Alcohol withdrawal syndrome is a series of symptoms that can occur after the reduction of alcohol use after a period of excessive use. Symptoms usually include anxiety, tremor, sweating, vomiting, rapid heartbeat, and mild fever. More severe symptoms may include seizures, seeing or hearing things that others do not, and delirium tremens (DTs). Symptoms usually start about six hours after the last drink, the worst at 24 to 72 hours, and improve for seven days.
Alcohol withdrawal can occur in those with alcohol dependence. This may occur after planned or unplanned alcohol deductions. The underlying mechanism involves a decreased response of GABA receptors in the brain. The withdrawal process is usually followed by the Clinical Institute of Alcohol Scale Scaling, revised (CIWA-Ar).
The typical treatment of alcohol withdrawal is with benzodiazepines such as chlordiazepoxide or diazepam. Often the amount given is based on a person's symptoms. Thiamine is recommended routinely. Electrolyte and low blood sugar problems should also be treated. Early treatment improves results.
In the Western world about 15% of people have problems with alcoholism at some point in time. About half of people with alcoholism will develop withdrawal symptoms after reducing their use, with four percent having severe symptoms. Among those with severe symptoms up to 15% died. The symptoms of alcohol withdrawal have been described at least as early as 400 BC by Hippocrates. Not believed to have been a widespread problem until the 1800s.
Video Alcohol withdrawal syndrome
Signs and symptoms
Signs and symptoms of alcohol withdrawal occur mainly in the central nervous system. The severity of the withdrawal may vary from mild symptoms such as sleep disturbances and anxiety to severe and life-threatening symptoms such as delirium, hallucinations, and autonomic instability.
Withdrawals usually begin 6 to 24 hours after the last drink. It can last up to a week. To be classified as an alcohol withdrawal syndrome, patients should show at least two of the following symptoms: increased hand tremor, insomnia, nausea or vomiting, transient hallucinations (hearing, sight or tactile), psychomotor agitation, anxiety, tonic-clonic seizures, and autonomous instability.
The severity of the symptoms is dictated by a number of factors, the most important is the level of alcohol intake, the length of time a person uses alcohol, and previous alcoholic withdrawal history. Symptoms are grouped together and grouped together:
- Alcoholin hallucinosis: the patient has visual, auditory, or tactile hallucinations, but is unclear.
- Seizure withdrawal: seizures occur within 48 hours of discontinuation of the alcohol and occur either as a single general tonic-clonic seizure or as a short episode of multiple seizures.
- Delirium tremens: hyperadrenergic state, disorientation, tremor, diaphoresis, attention/awareness disorders, and visual and auditory hallucinations. This usually occurs 24 to 72 hours after discontinuation of alcohol. Delirium tremens are the most severe form of withdrawal and occur in 5 to 20% of patients with detoxification and 1/3 of patients experience withdrawal seizures.
Progression
Usually the severity of symptoms experienced depends on the amount and duration of previous alcohol consumption as well as the amount and severity of previous withdrawals. Even the most severe of these symptoms can occur as soon as 2 hours after termination; this rapid onset as long as the uncertainty of this syndrome requires a pre-planned hospitalization, a doctor-coordinated treatment, or at least rapid access to medical care; friend or family support systems should also be introduced before handling detoxification. In many cases, however, symptoms follow a reasonably estimated time frame as exemplified below:
Six to 12 hours after the last beverage consumption, withdrawal symptoms such as shaking, headache, sweating, anxiety, nausea, or vomiting occur. Other comparable symptoms may also occur in this period. Twelve to 24 hours after discontinuation, this condition can develop into major symptoms such as confusion, hallucinations (with awareness of reality), tremor, agitation, and similar illnesses.
At 24 to 48 hours after consuming the last ethanol, the possibility of seizures should be anticipated. Meanwhile, no previous withdrawal symptoms will subside. Seizures carry a risk of death for alcoholics.
Although the patient's condition usually begins to improve after 48 hours, withdrawal symptoms sometimes continue to increase in severity and progress to the delirium tremens, characterized by hallucinations indistinguishable from reality, severe confusion, seizures, high blood pressure, and persistent fevers anywhere from 4 to 12 days.
Withdrawal drawn
The protracted alcohol withdrawal syndrome occurs in many alcoholics when withdrawal symptoms continue beyond the acute withdrawal stage but usually at a subacute intensity level and gradually decreases with severity over time. This syndrome is sometimes referred to as post-acute-withdrawal syndrome. Some withdrawal symptoms may persist at least one year after discontinuation of alcohol. Symptoms may include the desire to drink alcohol, the inability to feel the pleasures of the usually pleasant things (known as anhedonia), obscure the sensorium, disorientation, nausea and vomiting or headaches.
