Most of us clinical workers have been exposed to “alcohol” in our lifetime. Acute alcohol intoxication is also a common emergency in major hospitals, especially in cold climates, and most visits are late at night or early in the morning. As an emergency physician, when dealing with these common problems of acute alcohol overdose or poisoning, you need to realize that drinking can kill you; drinking generally does not kill you, and in the case of accidental death, very few patients die from genuine “intoxication”, while most have other causes. 1. Accidental inhalation Accidental inhalation is the main reason for accidental death of drunken patients. Drinkers often have a lot of food in their stomachs, and the stomach contents can easily enter the airway when vomiting, leading to asphyxiation and aspiration pneumonia; it can also stimulate the trachea and cause reflex cardiac arrest through the vagus nerve reflex. Therefore, in emergency work, it is often found that some cases of intoxication who have died before coming to the hospital are often aspirated from the trachea during cardiopulmonary resuscitation with a large amount of vomit, mostly due to misaspiration. Therefore, for patients with acute alcohol intoxication, the prevention of misaspiration is the “top priority”. Therefore, an intoxicated patient must not lie on his back; his head must be tilted to the side to prevent vomit from entering the trachea. Depending on the situation, gastric tube lavage and gastric emptying measures should be carried out, the latter of which is also aimed at preventing aspiration. In addition, the amount of gastric contents can be judged according to the orthopantomogram plain film, such as the disappearance of gastric bubbles, often suggesting that the patient’s stomach is in a state of filling. Cefoperazone is a second-generation cephalosporin, with a wide antibacterial spectrum and strong antibacterial effect, and is mainly excreted through the biliary tract; therefore, the usual amount can be used for those with renal impairment, and the usual amount can also be used for those with hepatic impairment or biliary obstruction, so that the renal excretion can increase and the biliary excretion can decrease. The toxicity of this product is low and easily tolerated. Therefore, it has been widely used in clinical practice in recent years; however, it should be noted that disulfiram-like reactions may occur when alcohol is consumed during the application of cefoperazone. Alcohol consumption during cefoperazone application and up to 5 days after drug administration may cause “disulfiram-like reaction”, therefore, patients should not drink alcohol, orally or intravenously enter drugs containing ethanol during drug administration and 5 d after drug withdrawal. The main drugs containing alcohol are nitroglycerin and hydrocortisone; during the use of cephalosporin antibiotics, such as intravenous nitroglycerin or hydrocortisone, disulfiram-like reactions may also occur, which can be easily misdiagnosed as drug allergy. Acetaldehyde poisoning is caused by the accumulation of acetaldehyde in the body after drinking alcoholic beverages (or being exposed to alcohol) after the application of drugs (cephalosporins), which is also called disulfiram reaction. Patients experience facial flushing, headache, dizziness, abdominal pain, stomach pain, nausea, vomiting, heartbeat, shortness of breath, increased heart rate, decreased blood pressure, and drowsy hallucinations, etc. In severe cases, it may lead to respiratory depression, myocardial infarction, acute heart failure, convulsions, and death. Clinically, disulfiram-like reactions are easily misdiagnosed as drug allergy or heart attack. Therefore, patients with acute alcohol intoxication should be asked for a history of recent drug use [2]. The drugs that can cause disulfiram-like reactions mainly include: ① Cephalosporins cefoperazone, cefmetazole, cefminox, laxative cephalosporin, cefmenoxime, cefamandole, ceftriaxone, cefadroxil, cefazolin, cefradine, cefaclor, etc. Cefoperazone has the most reported disulfiram-like reactions and is the most sensitive. ②Nitroimidazoles such as metronidazole, tinidazole, ornidazole, and secnidazole. ③ Other antibacterial drugs such as furazolidone, chloramphenicol, ketoconazole, and ashwagandha. In addition, when fresh cut flowers are preserved, alcohol is often added to the water in the flower arrangement, and human contact can also lead to disulfiram-like reactions or idiosyncratic reactions, which should be clinically noticed. If a patient eats wine core chocolate after medication, takes patchouli water, or even treats the skin with alcohol, disulfiram-like reactions can occur. It has also been pointed out that such reactions can occur when patients use cephalosporins with N-methylthiotetrazolium groups, i.e., when ethanol is used to disinfect the skin or scrub to cool down, and a small amount of ethanol enters the blood circulation. Especially in elderly people or patients with cardiovascular diseases, medical staff should try not to disinfect with ethanol but with povidone iodine when using such drugs. 