Guidelines for the diagnosis and treatment of chronic alcoholic toxic encephalopathy in China expert consensus

Chronic alcoholic toxic encephalopathy

Chronic alcoholic toxic encephalopathy is a common disease all over the world, and the harm to human health is becoming increasingly serious
.
With the gradual improvement of the living standards of Chinese residents, its incidence is also increasing
.
The results of the 1993 results of the epidemiological survey of mental illness in seven regions of the country showed
.
The lifetime prevalence of alcohol abuse (0.
68%) has risen to 4th
among psychiatric disorders.
Since the beginning of the 21st century, the proportion of drinking people in China has been increasing, and the incidence of alcohol-induced neuropsychiatric disorders has continued to rise, and has become a prominent or even ranked first neuromental health problem
in many regions.
In 2010-2012, the drinking rate of residents aged 15 and over was 34.
3%, the drinking rate of men (54.
6%) was about 4.
1 times that of women (13.
3%), and the highest drinking rate was among people aged 45-59 (38.
6%), of which the excessive drinking rate was 30.
4% among drinkers, and the male (34.
8%) was higher than that of female (11.
7%)
。 The results of the survey on diseases and alcohol consumption in the Department of Internal Medicine of West China Hospital of Sichuan University from 1999 to 2008 also showed that alcohol-related internal medicine diseases accounted for a high proportion of inpatients in general hospitals, and involved multiple organs and systems, such as type 2 diabetes, liver cirrhosis, stroke, etc
.

Chronic alcoholic toxic encephalopathy is an important manifestation
of alcohol abuse and alcoholism.
The damage caused by alcoholism to human brain tissue, as well as the family, medical and social problems that accompany it, lead to the waste
of a large number of social resources (such as medical services, social security, etc.
).
At present, some neurologists still cannot diagnose and treat the disease in a timely and accurate manner, prolonging the diagnosis time and even delaying the treatment of
patients.

In order to promote the attention and understanding of domestic neurologists on chronic alcoholic toxic encephalopathy, popularize the standardized diagnosis and treatment of chronic alcoholic toxic encephalopathy, and help clinicians make correct decisions on the diagnosis and treatment of chronic alcoholic toxic encephalopathy, the Brain and Spinal Cord Injury Professional Committee of the Neurologist Branch of the Chinese Medical Doctor Association reached the following consensus
on the relevant principles of clinical diagnosis and treatment of chronic alcoholic toxic encephalopathy after extensive discussion, combined with the existing research and clinical evidence at home and abroad.

1 Definition of chronic alcoholic toxic encephalopathy

Alcoholic toxic encephalopathy includes acute and chronic alcoholic toxic encephalopathy
.
Chronic alcoholic toxic encephalopathy refers to a chronic, easily recurrent brain disease caused by long-term drinking caused by alcohol acting on brain tissue, which is a serious poisoning of the central nervous system caused by long-term excessive drinking, and almost all patients have the pathogenesis of
chronic alcohol dependence syndrome.

2 Clinical manifestations and features of chronic alcoholic toxic encephalopathy

According to the clinical manifestations of patients, the onset of the disease, the length of the disease, etc.
, chronic alcoholic toxic encephalopathy is divided into six syndromes
: Wernicke encephalopathy, Korsakoff syndrome, chronic alcoholic toxic dementia, alcoholic tremor-delirium, alcoholic epilepsy, and alcoholic mental and behavioral disorders.

1 Wernicke encephalopathy

A typical patient with Wernicke's encephalopathy presents with three characteristic sets of symptoms: ophthalmoplegia, psychiatric abnormalities, and ataxia.

More acute or subacute onset, vomiting and nystagmus are the earliest symptoms, ophthalmoplegia is one of
the characteristic manifestations of the disease.

Ataxia often follows ocular symptoms
.
Most patients have severe symptoms at first and progress to difficulty standing and walking within a few days; Mild patients have cerebellar ataxia, with a wide step base when walking, which is easy to fall; Individual patients may also be accompanied by slurred speech and incoherent arthria
.
More than 80% of patients have psychiatric symptoms, but sometimes the manifestations are insidious and require careful examination
by a physician.