Insomnia is a common dotted symptom that continues after the phase of acute alcohol withdrawal. Insomnia has also been found to affect recurrence rates. Research has found that magnesium or trazodone can help treat the ongoing dashed symptoms of insomnia in restoring an alcoholic. Insomnia can be difficult to treat with alcoholics as many traditional sleeping aids (eg, benzodiazepine receptor agonists and barbituric receptor agonists) work through GABA A and cross-tolerant receptor mechanisms with alcohols. However, trazodone is not tolerant of alcohol. The acute phase of alcohol withdrawal syndrome can sometimes be protracted. Spinning of delirium tremens has been reported in the medical literature as a possible but unusual feature of alcohol withdrawal.
Maps Alcohol withdrawal syndrome
Pathophysiology
The use of chronic alcohol causes changes in brain chemistry especially in GABAergic systems. Various adaptations occur such as changes in gene expression and GABA receptor down regulation A . During the withdrawal of acute alcohol, changes also occur such as increased alpha regulation containing GABA receptors A and decreased regulation of alpha1 and alpha3 receptors containing GABA A . The neurochemical changes that occur during alcohol withdrawal can be minimized with drugs used for acute detoxification. With abstinence from alcohol and cross-tolerant drugs this change in neurochemistry gradually returns to normal. Adaptation to the NMDA system also occurs as a result of recurrent alcohol poisoning and is involved in hyper-stimulation of the central nervous system during the alcohol withdrawal syndrome. Homocysteine ​​levels, which increase during chronic drinking, increase further during the withdrawal state, and can lead to excitotoxicity. Changes to ECG (especially increased QT interval) and EEG abnormalities (including abnormally measured EEGs) may occur during early withdrawal. The dysfunction of the hypothalamic-pituitary-adrenal axis and the increased release of corticotropin-releasing hormone occur during both acute and protracted abstinence from alcohol and contribute to both acute and prolonged withdrawal symptoms. Anhedonia/dysphoria symptoms, which can survive as part of a protracted drawdown may be due to lack of dopamine activity.
Kindling
Kindling is a phenomenon in which the detoxification of recurrent alcohol leads to an increase in the severity of the withdrawal syndrome. For example, party drinkers may initially not experience withdrawal symptoms, but with each period of alcohol use followed by discontinuation, their withdrawal symptoms intensify in severity and can eventually produce delirium tremens filled with convulsive convulsions. Alcoholics who experience seizures during detoxification are more likely to have an earlier episode of alcohol detoxification than patients who have not experienced seizures during withdrawal. In addition, patients with earlier withdrawal syndromes are more likely to have more medically complicated alcohol withdrawal symptoms.
Rangsel can cause complications and may increase the risk of recurrence, alcohol-related brain damage and cognitive deficits. Chronic alcohol abuse and firewood through double alcohol withdrawal may cause permanent changes to GABA receptors A . The mechanism behind kindling is the sensitization of some neuronal systems and the desensitization of other nervous systems that leads to higher neurochemical imbalances. This in turn leads to deeper withdrawal symptoms including anxiety, seizures and neurotoxicity.
A drinking party is associated with an increase in impulsivity, a disruption in spatial working memory and emotional learning disruption. These side effects are believed to be due to the neurotoxic effects of repeated withdrawal from alcohols on deviant neuronal plasticity and cortical damage. Recurrent periods of acute poisoning followed by acute detoxification have profound effects on the brain and are associated with an increased risk of seizures as well as cognitive deficits. The effects on the brain are similar to those seen in alcoholics that have been detoxified several times but are not as severe as alcoholics who have no previous detoxification history. Thus acute withdrawal syndrome appears to be the most important factor in causing damage or malfunction of the brain. The part of the brain that is most sensitive to the dangers of binge drinking is the amygdala and prefrontal cortex.
People in adolescence who experience a lot of withdrawal from binge drinking shows long-term nonverbal memory impairment. Alcoholics that have had two or more alcohol withdrawals show more frontal lobe cognitive dysfunction than alcoholics who have experienced one or no previous withdrawal. Kindling neuron is the proposed cause of cognitive impairment related withdrawal. The exile from many withdrawals leads to the accumulation of neuro-regional changes. Twigs can also be the reason for the cognitive impairment seen in party drinkers.
Diagnosis
Many hospitals use the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol to assess the current withdrawal rate and therefore the amount of drug required. When overuse of alcohol is suspected but the history of drinking is unclear, testing for high values ​​of carbohydrate-deficient transferrin or gammaglutamyl transferase may help make the diagnosis of alcohol use and over-dependence more pronounced. CIWA has also been shortened (now called CIWA-Ar), while maintaining its validity and reliability, to help assess patients more efficiently because of the life-threatening nature of life-threatening discontinuation.
