can linger for at least a year after discontinuation of alcohol. Symptoms can include a craving for alcohol, inability to feel pleasure from normally pleasurable things (also known as anhedonia), clouding of sensorium, disorientation, nausea and vomiting or headache. Insomnia is also a common protracted withdrawal symptom which persists after the acute withdrawal phase of alcohol. Insomnia has also been found to influence relapse rate. Studies have found that magnesium or trazodone can help treat the persisting withdrawal symptom of insomnia in recovering alcoholics. Insomnia can be difficult to treat in alcoholics because many of the traditional sleep aids (e.g. benzodiazepine receptor agonists and barbiturate receptor agonists) work via a GABAA receptor mechanism and are cross tolerant with alcohol. However, trazodone is not cross tolerant with alcohol. The acute phase of the alcohol withdrawal syndrome can also occasionally be protracted. Protracted delirium tremens has been reported in the medical literature as a possible but unusual feature of alcohol withdrawal.
Diagnostic Criteria for Alcohol Withdrawal
A. Cessation of (or reduction in) alcohol use that has been heavy and prolonged.
B. Two (or more) of the following, developing within several hours to a few days after criterion A:
1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 beats per minute)
2. Increased hand tremor
3. Insomnia
4. Nausea or vomiting
5. Transient visual, tactile, or auditory hallucination s or illusions
6. Psychomotor agitation
7. Anxiety
8. Grand mal seizures
C. The symptoms in criterion B cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D. The symptoms are not due to a general medical condition and are not better accounted for by another mental disorder.
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.”
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,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 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.Oder -medications includes
-antipschotics
-anticovulsants
-baclofen
-barbiturates
-clomethiazole
-clonidine
-ethanol (low dose)
-flumazenil
-trazodone
-magnesium
Prevention of brain damage
Failure to manage the alcohol withdrawal syndrome appropriately can lead to permanent brain damage or death. It has been proposed that brain damage due to alcohol withdrawal may be prevented by the administration of NMDA antagonists, calcium antagonists, and glucocorticoid antagonists. The NMDA antagonist acamprosate reduces excessive glutamate rebound thereby suppressing excitotoxicity and potential withdrawal related neurotoxicity. A cheaper, non prescription substance would be dextromethorphan, with is metabolized into dextrothrophan, which has calcium channel and NMDA blocking effects. Any NMDA antagonist is likely to be of benefit in alcohol withdrawal, due to the upregulated nature of ligand gated calcium channels due to the downregulated GABAA Cl- channel.
Substances impairing recovery
Continued use of benzodiazepines may impair recovery from psychomotor and cognitive impairments from alcohol. Cigarette smoking may slow down or interfere with recovery of brain pathways in recovering alcoholics.