2 Coossakov syndrome

Also known as alcohol amnesia syndrome
.

Typical clinical manifestations include amnesia, fiction, misarthronism, cognitive dysfunction, disorientation, and personality changes
.

These clinical manifestations are often based on cognitive dysfunction, decreased learning ability, and personality changes
.
Patients often fail to retain new information and show forgetting, but in order to fill the gap in this regard, the patient describes events that have occurred in the past time as having occurred at this time, or fills in the forgotten passage with a ridiculous, changeable, rich and diverse fictional fact, and firmly believes in it
.
In addition, patients often show indifference in personality, lack of initiative, lack of initiative and concern for the surrounding personnel, but sometimes appear selfish and stubborn, euphoric and superficial, or emotional fluctuations are very intense
.

3 Chronic alcohol toxic dementia

It is a pronounced cognitive dysfunction due to chronic alcoholism, which can develop from Wernicke's encephalopathy or Korsakov syndrome, a significant decline in personal life capacity, slovenliness, poor personal hygiene, and the need to drink more than anything
.
Late speech function is also seriously impaired, can only speak, and finally bedridden, urinary incontinence, and death
due to various complications.

4 Alcoholic tremor - delirium

The disease can be triggered by some factors that weaken the body's resistance
, such as trauma and infection.
The classic prodrome is insomnia, fear, and tremor, and the classic triad is delirium with vivid hallucinations or delusions, behavioral disturbances, and overt tremor
.
Tremor is mostly gross tremor, especially in fingers, face, tongue and other parts, sometimes lack of regularity, manifested as rocking tremor
.
Delirium appears within a few days, the patient loses orientation, accompanied by a variety of vivid hallucinations, mainly visual hallucinations, often accompanied by misrepresentation and fiction
.
It may be accompanied by delusions of victimization, and even suicidal or self-injury or aggression, impulsive manifestations
.
The disease usually lasts for several days, and patients usually have no memories
of the experience.
The case fatality rate is lower in patients without complications with prompt management, but significantly higher
when complications (eg, pneumonia, heart failure) occur.

5 Alcoholic epilepsy

The clinical manifestations are a variety of types of seizures, with generalized tonic-clonic seizures being common, and status epilepticus
in severe cases.

6 Alcoholic mental and behavioral disorders

Includes withdrawal from long-term alcohol use disorder and accompanying personality, mood disorder, or psychotic disorder
.
Mood disorders are often manifested as depression, anxiety and other manifestations, patients have mixed emotions, changeable, poor stability, long duration, poor response to drugs, and accompanied by personality abnormalities, hallucinations, sleep disorders, or cognitive dysfunction
.

3 Pathological and imaging manifestations of chronic alcoholic toxic encephalopathy

(1) Pathological manifestations of chronic alcoholic toxic encephalopathy

Different types of syndromes may have different pathologic manifestations
.
The pathological characteristics of central myelinolysis of the pontine brain are symmetrical demyelinating at the center of the base of the pontine, starting from the middle suture and developing to both sides, the myelin sheath is severely lost, but the nerve cells and axons are still relatively intact and there is no inflammatory response; In severe cases, the lesion may spread to the pontine cover and spread upward to the midbrain, but does not involve the subleptomeninges and periventricular areas
.
The pathology of corpus callosum (Marchiafava-Bignami disease) is characterized by symmetrical demyelinating, necrosis, and atrophy of the corpus callosum, and often involves nearby white matter and central pons white matter
.
The pathology of Wernicke's encephalopathy-like changes is manifested as small focal hyperemia and hemorrhage in the upper brainstem, hypothalamus and periventricles (third ventricle and aqueduct), which can be manifested as cellular edema, vasogenic edema, neuronal degeneration, necrosis, deletion, relaxation of nerve fibers, myelin sheath structural degeneration, necrosis, astrocytes, oligodendrocytes and capillary hyperplasia, intracellular edema and spotted hemorrhage
.