Other conditions that may be present together include benzodiazepine withdrawal syndrome (condition is also mainly due to GABA A adaptation receptor).
Treatment
Benzodiazepines are effective for symptom management as well as prevention of seizures. Certain vitamins are also an important part of the management of alcohol withdrawal syndrome. In those with severe hospitalization symptoms are often necessary. In those with lower symptomatic care at home may be possible with daily visits with health care providers.
Benzodiazepines
Benzodiazepines are the most commonly used drugs for the treatment of alcohol withdrawal and are generally safe and effective in suppressing alcohol withdrawal symptoms. This type of drug is generally effective in controlling symptoms, but should be used with caution. Although benzodiazepines have a long history of successfully treating and preventing withdrawal, there is no consensus about which is ideal to use. The most commonly used agents are long-acting benzodiazepines, such as chlordiazepoxide and diazepam. It is believed to be superior to other benzodiazepines for the treatment of delirium and allows for a longer time between dosing. However, medium-term benzodiazepines such as lorazepam may be safer in people with liver problems.
The main debate between the use of long-acting benzodiazepines and short-acting is ease of use. Longer-acting drugs, such as diazepam, may be given less frequent doses. However, evidence exists that "symptom-induced regimens" such as those used when treating with lorazepam, are safe and effective, but have reduced the duration of treatment and the amount of drug used.
Although benzodiazepines are very effective at treating alcohol withdrawal, they should be used with caution. Benzodiazepines should only be used for short periods of alcoholics who are not yet dependent on them, because they share cross-tolerance with alcohol. There is a risk of replacing alcohol addiction with benzodiazepine dependence or adding to other addictions. Furthermore, impaired GABA receptor benzodiazepine function is part of alcohol dependence and chronic benzodiazepines may prevent full recovery of alcohol-induced mental effects. The combination of benzodiazepines and alcohols may reinforce the adverse psychological effects of one another that lead to increased depression effects in mood and increase suicide and are generally contraindicated except for alcohol withdrawal.
Vitamins
Alcoholics often lack a variety of nutrients, which can cause severe complications during alcohol withdrawal, such as the development of Wernicke's syndrome. To help prevent Wernicke's syndrome, alcoholics should be given adequate multivitamin preparations of thiamine and folic acid. During alcohol withdrawal, thiamine prophylaxis, folic acid, and intravenous pyridoxine are recommended before starting any liquid or carbohydrate-containing foods. These vitamins are often incorporated into banana bags for intravenous administration.
Antikonvulsan
Very limited evidence suggests that topiramate or pregabalin may be useful in the treatment of alcohol withdrawal syndrome. Limited evidence supports the use of gabapentin or carbamazepine for the treatment of mild or moderate alcohol withdrawal as the only treatment or as a combination therapy with other drugs; however, gabapentin appears to be ineffective for treatment of severe alcohol withdrawal and is therefore not recommended for use in this setting. The 2010 Cochrane Review also reports that evidence to support the role of anticonvulsants against benzodiazepines in the treatment of alcohol withdrawal is not supported. Paraldehyde in combination with chloral hydrate exhibits excellence over chlordiazepoxide with regard to life-threatening side effects and carbamazepine may have advantages for certain symptoms.
Prevention for further drinking
There are three drugs used to help prevent the return of drinking: disulfiram, naltrexone, and acamprosate. They are used after the withdrawal has occurred.
More
Clonidine can be used in combination with benzodiazepines to help some symptoms. There is insufficient evidence to support the use of baclofen for alcohol withdrawal syndrome.
Antipsychotics, such as haloperidol, are sometimes used in addition to benzodiazepines to control agitation or psychosis. Antipsychotics potentially exacerbate alcohol withdrawal because it lowers the seizure threshold. Clozapine, olanzapine, or low-potency phenothiazines (such as chlorpromazine) are very risky; if used, extreme caution is required.
While intravenous ethanol can theoretically be used, the evidence to support this use, at least in those who are very ill, is inadequate.
Prognosis
Failure to properly manage alcohol withdrawal syndrome can lead to permanent brain damage or death. It has been proposed that brain damage due to alcohol withdrawal can be prevented by administration of NMDA antagonists, calcium antagonists, and glucocorticoid antagonists.
Substances that damage recovery
Continuing use of benzodiazepines may damage recovery from psychomotor and cognitive impairment of alcohol. Cigarette smoking can slow or impair the restoration of brain pathways in restoring an alcoholic.
References
External links
- CIWA-Ar for Alcohol Withdrawal
- Alcohol Detox Guidelines Example
Source of the article : Wikipedia
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