What are the thirteen ways to die drunk

Thirteen Ways to Die of Drunkenness Most of us clinicians have been exposed to “alcohol” in our lives. Acute alcohol poisoning is one of the most common emergencies in major hospitals, especially in colder climates, and is often seen late at night or early in the morning. As an emergency physician, dealing with acute alcohol overdose or poisoning of these common problems, need to realize that drinking can be dead; drinking is generally not dead, such as accidental death, a very small number of patients are really “drunk” death, and most of them have other reasons. Misinhalation is the main reason for the accidental death of drunken patients. Drinkers often have a lot of food in the stomach, and when they vomit, the stomach contents can easily enter the airway, leading to asphyxiation and aspiration pneumonia; it can also stimulate the trachea, and cause reflex cardiac arrest through the vagus nerve reflex. Therefore, in the emergency work, often found that some of the hospital before the death of intoxicated cases, in cardiopulmonary resuscitation, often from the trachea sucked out a large number of vomitus, most of which is due to misinhalation. Therefore, for patients with acute alcohol intoxication, preventing the occurrence of aspiration is a “top priority”. Therefore, the drunken patient must not lie on his back; his head must be tilted to one side to prevent the vomit from entering the trachea. And according to the situation, the gastric tube for gastric lavage, gastric emptying measures, the latter is also aimed at preventing the occurrence of aspiration. In addition, to determine the amount of gastric contents, can also be based on orthopantomogram, 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 broad antibacterial spectrum, strong antibacterial effect, mainly excreted through the biliary tract; therefore, those with renal impairment can use the usual amount, those with hepatic impairment or biliary obstruction can also use the usual amount, so that the renal excretion can be increased to compensate for the decrease in biliary excretion. The toxicity of this product is low and easy to tolerate. Therefore, it has been widely used in clinical practice in recent years; however, it should be noted that alcohol consumption during the application of cefoperazone may result in disulfiram-like reactions. Drinking alcohol during the application of cefoperazone until 5 days after the administration of the drug can cause “disulfiram-like reaction”, therefore, during the administration of the drug and within 5d after discontinuation of the drug, the patient should not drink alcohol, oral or intravenous ethanol-containing drugs. Alcohol-containing drugs mainly include nitroglycerin and hydrocortisone; during the use of cephalosporin antibiotics, such as intravenous nitroglycerin or hydrocortisone, disulfiram-like reaction can also occur, and it is easy to be misdiagnosed as drug allergy. After the application of drugs (cephalosporins) drinking drinks containing alcohol (or exposure to alcohol) caused by the body’s acetaldehyde can not be degraded, accumulation in the body, resulting in the phenomenon of acetaldehyde poisoning, also known as disulfiram reaction. Patients appear facial flushing, v. headache, dizziness, abdominal pain, stomach pain, nausea, vomiting, heartbeat, shortness of breath, accelerated heart rate, lowered blood pressure, and drowsiness and hallucinations, etc., and in severe cases, it can lead to respiratory depression, myocardial infarction, acute heart failure, convulsions and death. Clinically, disulfiram-like reaction is easily misdiagnosed as drug allergy or heart attack. Therefore, patients with acute alcoholism should be asked about recent medication history [2]. Drugs that can cause disulfiram-like reactions include: ① Cephalosporins Cefoperazone, cefmetazole, cefminox, cephalexin, cephalexin, cefmenoxime, cefamandole, ceftriaxone, cephalexin, cefradine, cefaclor, and so on. Cefoperazone is the most reported bisulfite-like reaction, the most sensitive. ② Nitroimidazole drugs such as metronidazole, tinidazole, ornidazole, Secnidazole. ③ other antibacterial drugs such as furazolidone, chloramphenicol, ketoconazole, ashwagandha. In addition, when fresh cut flowers are preserved, alcohol is often added to the water in which the flowers are inserted, and disulfiram-like reactions or idiosyncratic reactions can occur after human contact, which should be noted in the clinic. If a patient eats alcohol-cored chocolate after medication, takes patchouli, or even treats the skin with alcohol, a disulfiram-like reaction can occur. Some scholars also pointed out that when patients use N – methyl thiotetrazole group of cephalosporins, even if the use of ethanol to disinfect the skin or scrub to cool down, a small amount of ethanol into the blood circulation, such reactions can also occur. Especially the elderly or cardiovascular disease patients, so medical personnel in the patients with such drugs, try not to use ethanol disinfection, and use povidone-iodine disinfection. 