(2) Imaging manifestations of chronic alcoholic toxic encephalopathy

1.
Head CT scan: Degeneration of corpus callosum can be manifested as symmetrical low-density opacities of corpus callosum pressure, body and knee on CT, and enhanced scanning is not enhanced
.
Wernicke's encephalopathy shows low-density changes in the aqueduct area of the midbrain on CT, but due to the low resolution of CT, the sensitivity and accuracy are not ideal
.
Low-density changes in bilateral paraventricles adjacent to the thalamus or around aqueducts can also be seen on CT, and papillary body density changes can also be seen, but sensitivity and specificity are low
.

2.
Head MRI examination: At present, MRI is an ideal imaging method for chronic alcoholic toxic encephalopathy, with a sensitivity of about 50% and a specificity of about 90%.

Non-MRI T2WI sequence can detect symmetric abnormal signals in the bilateral thalamus and brainstem in patients with chronic alcoholic toxic encephalopathy, and its typical changes are symmetric long T2 signals around the third ventricle and aqueduct, and papillary body atrophy, which is considered to be a characteristic neuroimaging abnormality
of chronic alcoholic toxic encephalopathy.
A marked reduction in the volume of the nipple body is a particular marker of
thiamine deficiency.
White matter demyelination on MRI can be manifested as multiple punctate or patchy long T1 long T2 signal shadows around the subcortical white matter and lateral ventricles, and corpocysts, cavitation, and division of corpus callosum and suggest that stratification necrosis of corpus callosum is a typical manifestation of
chronic alcoholic toxic white matter injury.
In the early stages of chronic alcoholic toxic encephalopathy, MRI shows an increase in T2WI signal in the third ventricle and the area around the aqueduct; During the recovery period (June-December), the T2WI high signal will gradually decrease or disappear.

In addition, abnormal signal foci of Wernicke encephalopathy on MRI often manifest as T1 long T2 signals such as bilateral symmetry, most commonly around the third and fourth ventricles, around the aqueduct, and in the papillary body, quadrilogue, and thalamus
.
Central myelin sheath of pontine brain is manifested on MRI as a long T1 long T2 abnormal signal of bilateral symmetry at the base of the pontine, no mass effect, generally does not invade the midbrain and invades the central fibrous tract backwardly, the lesion often involves the prefrontal lobe, and the enhanced scan is not enhanced
.
Degeneration of corpus callosum on MRI mainly involves the central layer of corpus callosum, mostly distributed along the long axis of corpus callosum, and the transection shows bilateral symmetry of the lesion, equal or slightly lower signal on T1WI, high signal on T2WI, and the boundary is blurred, and the sagittal T2WI can show that the upper and lower edges of the corpus callosum are not affected, thus forming a layered change, that is, the "sandwich biscuit sign"
.
The corpus callosum in the acute stage is mainly marked by swelling, the corpus callosum in the subacute stage can be normal or mildly swollen and atrophied, and the corpus callosum atrophies
in the chronic stage.
Extensive cortical cerebral atrophy on MRI manifests as age-inappropriate extensive cortical atrophy, thinning of the cortex, widening of the sulci and gyrus, partly with white matter demyelination, or coexisting
with other types of brain damage.
The imaging characteristics of cerebellar degeneration are cerebellar atrophy, mainly cerebellar vermist atrophy, severe cerebellar cortex, vermise and olive body atrophy, accompanied by enlargement
of brain cisterns such as annular cistern, supracerebellar cistern and occipital large cistern.

The magnetic resonance fluid attenuate inversion recovery (FLAIR) sequence clearly shows abnormal signals
in the lateral ventricles.
Because alcohol damage to the blood-brain barrier is slow and insidious, MRI contrast is not very helpful in the diagnosis of chronic alcoholic toxic encephalopathy, but in some cases it is beneficial to the differential diagnosis
of other diseases.
Magnetic resonance diffusion-weighted imaging (DWI) sequences may be more sensitive (increased signal expression)
to early white matter foci of chronic alcohol-toxic encephalopathy.
Magnetic resonance spectroscopy (MRS) of the brain in patients with chronic alcohol-toxic encephalopathy often shows a decrease in the N-acetylaspartate/creatine ratio (NAA/Cr) of the thalamus and cerebellum, while the ratio increases after response to thiamine therapy and is consistent with clinical improvement, so MRS can be used to compare
the efficacy before and after treatment of chronic alcoholic toxic encephalopathy.

