There are at least eight causes of sudden death after alcohol consumption: aspiration, acute pancreatitis, cardiac emergencies, cerebral hemorrhage, disulfiram-like reaction, hypothermia, rhabdomyolysis, and hypotonicity after gastric lavage. Only by understanding these mechanisms of sudden death can we better diagnose and treat them. “Pathophysiologically oriented”, which is the key to clinical diagnosis and treatment.
I. Misaspiration: “One bite of food means one life”.
Accidental aspiration is the main cause of accidental death in intoxicated patients. Drinkers often have a large amount of food in their stomachs, and the stomach contents can easily enter the airway when vomiting, leading to asphyxia 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, preventing misaspiration is the “top priority”. “One bite of food means one life.
1. Typical case.
Several years ago, there was a case of a young woman who came to the clinic at about two o’clock at night after drinking about one pound of highly alcoholic beverage. The patient was intubated and a large amount of vomit was aspirated from the airway, and bronchial lavage was performed, which washed out a large amount of turbid liquid. Gastric lavage with a gastric tube was then performed, and a large amount of gastric contents with the smell of alcohol was washed out. After aggressive treatment, the patient regained consciousness only at noon the following day and began to have fever. A chest X-ray showed scattered patchy shadows on the back of both lungs, which was diagnosed as aspiration pneumonia, and the patient was treated for up to two weeks before being discharged. This patient would have had a high probability of death if he had come to the clinic later.
Therefore, the intoxicated patient must not be placed in the supine position; the head must be tilted to the side to prevent vomit from entering the trachea. And depending on the situation, gastric lavage with a gastric tube and gastric emptying measures are performed, the latter also aiming to prevent the occurrence of aspiration by mistake.
In addition, to determine how much gastric contents, you can also be based on an orthopantomograph of the chest, such as the disappearance of gastric bubbles, often suggesting that the patient’s stomach is in a state of fullness.
2, the prevention of misaspiration in critically ill patients.
The main mechanism of misaspiration is the reduced level of consciousness due to various causes, accompanied by diminished vocal or cough reflexes, and when the natural defense of the upper gastrointestinal tract is impaired (e.g., incomplete closure of the esophageal sphincter). The danger of misaspiration is twofold, physical and biological, and must be fully recognized. The main preventive measures for misaspiration are: gastrointestinal decompression; use of antiemetics or antacids or drugs that accelerate gastrointestinal motility; attention to posture and feeding.
(1) Simple two-step swallowing stimulation test
Recently, Teramoto et al. in Japan reported a simple and easy two-step swallowing stimulation test (STS-SPT) with only one fine nasal catheter, which can detect swallowing dysfunction in various patients prone to aspiration pneumonia. Therefore, the STS-SPT is particularly useful for differentiating between those prone to aspiration and those with normal swallowing function. Since the STS-SPT does not require a special device, but only a thin nasal cannula, it is suitable for all frail elderly patients and can be done at the bedside.
Method: patient in supine position via nasal catheter (0.5 mm inner diameter) to the upper pharynx.
Step 1: Injection of 0.4 ml of water.
Step 2:injection of 2.0 ml of water.
Observe swallowing response and swallowing latency. The appropriate position of the catheter opening in the upper pharynx can be determined by visual inspection. The latency period refers to the time between the injection of water and the start of swallowing, which is determined by observing the characteristic movements of the larynx and measured with a running meter; the swallowing reaction is normal if it occurs within 3 seconds after the injection of water.
(2) Feeding of patients prone to aspiration
①Adjust the feeding position. During feeding, the patient takes a 30° to 45° supine position with the neck flexed forward and the head turned to the side of pharyngeal paralysis so that the food can pass smoothly through the pharynx. The forward-flexed neck position can reduce the time for food to pass through the pharynx and is a way to prevent misaspiration, while the backward neck extension has the opposite effect. Studies have shown that eating from a 45° lateral position is less likely to cause aspiration than from an upright position. Fatigue will increase the risk of misaspiration, and rest should be paid attention to before eating, lying still for 1 to 2 hours, and after eating to avoid esophageal reflux, the sitting and standing position should be maintained for 0.5 to l hours.
②Change the method of food properties. Generally use semi-liquid, soft food, paste or jelly-like viscous food, food should be soft, with appropriate viscosity, not easy to loose, so that it is not easy to remain and easily deformed when passing through the pharynx. It is important to pay attention to the amount of each intake, i.e., the amount of one bite. Too much of one bite can be retained in the pharynx and lead to accidental aspiration or spillage from the mouth, while too little of one bite is difficult to induce the swallowing reflex, generally starting from 5 ml and increasing as appropriate. The temperature of the food and the patient’s oral hygiene should also be taken seriously.
Second, disulfiram-like reaction: “A medical history, means a life.”