3, acute pancreatitis Drinking alcohol can lead to an attack of acute pancreatitis, the latter of which can produce myocardial inhibitory factors that can cause cardiac arrest. Therefore, patients with alcoholism should be routinely checked for serum amylase. In Western countries, alcoholism is the main cause of acute and chronic pancreatitis. Each year in the United States, 1/2-2/3 of acute pancreatitis is related to alcoholism. If you do not stop drinking after an episode of acute alcoholic pancreatitis, there are those who can recover completely. According to foreign statistics, about 0.9%-9.5% of alcoholism occurs in clinical-type pancreatitis, and 17%-45% have evidence of pancreatitis in pathology. Alcoholic pancreatitis is less common in China, which may be related to the small amount of alcohol consumption, the habit of slow drinking and wine and vegetables together. Alcohol may cause acute pancreatitis through several pathways: (1) causing hypertriglyceridemia or direct toxic effects; (2) increased intra-duodenal pressure and reflux of duodenal fluid into the pancreatic duct; (3) spasm of Oddi’s sphincter, papillitis, edema, resulting in increased pressure in the pancreatic duct; (4) stimulating G-cells in the gastric sinus to secrete gastrin and stimulate pancreatic secretion; (5) absorption from the stomach, stimulating gastric lining cells to secrete hydrochloric acid, which in turn causes secretion of pancreatin and glucagon in the duodenum, eventually leading to pancreatic hypersecretion, etc. 4. Hypothermia Since alcohol can cause vasodilation, increase heat dissipation, and reduce judgment or cause retardation; especially in a cold environment, it is easy to cause hypothermia. The latter can cause hypercoagulability, hyperglycemia and cardiac arrhythmia in the body, resulting in the unexpected death of the patient. Some statistics show that in some rural areas, more than 90% of deaths caused by hypothermia are related to elevated blood alcohol concentration. Therefore, warming is a necessary measure when dealing with acute alcohol poisoning, both out-of-hospital and in the emergency department. Systemic cold injury is also called cold stiffness and freezing cold injury. It is caused by a large loss of body heat caused by prolonged exposure of the body to a cold environment, and the metabolic function of the whole body is reduced, so that the normal central body temperature cannot be maintained. As a result of hypothermia, loss of consciousness and coma eventually occur. Freezing stiffness occurs, and in severe cases, death by freezing. Severe hypothermia (body temperature below 30°C) can cause a significant decrease in cerebral blood flow and oxygen demand, a decrease in cardiac output, and a decrease in arterial pressure, and because brain function is significantly depressed, patients with hypothermia can show signs similar to clinical death. However, it is not common for patients with acute alcohol intoxication to die from freezing cold injury caused by hypothermia, i.e., complete “freezing”, because of the rapid loss of body temperature, which often precedes complete “freezing” and can lead to cardiac arrhythmias and death. If a patient develops hypothermia, the temperature should be slowly raised to normal (≤0.6°C per hour). A more rapid rewarming can often cause irreversible hypotension. Insulation can be achieved in a warm room with the use of blankets or other higher-grade insulating substances. Careful monitoring of the patient and the ability to anticipate common complications are necessary for successful treatment. 5, rhabdomyolysis Patients who drink alcohol often fall asleep for a long time, and if the limb is inactive, prolonged compression of the site can also result in ischemic necrosis of the muscle, the latter of which can lead to rhabdomyolysis (rhabdomyolysis). When the limb is released from compression, acute alcoholic myopathy (alcoholicmyopathy) occurs, and the large amount of necrotic material released from muscle lysis into the blood can cause multiple organ insufficiency and even sudden death. Among them, a large amount of myoglobin blocks the renal tubules, often resulting in renal failure (acultrenalfailure), and the morbidity and mortality rate is high. Therefore, patients with acute alcoholism, must be turned regularly to prevent prolonged pressure on the limbs. 6. Acute alcoholic myopathy Acute alcoholic myopathy occurs mostly in long-term alcoholics after a large amount of alcohol consumption. The main types are: (1) acute alcoholic myopathy with rhabdomyolysis; (2) acute alcoholic myopathy with hypocalcemia; (3) acute alcoholic myopathy with hypokalemia. The pathogenesis is unclear, and it is speculated that it may be related to the following factors: (1) acetaldehyde decreases glycolytic enzyme activity and inhibits sugar metabolism; (2) alcohol and the metabolite acetaldehyde have toxic effects on myocytes causing toxic damage to mitochondria and mitochondrial dysfunction; or blocking myoglobin kinase, blocking metabolic abnormalities such as low blood sodium, low blood phosphorus, low blood calcium and low blood magnesium, as well as seizures, tremors, delirium and hyperthermia can increase somatic activity and myocyte metabolism, leading to myocyte injury; seizures and limb compression can induce rhabdomyolysis. Pathological manifestations include muscle necrosis with or without inflammatory response muscle fiber regeneration, type I brain tissue ischemia even causing platelet hyperfunction and blood hypercoagulation; fibrinolysis is reduced and fibrin spontaneous lysis time is significantly prolonged. Heavy alcohol consumption can also induce platelet aggregation and increased thromboxane A2, which is a strong platelet aggregation and cerebral vasoconstrictor. Therefore, alcohol intoxication can put the patient’s blood in a hypercoagulable state and cerebral vasoconstriction through a variety of factors, decreasing cerebral blood flow, causing brain tissue ischemia and hypoxia, and even causing cerebral edema. ②After heavy drinking intoxication, the body is often in deep sleep or coma after drinking, and the body is in a variety of abnormal postures and positions, causing compression of extracranial blood vessels and leading to further impairment of blood supply to the cerebral circulation. 