4 Screening, evaluation and clinical diagnosis of chronic alcoholic toxic encephalopathy

(1) Screening and evaluation scale for chronic alcoholic toxic encephalopathy

Appropriate use of chronic alcohol toxic encephalopathy screening and assessment scales can help clinicians improve the efficiency and accuracy of diagnosis
.
The CAGE scale includes 4 easy-to-understand questions that are commonly used
in clinical practice.
The drawback of the CAGE scale is that it does not cover acute alcoholic toxic brain injury caused by heavy drinking at one time, while the alcohol use disorders identification test (AUDIT) makes up for the shortcomings
of the CAGE scale.
The AUDIT scale consists of 10 questions that take the clinician about 2-3 minutes to complete, and finally gives a score
of 0-40.
Although the accuracy of the AUDIT scale has improved, its clinical efficiency is low
.
Combined with foreign clinical applications, we recommend using a simplified clinical version of the AUDIT scale, such as the AUDIT-C scale, the fast alcohol screening test (FAST) scale, the AUDIT-PC scale, or the Five-SHOT scale derived from the AUDIT scale and CAGE scale
.

Memory impairment is also a common clinical manifestation in patients with chronic alcohol-toxic encephalopathy, which requires physicians to cooperate with the use of cognitive function rating scales to assist in diagnosis
.
Commonly used cognitive function rating scales include the Mini-mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA).

Because the MoCA scale involves more cognitive domains, especially the detection of visuospatial and executive ability, it is more recommended
for patients with chronic alcoholic toxic encephalopathy.

(2) Clinical diagnosis of chronic alcoholic toxic encephalopathy

A history of long-term alcohol consumption or alcohol
dependence should be the first step.
The core symptoms/diagnostic criteria for alcohol dependence are described in DSM-4/ICD-10 as follows (3 or more of the following within 12 months):(1) Alcohol tolerance (requires greater intake to achieve a sense of pleasure); (2) withdrawal symptoms/reactions after stopping drinking; (3) excessive intake; (4) Uncontrollable and abstaining; (5) Spending a lot of time seeking, obtaining, and ingesting alcohol; (6) Decreased willingness to engage in social interactions; (7) Regardless of any adverse consequences (physical/psychological problems).

Since the clinical manifestations and severity of patients may also be closely related to factors such as the type of alcohol, the time of initiation, the amount and frequency of drinking, whether the alcohol is accompanied by food, and the functional status of the nervous system, clinicians should make a comprehensive judgment
based on the above diagnostic criteria, combined with clinical manifestations and imaging features.

5 Treatment of chronic alcoholic toxic encephalopathy

(1) Abstaining from alcohol

The first treatment for chronic alcoholic toxic encephalopathy is abstinence
.
Treatment is generally divided into 2 stages: one is the abstinence stage, also known as the detoxification stage; The other stage is the rehabilitation phase
.
Aggressive drug therapy can help patients wean themselves off alcohol dependence and prevent recurrence
.
Alcohol withdrawal in patients with severe alcoholism should be hospitalized to prevent serious complications
.