3, acute pancreatitis Drinking alcohol can lead to an attack of acute pancreatitis, the latter can produce myocardial inhibitory factor, so that cardiac arrest. Therefore, patients with alcoholism should routinely check 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. There are also those who can recover completely after an attack of acute alcoholic pancreatitis if they don’t quit drinking. According to foreign statistics, clinical pancreatitis occurs in about 0.9%-9.5% of alcoholics, 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 consumed, the habit of slow drinking and wine and food together. Alcohol may cause acute pancreatitis through the following pathways: (1) cause hypertriglyceridemia or direct toxic effects; (2) elevated intraduodenal pressure, duodenal fluid reflux into the pancreatic duct; (3) spasm of Oddi’s sphincter, papillitis, edema, resulting in increased intraductal pressure in the pancreatic duct; (4) stimulate the gastric sinus G-cells to secrete gastrin, which stimulates the secretion of pancreatic secretion; (5) absorbed from the stomach, stimulate the gastric wall cells to secrete hydrochloric acid, which in turn causes the gastric wall cells to secrete hydrochloric acid, which in turn causes the pancreatic secretion. cells to secrete hydrochloric acid, which in turn causes secretion of pancreatin and glucagon in the duodenum, ultimately leading to pancreatic hypersecretion and so on. 4, hypothermia As alcohol can cause vasodilation, increased heat dissipation, and reduce judgment or lead to retardation; especially in cold environments, easy to cause hypothermia. The latter can make the body appear hypercoagulable, hyperglycemia and arrhythmia, resulting in accidental death of the patient. Some statistics show that in certain rural areas, more than 90% of deaths caused by hypothermia are related to elevated blood alcohol concentrations. Therefore, insulation is a necessary measure when dealing with acute alcohol poisoning, whether out of hospital or in the emergency department. Generalized cold injury is also known as cold stiffness and is a freezing cold injury. It is a massive loss of body heat caused by prolonged exposure of the body to cold temperatures and a decrease in the metabolic function of the whole body, so that the normal central body temperature cannot be maintained. Due to hypothermia, the final loss of consciousness, coma. Frozen stiffness occurs, and in severe cases, frozen to death. Severe hypothermia (body temperature below 30 ℃ ) can cause a significant reduction in cerebral blood flow and oxygen demand, reduced cardiac output, arterial pressure drop, due to the obvious suppression of cerebral function, hypothermia patients can appear similar to clinical death. However, acute alcoholism patients due to hypothermia caused by freezing cold injury, that is, complete “freezing” and death is not common, due to its faster loss of body temperature, often preceded by complete “freezing” before the cardiac arrhythmia and death. If the patient is hypothermic, the body temperature should be raised slowly to a normal level (≤0.6°C per hour). More rapid rewarming can often cause irreversible hypotension. In a warm room, insulation can be achieved with the use of blankets or other superior insulating substances. Successful treatment requires careful monitoring of the patient and the ability to anticipate common complications. 5, rhabdomyolysis Drinking patients often sleep for a long time, such as limb inactivity, prolonged compression sites, there will also be muscle ischemic necrosis, the latter can lead to rhabdomyolysis (rhabdomyolysis). When the limb is released from compression, acute alcoholic myopathy (alcoholicmyopathy) occurs, and a large amount of necrotic material released from muscle lysis into the bloodstream can cause multiple organ insufficiency and even sudden death. Among them, a large number of myoglobin clogged renal tubules, often resulting in renal failure (acute renal failure), the death rate is high. Therefore, patients with acute alcoholism, must turn over regularly to prevent prolonged limb pressure. Acute alcoholic myopathy occurs mostly in chronic alcoholics after a single heavy drinking, and the main types are: (1) acute alcoholic myopathy with rhabdomyolysis; (2) acute alcoholic myopathy with hypocalcemia; and (3) acute alcoholic myopathy with hypokalemia. Its pathogenesis is unclear, it is speculated that the following factors may be related: ① acetaldehyde reduces the activity of glycolytic enzymes, inhibit the metabolism of sugar; ② alcohol and metabolite acetaldehyde has a toxic effect on the myocyte mitochondrial toxicity damage to mitochondrial dysfunction; or prevent myoglobin kinase, prevent metabolic anomalies, such as hyponatremia, hypophosphate, hypocalcemia, hypomagnesium and epileptic seizures, tremor, delirium and hyperthermia can be Increase somatic activity and myocyte metabolism, leading to myocyte injury; seizures and limb compression can induce rhabdomyolysis. Pathological manifestations of muscle necrosis, with or without inflammatory response muscle fiber regeneration, type I brain tissue ischemia and even cause platelet hyperfunction and hypercoagulable state of the blood; fibrin solubility is reduced, and the time of spontaneous fibrin dissolution is significantly prolonged. Large amounts of alcohol can also induce platelet aggregation and thromboxane A2 increase, which is a strong platelet aggregation and cerebral vasoconstrictor. Therefore, alcohol poisoning can make the patient’s blood in a state of hypercoagulability and cerebral vasoconstriction through a variety of factors, cerebral blood flow decreases, so that the brain tissue ischemia, hypoxia, and even cause cerebral edema. ② After a large number of alcohol poisoning, alcohol is often deep sleep or coma, the body is in a variety of abnormal posture and position, causing the compression of extracranial blood vessels, resulting in further obstacles to cerebral circulation and blood supply. 