What to do about acute alcoholism

  Alcohol is ethanol. All kinds of alcoholic beverages contain different concentrations of alcohol, among which the alcohol content in white wine can reach 50%-60%, while the alcohol content in beer is only 2%-5%. In recent years, the number of alcohol drinkers in China has been increasing year by year, and the number of alcoholics has been increasing, so the incidence of acute and chronic alcoholism has also increased, and the condition can be life-threatening in serious cases.  Mechanism of toxic effects】 Under normal circumstances, after the intake of alcohol, about 80% is absorbed by the duodenum and jejunum, the rest is absorbed in the stomach and only 2-10% is excreted in its original form by the respiratory tract, urine and sweat glands. When drinking alcohol on an empty stomach, more than 95% of the alcohol is absorbed within 1.5 hours, and all of it is absorbed within 2.5 hours. The absorption of alcohol can be delayed when there is food in the stomach. About 90-98% of alcohol absorbed in the gastrointestinal tract enters the blood circulation through the portal vein and is oxidized to acetaldehyde by ethanol dehydrogenase and catalase in the liver, then further oxidized to acetic acid by acetaldehyde dehydrogenase, and finally produced as carbon dioxide and water through the tricarboxylic acid cycle. About 2% of alcohol is not oxidized and is slowly excreted by the lungs and kidneys. When excess alcohol enters the body, it exceeds the oxidative metabolic capacity of the liver, that is, it accumulates in the body and enters the brain. In addition, acetaldehyde, a metabolite of ethanol, is condensed into opioid-like substances with dopamine in the body, which acts directly or indirectly on opioid receptors in the brain, causing the patient to first be in an excited state and gradually turn into an inhibited state, followed by the subcortical center, cerebellum, vasomotor center and respiratory center of the delayed brain. Inhibited, severe acute intoxication can occur respiratory and circulatory failure.  The clinical manifestations of acute alcohol poisoning vary from person to person, and the early and late appearance of symptoms varies, and is positively related to the amount of alcohol consumed and the concentration of ethanol in the blood, as well as to individual sensitivity. The symptoms of acute intoxication are mainly for the nervous system and digestive system, with the most common damage to the nervous system. The damage to the central nervous system is roughly divided into three phases: 1. excitement phase: when the blood alcohol content is 200-990mg/L, dizziness, weakness, loss of self-control, self-expression, increased speech, sometimes rude and rude, easy to be emotional, flushed or pale face, and days with the smell of alcohol in the air.  2.Ataxia period: the blood alcohol level reaches 1000-2999mg/L. The patient has uncoordinated movements, stumbling gait, clumsy movements, incoherent speech, nystagmus, agitation, diplopia.  3. Coma stage: Blood alcohol content reaches 3000mg/L or more. Patients are asleep, pale face, lowered body temperature, wet and cold skin, slightly clamped mouth and lips, and in severe cases, coma, Chen-Schi breathing, rapid heartbeat, incontinence, and death due to respiratory failure. There are also cases of death due to aspiration pneumonia or asphyxia due to reduced pharyngeal reflex and vomiting after a full meal. Secondary lacunar cerebral infarction and acute alcoholic myopathy (myalgia, tenderness, muscle swelling, muscle weakness, etc.) have also been reported. Alcohol causes a significant decrease in liver glycogen due to inhibition of glycogen isogenesis, causing hypoglycemia and can aggravate coma.  The patient’s exhaled breath and vomit have the smell of alcohol, and ethanol can be measured in blood and urine, which helps in the diagnosis.  Treatment] Acute poisoning generally does not require special treatment, bed rest, pay attention to warmth, can recover on its own. If the symptoms of poisoning are serious, the patient can be induced to vomit (Apomorphine is prohibited), and if necessary, the stomach can be lavaged with water or 1% sodium bicarbonate, and aspiration pneumonia should be prevented during the period. For those who are restless or overexcited, use small doses of Dixie and avoid morphine, chlorpromazine, and phenobarbital sedatives. Intravenous push of 50% glucose 100mI, intramuscular injection of vitamin B1, vitamin B6, nicotinamide 100mg each to accelerate the oxidation of ethanol in the body.  Naloxone is a specific antagonist of opioid-like substances, which can cross the blood-brain barrier and bind to opioid peptide receptors, leading to opioid peptide inactivation, relieving the inhibitory effect of opioid peptides on cardiovascular system and nervous system, having non-opioid receptor effects such as inhibiting oxygen free radical release and stabilizing liver lysosomal membranes, having a hypnotic effect on disorders of consciousness, and promoting the conversion of ethanol in the body. It can be injected intramuscularly or intravenously, 0.4-O.8mg each time. 1-2min intravenous injection, the blood concentration will reach the peak, and the clearance half-life is 1 hour. If necessary, the application can be repeated at intervals of about 1 hour until the patient is awake. In case of severe poisoning, the first dose can be 0.8-1.2mg. If complications such as respiratory failure, cerebral edema and hypoglycemia occur, symptomatic and supportive treatment should be given accordingly.  In case of severe poisoning, peritoneal dialysis or hemodialysis can be used to promote the excretion of ethanol from the body. Indications for dialysis treatment: blood ethanol level >5g/L, acidosis, or concomitant use of methanol or other suspected drugs.  In case of severe intoxication, hemodialysis can be used to promote the elimination of ethanol from the body. Indications for dialysis treatment: blood ethanol level >5g/L with acidosis, or concomitant use of methanol or other drugs of interest.