At present, the first-line treatment drugs are: (1) nalmefine, naloxone, naltrexone: nalmefen is a μ and some K opioid receptor antagonists, naloxone, naltrexone is μ opioid receptor antagonists
.
Opioids stimulate the paraventricular nucleus of the hypothalamus, which leads to alcohol intake
.
Therefore, the opioid antagonists nalmefine, naloxone, and naltrexone can block these processes and reduce the patient's dependence
on alcohol.
In terms of effectiveness, nalmefen improved the amount and frequency of alcohol consumption in patients better than naloxone and naltrexone, but there was no significant difference
in safety.
However, due to the diversity of opioid receptor genes, there are large individual differences
in treatment effectiveness.
(2) Disulfiram: The pharmacological mechanism of disulfiram is to block acetaldehyde dehydrogenase
.
When the patient ingests alcohol, due to the blockade of acetaldehyde dehydrogenase, acetaldehyde accumulates in the body, and then disulfiram reaction, that is, tachycardia, flushing, nausea, vomiting and other symptoms
.
Therefore, disulfiram mainly reduces the patient's dependence on alcohol psychologically, but has no therapeutic effect
on the core symptoms of alcohol dependence.
In addition, disulfiram has a good effect
mainly in patients who are well compliant and well supervised.
(3) Acampronic acid: The pharmacological mechanism may be to reduce withdrawal symptoms by blocking N-methyl-D-aspartate (NMDA) receptors, such as drinking desire, anxiety, insomnia, etc
.
However, its efficacy is weak, oral bioavailability is low, the efficacy is short, and the number of doses is more
.

At present, the second-line treatment drugs are: (1) baclofen: baclofen has a sedative effect in the withdrawal process of patients, and the efficacy may be related to
the dose of medication and the amount of alcohol consumed before abstinence.
However, its therapeutic effect on alcohol dependence is currently controversial
.
(2) Topiramate: topiramate has a certain effect
on preventing the recurrence of alcohol dependence.
However, it has dose-related side effects such as paresthesia, mistaste, anorexia, difficulty concentrating, and pruritus
.
(3) Benzodiazepines: commonly used to treat alcohol withdrawal symptoms such as anxiety and insomnia, can also be used to prevent and treat seizures and delirium, but attention should be paid to the addictive nature
of such drugs.
(4) Tricyclic antidepressants: can be used to control anxiety and depression caused by any cause, but because these symptoms may disappear with alcohol withdrawal, such drugs
can be considered if these symptoms still exist after the end of the abstinence period.
(5) Large doses of antioxidants: such as vitamin C and vitamin E, may have a certain protective effect
on alcoholic toxic encephalopathy.
After drinking a lot, ethanol is metabolized in the body to produce a large number of free radicals, and reduced glutathione has been used in the treatment
of alcoholism.

(2) Treatment of etiology

The cause of chronic alcoholic toxic encephalopathy is ammonium sulfate (vitamin B1) deficiency caused by gastrointestinal malabsorption, so the key to treatment is to target
the cause and pathogenesis.
Because patients with chronic alcohol-toxic encephalopathy have gastrointestinal malabsorption and oral vitamin B1 are not effective, parenteral administration
is generally selected.
When thiamine reserves in the body are severely insufficient, patients who ingest a large amount of carbohydrate fluid may induce acute brain injury, manifested as the acute onset or exacerbation of chronic alcoholic toxic encephalopathy, so chronic alcoholic toxic encephalopathy is expected to be fully recovered
by rapid parenteral supplementation of thiamine at the beginning of the disease.
For patients with chronic alcohol-toxic encephalopathy with cognitive dysfunction, malnutrition, hypoglycemia, liver disease, etc.
, high-dose vitamin B1 should be supplemented non-enterally before intravenous infusion of sugary liquids, and intravenous injection (500mg/d, continuous 3d)
can be used.
If chronic alcohol-toxic brain injury is not treated in time, its natural history can continue to develop, eventually leading to coma, shock, cardiovascular and neurological failure
.

(3) Correct nutritional disorders

Nutritional disorders are an important factor in causing and aggravating chronic alcoholic toxic encephalopathy, and such patients are often accompanied by malnutrition, so correcting nutritional disorders is the basis for
alleviating the disease and early recovery.
First, intravenous water, electrolytes, vitamin B1, and vitamin C should be given
.
Patients are deficient in vitamin A, B complex vitamins and C, carnitine, magnesium, selenium, zinc, and essential fatty acids and antioxidants, and supplementation of nutrients, especially B vitamins, can help recovery
.
Secondly, help patients restore appetite, keep the mouth clean and hygienic, eat small and frequent meals, and try to meet the dietary requirements
of patients.
Patients are encouraged to eat vitamin-rich foods
.
Patients should avoid sugar, even fruit juices, which may contain more sugar than whole fruit; Reduce diets high in simple sugars, such as white flour and prepared potatoes; Increase the consumption
of plant protein and polysaccharides.
These substances are found in higher amounts in
cereals, legumes, and vegetables.