6, cardiac emergencies Drinking alcohol can induce acute myocardial infarction, this point need not be repeated. In emergency work, alcoholism patients need to do a copy of the electrocardiogram, especially the elderly and patients with underlying pathologies such as diabetes mellitus, and the occurrence of acute myocardial infarction in drowsy drinkers is relatively insidious and can be asymptomatic [4]. In addition, acute alcoholism itself can cause cardiac damage. In patients with acute alcohol poisoning, some cases of ECG abnormalities and cardiac enzymology changes exist, and the degree of acute alcohol damage to the heart is proportional to the time and degree of poisoning. 7, cerebral hemorrhage, a patient due to deep alcohol poisoning was rushed to the hospital, doctors diagnosed as acute alcohol poisoning, in a few hours to give the appropriate active treatment, but the patient is still in a coma, at this time the doctor suspected that whether there are other problems at the same time, after the cranial brain CT showed cerebral hemorrhage. It is estimated that 110,000 people die of cerebral hemorrhage caused by alcohol poisoning every year in China, accounting for 1.3% of the total mortality rate. 8, methanol poisoning Methanol, also known as wood alcohol, wood alcohol, colorless, transparent, slightly ethanol-flavored liquid, is one of the main components of industrial alcohol. It is one of the main components of industrial alcohol. The cause of poisoning is drinking industrial alcohol containing methanol or “bulk liquor” blended with it. Intake of methanol 5 to 10 ml can cause poisoning, 30 ml can be fatal. The toxic effect of methanol on the human body is caused by methanol itself and its metabolites formaldehyde and formic acid, mainly characterized by central nervous system damage, eye damage and cell metabolism in the important coenzymes, so that the pyruvate dehydrogenase α-ketoglutarate dehydrogenase and ketotransferase play a role in the decarboxylation of pyruvate converted into acetyl-coenzyme A, the anaerobic glycolysis and the tricarboxylic acid cycle; so that the α-ketoglutarate is converted to succinic acid, the latter of which is also an important link in the tricarboxylic acid cycle. Thiamine or thiamine pyrophosphate deficiency prevents the tricarboxylic acid cycle from proceeding normally cannot be generated by Korsakoff psychosis. Etiologic treatment is most important in patients with chronic alcoholism due to gastrointestinal malabsorption, B thiamine). Accompanied by consciousness disorder of chronic alcoholism, malnutrition, hypoglycemia and liver disease patients, intravenous glucose should be supplemented through the non-intestinal vitamin B1, to prevent the induction of Wernicke’s encephalopathy caused by chronic alcoholism Wernicke’s encephalopathy patients can be accompanied by magnesium deficiency in the dependence on thiamine metabolism of several biochemical processes of magnesium is a co-factor, magnesium deficiency can reduce the role of thiamine to make the thiamine deficiency of the disease worsened, so it should be supplemented with magnesium. 9, osmotic demyelination syndrome osmotic demyelination syndrome (osmotic demyelination syndrome, ODS), also known as osmotic myelinolysis syndrome (osmotic myelinolysis syndrome, OMS), is a rare acute non-inflammatory central demyelinating disease, mainly due to chronic hyponatremia when the brain cells have adapted to the hyponatremia. In chronic hyponatremia, brain cells have adapted to a hypotonic state, and once sodium is rapidly replaced, plasma osmolality rises rapidly, causing dehydration of brain tissue and secondary demyelination. Chronic alcoholism and malnutrition are the more certain etiologic factors, accounting for about 39% of cases. And too rapid correction of hyponatremia became the second most important etiology after 1986, accounting for about 21.5%. Silver et al. proposed that osmotic demyelination syndrome is closely related to organic osmolality, and that not only electrolytes are altered in hyponatremia, but also organic osmolalities such as amino acids (e.g., alanine, glutamate, taurine, glycine) and sugars (e.g., inositol) are altered, and that rapid correction of hyponatremia restores intracellular electrolytes very quickly but fails to quickly correct the lost organic osmolalities, leading to cellular damage and demyelination. In experimental animal models, it has been found that the brain regions with the slowest recovery of organic osmolytes after rapid correction of hyponatremia are the most severely demyelinated. Alcoholism and malnutrition patients are generally lack of organic osmolality, they will be in a high-risk environment of cellular crumpling, when the blood sodium is lowered adjacent to the blood vessels of the gray matter is more susceptible to damage, so that the brain bridge is particularly vulnerable to myelin toxicity from the vascular leakage of the material damaged. 10, drunken accidents car accidents caused by drunk driving is the emergency department trauma patients, “the head of the problem”, surgical patients accounted for about three to fifty percent of the emergency room patients. In the past, most surgical patients were injured in car accidents caused by drunk driving. There have been reports of a person who drank too much alcohol and was so drunk that he became unconscious after lighting the paper money for rituals, and he was buried in his own graveyard without realizing that the fire had reached him. There have been cases of drunken falls resulting in cranial epidural hemorrhages and aortic coarctation.