7. Cardiac emergencies Drinking alcohol can induce acute myocardial infarction, and there is no need to elaborate on this point. In emergency workups, alcoholic patients require an ECG, especially in the elderly and those with underlying pathologies such as diabetes mellitus, and acute myocardial infarction in a drowsy drinker is relatively insidious and can be asymptomatic [4]. In addition, acute alcohol intoxication itself can cause cardiac damage. In some cases of patients with acute alcohol intoxication, there are abnormal electrocardiograms and myocardial enzymatic changes, and the degree of acute alcohol damage to the heart is directly proportional to the duration and degree of intoxication. 8. Cerebral hemorrhage A patient was rushed to the hospital for resuscitation due to deep alcohol intoxication. The doctor diagnosed acute alcohol intoxication and gave appropriate active treatment for several hours, but the patient was still in a coma, and only then did the doctor suspect whether there were other problems at the same time, and later the cranial CT showed cerebral hemorrhage. It is estimated that 110,000 people die each year in China from brain hemorrhage caused by alcohol poisoning, accounting for 1.3% of the total mortality rate. 9, methanol poisoning Methanol, also known as wood alcohol, wood alcohol, is a colorless, transparent, slightly ethanolic liquid, and is one of the main components of industrial alcohol. The cause of poisoning is mostly the consumption of industrial alcohol containing methanol or “bulk white wine” blended with it. Intake of 5-10 ml of methanol can cause poisoning, and 30 ml can be fatal. The toxic effect of methanol on human body is caused by methanol itself and its metabolites formaldehyde and formic acid, which are mainly characterized by central nervous system damage, eye damage and important coenzymes in cell metabolism, making pyruvate dehydrogenase α-ketoglutarate dehydrogenase and transketolase work, converting pyruvate decarboxylation into acetyl coenzyme A, linking anaerobic glycolysis with tricarboxylic acid cycle; converting α-ketoglutarate into butanedioic acid, the latter also being an important link in the tricarboxylic acid cycle. Thiamine or thiamine pyrophosphate deficiency prevents the tricarboxylic acid cycle from proceeding properly cannot be generated by Korsakoff psychosis. Etiological treatment is most important in patients with chronic alcoholism due to gastrointestinal malabsorption and group B thiamine). With impaired consciousness of chronic alcoholism, malnutrition, hypoglycemia and liver disease patients, intravenous input of glucose should be supplemented with vitamin B1 through the non-intestinal tract before to prevent the induction of Wernicke’s encephalopathy chronic alcoholism caused by Wernicke’s encephalopathy patients can be accompanied by magnesium deficiency, in several biochemical processes dependent on thiamine metabolism magnesium is a cofactor, magnesium deficiency can reduce the role of thiamine to worsen the condition of thiamine deficiency so should be supplemented with magnesium. 10, osmotic demyelination syndrome osmotic demyelinationsyndrome, ODS, also known as osmotic myelinolysis syndrome (osmoticmyelinolysyndrome, OMS), is a rare acute non-inflammatory central demyelination disease, mainly due to chronic In hyponatremia, brain cells have already adapted to a hypotonic state, and when given rapid sodium replacement, the plasma osmolality rapidly increases, causing dehydration of brain tissue and secondary demyelination. Chronic alcoholism and malnutrition are the more certain causes, accounting for about 39% of cases. In contrast, too rapid correction of hyponatremia after 1986 became the second leading cause, accounting for about 21.5% of cases. Silver et al. proposed that osmotic demyelination syndrome is closely related to organic osmolytes, and not only electrolytes are altered in hyponatremia, but also organic osmolytes such as amino acids (e.g. alanine, glutamate, taurine, glycine) and sugars (e.g. inositol) are altered, and rapid correction of hyponatremia results in rapid recovery of intracellular electrolytes, but the lost organic osmolytes cannot be corrected quickly, leading to cell damage and demyelination. In experimental animal models, it was found that the brain regions with the slowest recovery of organic osmolality after rapid correction of hyponatremia were the most severely demyelinated. Patients with alcoholism and malnutrition generally lack organic osmolytes, and they are then in a high-risk environment of cellular crumpling, and the gray matter adjacent to blood vessels is more susceptible to damage when blood sodium decreases, making the cerebral bridge especially vulnerable to damage by myelin toxic substances leaking from the vessels. 11, drunkenness accident drunk driving caused by car accidents is the emergency department trauma patients “disaster”, surgical patients accounted for about thirty to fifty percent of emergency patients. In the past, most surgical patients were injured in car accidents caused by drunk driving. There was a report of a person who drank too much alcohol and was so drunk that he was unconscious after lighting the paper money for the sacrifice, and did not notice that the fire had run into him and he was buried in his own grave. Cases of cranial epidural hemorrhage and aortic coarctation occurred after falling into drunkenness.