(4) Brain-protective therapy

Patients with chronic alcoholism suffer from cerebral peroxide and free radical damage and significantly low levels of neurotrophic factors, so appropriate and effective neuroprotective therapy can help improve the symptoms
of chronic alcohol-toxic encephalopathy.
In addition to the use of high-dose vitamin C and supplementation of B vitamins such as methylcobalamin, free radical scavengers such as edaravone, mitochondrial protectors such as idebenone, coenzyme Q10, etc.
, and neurotrophic drugs such as murine nerve growth factor, oxiracetam, etc
.
can also be given.

(5) Treatment of various types of syndromes

1.
Wernicke encephalopathy and Korsakoff syndrome: The pathogenesis of Wernicke encephalopathy and Korsakov syndrome is mainly ammonium sulfide deficiency, so B vitamins can be actively supplemented through non-enteral supplementation, including intramuscular injection of vitamin B1 injection and intramuscular or intravenous injection of methylcobalamin injection (1000μg, 1 time/day).

2.
Chronic alcohol toxic dementia: impaired cholinergic function of the brain is the main mechanism of chronic alcohol toxic dementia, alcohol inhibits acetylcholine activity, resulting in loss of hippocampal and frontal cholinergic neurons, causing cognitive decline
.
Clinical use of cholinesterase inhibitor donepezil and NMDA receptor non-competitive antagonist memantine, the recommended dose is: donepezil 5-10mg orally, once / d, 4-6 weeks later to increase to 10mg oral, once / d; For the first 3 weeks of memantine treatment, the dose is increased by 5 mg/d to 10 mg orally twice a day
.

3.
Alcoholic tremor-delirium: short-term use of benzodiazepines is preferred, with antipsychotics such as haloperidol or olanzapine
if necessary.

4.
Alcoholic epilepsy: seizures during withdrawal or convalescent should be actively treated with antiepileptic drugs, preferably benzodiazepines, such as lorazepam or diazepam, if necessary, sodium valproate extended-release tablets or levetiracetam can be combined to adjust to the lowest safe and effective dose, and the drug should be considered after 1-2 years of abstinence from alcohol and complete control of seizures, and appropriately prolonged
according to the patient's brain injury.

5.
Alcoholic Mental and Behavioral Disorders: Alcohol can have significant effects on the central neurotransmitter system, including central neurotransmitters
such as dopamine, γ-aminobutyric acid, and serotonin.
Therefore, patients should be actively treated for anxiety and depression disorders, including the use of selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, or serotonin and norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine or duloxetine, or thiatonic neuroleptic drugs such as haloperethan melitrexine tablets, or in combination with proprietary Chinese medicines such as Shuhepatic antidepressant capsules and Wuling capsules
.
For mild anxiety and depressive disorders, the above proprietary Chinese medicines alone also have certain effects, and there are fewer
side effects.

6.
White matter demyelination and central pontine myelinolysis: glucocorticoids are not effective
in alcoholic white matter demyelination.
Given the mechanism of action of statin lipid-lowering drugs on atherosclerotic arterial lesions and vasculitic injury, such drugs as atorvastatin or rosuvastatin may also have a therapeutic effect on alcoholic white matter demyelination and alcoholic cognitive dysfunction, but more attention should be paid to monitoring liver function and muscle enzymes
during medication.
At the same time, neurotrophic protective drugs such as murine nerve growth factor and B vitamins such as idebenone, methylcobalamin and edaravone can be given in large doses
.

(6) Rehabilitation treatment

For patients with cerebellar ataxia who cannot walk independently, have difficulty with fine skills and movements of the upper limbs, and have worsening speech dysfunction, motor function should be maintained as much as possible to prevent the occurrence
of secondary movement disorders.
It is necessary
to maintain a certain degree of daily living ability and quality of life, and timely rehabilitation treatment.

(7) Other treatments

Acupuncture treatment can reduce withdrawal symptoms in alcoholics, help prevent seizures and relapse alcoholism, and help patients successfully complete their abstinence programs
.
Hyperbaric oxygen therapy can increase aerobic metabolism of brain tissue in patients with chronic alcoholic toxic encephalopathy, which is beneficial
to speed up the recovery of patients.
Transcranial magnetic stimulation (TMS) has the advantages of painless, non-injury, and safety, especially transcranial magnetic stimulation (rTMS) with continuous adjustable repetitive stimulation can play a certain auxiliary role
in the treatment of chronic alcoholic toxic encephalopathy by regulating neuroplasticity and affecting nerve activity in the short or long term.

6 Care of chronic alcoholic toxic encephalopathy

(1) Care for alcohol abstinence

Chronic alcohol-toxic encephalopathy is caused by long-term alcoholism, so abstinence from alcohol is the key
to treating the disease.
In the care of alcohol abstinence, health guidance cannot be ignored
.
The patient is in a passive abstinence period during the hospital stay, which is a good start
to abstinence.
In order to stop drinking alcohol when the patient goes home, we should chat with the patient when he is calm and explain the causes and harms
of chronic alcoholic toxic encephalopathy.
Requirements for patients: (1) Good habit
of "drinking without getting drunk" when drinking.
(2) When drinking, you should not disrupt the rules of diet, and you must not "use wine as a meal" to avoid malnutrition
.
(3) Once addicted, you should quickly quit drinking, and the patient should be carefully cared for, and the serious case must be hospitalized
.
At the same time, family members should understand the knowledge of caring for the disease, assist in the persuasion and supervision tasks of patients, and ensure that patients are given family care
such as diet and living after discharge.

(2) Closely observe changes in the condition

Long-term alcohol consumption can cause atrophic gastritis and damage to the small intestine and liver, followed by systemic malnutrition and vitamin B1 deficiency
.
Vitamin B1 deficiency can lead to disorders of glucose metabolism, which can lead to dysfunction of organs with strong glucose metabolism
.
The nervous system and heart are affected first, with particularly severe
damage to the brain.
Therefore, changes in the patient's consciousness, mental status, and vital signs should be monitored, and ECG monitoring
should be given if necessary.

(3) Safe care

Patients with chronic alcohol-toxic encephalopathy with ataxia often have decreased sense of balance
.
Loss of balance and risk avoidance response should be
corrected.
Therefore, ensuring the safety of patients is also an issue
that should be paid attention to in care.
The patient's health status and mobility should be correctly assessed, and the patient should be educated so that he can understand his own activity ability and improve safety awareness
.

(4) Psychological care

Patients with chronic alcohol-toxic encephalopathy often have frustration, anxiety, and low self-esteem
.
The patient's psychological state should be understood in time, help the patient understand his own condition, encourage the patient to admit the reality, and patiently explain
the problems raised.
After discharge, patients should be followed up by telephone or home when appropriate
.
To learn to live without drinking, you must do the following: (1) Avoid contact with people who drink and go
to places where they drink.
Make friends
who don't drink.
(2) Get help
from family and friends.
(3) Replace dependence on alcohol with positive dependence, such as new hobbies or volunteer labor
.
(4) Participate in exercise
.
Proper exercise allows the brain to release chemical transmitters.
Even a walk after a meal helps to calm
the mind.

The main problem affecting the recovery of alcoholics is re-drinking
.
Preventing alcohol consumption can be difficult, requiring sustained treatment, motivation and strong social support to consolidate the results
achieved.
Other ways to prevent re-drinking include changing daily habits and avoiding contact or activities
with people who are drinking.
90% of alcoholics smoke, and those who quit are more likely to achieve long-term abstinence and other health benefits
.
In addition
, psychological counseling and psychotherapy should be added.