The molecular structure of some antibiotics, such as cefoperazone, contains groups such as N -methyl thiotetrazole, which can inhibit the activity of acetaldehyde dehydrogenase, thus making acetaldehyde unable to degrade and accumulate in the body, causing the phenomenon of acetaldehyde poisoning – disulfiram reaction, also known as disulfiram wake reaction. Patients may experience facial flushing, headache, dizziness, abdominal pain, stomach pain, nausea, vomiting, heartbeat, shortness of breath, accelerated heart rate, decreased blood pressure, and drowsy hallucinations, etc. Severe cases may result in 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 alcoholism should be asked for a history of recent drug use. “A medical history means a life.”
1. Mechanism.
Cefoperazone is a second-generation cephalosporin, with a wide antibacterial spectrum and strong antibacterial effect, mainly excreted through the biliary tract; therefore, the usual amount is available for those with renal impairment, and the usual amount is also available for those with hepatic impairment or biliary tract obstruction, so that renal excretion can increase and compensate for the decrease in biliary excretion. 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.
Disulfiram-like reactions can occur when alcohol is consumed during the application of cefoperazone up to 5 days after the drug is administered. Therefore, patients should not drink alcohol, orally or intravenously administer drugs containing ethanol during the drug administration and within 5 d after stopping the drug.
2. Drugs that can cause disulfiram-like reactions.
(1) Cephalosporins: cefoperazone, cefmetazole, cefminox, cephalexin, cefmenoxime, cefamandole, ceftriaxone, cefadroxil, cefazolin, cefradine, cefaclor, etc. Cefoperazone has the most reported disulfiram-like reactions and is the most sensitive.
(2) Nitroimidazoles: such as metronidazole, tinidazole, ornidazole, Secnidazole.
(3) other antibacterial drugs: such as furazolidone, chloramphenicol, ketoconazole, ashwagandha.
3.Other.
(1) fresh cut flowers to preserve freshness. Alcohol is often added to the water used in flower arrangements, and human contact can also lead to disulfiram-like reactions or idiosyncratic reactions, which should be clinically noted. For example, some patients eat wine core chocolate after medication, take patchouli water, or even treat the skin with alcohol can also occur disulfiram-like reactions.
(2) It has been pointed out that such reactions can also 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, so medical personnel try not to disinfect with ethanol but with povidone-iodine when giving patients such drugs.
(3) Alcohol-containing drugs: nitroglycerin and hydrocortisone; during the use of cephalosporin antibiotics, such as intravenous nitroglycerin or hydrocortisone, can also occur disulfiram-like reactions, which are easily misdiagnosed as drug allergies.
4, acute pancreatitis: “A lab test, means a life.”
Alcohol consumption can lead to an attack of acute pancreatitis, and the latter can produce myocardial depressor factors that can cause cardiac arrest. Therefore, patients with alcoholism should be routinely checked for serum amylase. “One lab test means one life.”
More than twenty years ago, there was a case of an elderly patient who came to the clinic after drinking alcohol at dinner with abdominal pain, the receiving doctor gave routine serum biochemical tests and found that the blood amylase was normal, and went home after symptomatic treatment; the next morning the family found that the patient did not get up, called out and pushed, before confirming that the patient had died, and later the autopsy revealed that it was severe pancreatitis. In patients with severe pancreatitis, the amylase in the tissues could not enter the blood because of the extremely poor blood flow of the pancreas, so the blood amylase was normal. The diagnosis and treatment of this case is a profound lesson.
Alcoholism is the leading cause of acute and chronic pancreatitis in Western countries. In the United States, 1/2-2/3 of acute pancreatitis is associated with alcoholism each year. If you do not stop drinking after an episode of acute alcoholic pancreatitis, there are those who can fully recover. 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 consumed, the habit of slow drinking and eating with wine and vegetables.
Alcohol may cause acute pancreatitis through several pathways.
(1) Causing hypertriglyceridemia or direct toxic effects.
(2) Increased duodenal pressure and reflux of duodenal fluid into the pancreatic duct.
(3) Spasm of the sphincter of Oddi, papillitis, and edema, leading to increased pressure in the pancreatic duct.
(4) Stimulation of gastrin secretion from G-cells in the gastric sinus, which stimulates pancreatic secretion.
(5) Absorption from the stomach, stimulating the secretion of hydrochloric acid from the cells of the stomach wall, which then causes the secretion of pancreatin and glucagon in the duodenum, eventually leading to pancreatic hypersecretion, etc.
5. Hypothermia: “A blanket, means a life”.
(1) Death caused by alcohol-related hypothermia
Since alcohol can cause vasodilation, increase heat dissipation, and reduce judgment or cause sluggishness; especially in a cold environment, it tends to cause hypothermia. The latter can cause hypercoagulability, hyperglycemia and cardiac arrhythmias 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, insulation is a necessary measure when dealing with acute alcohol poisoning, both out-of-hospital and in the emergency department. “A blanket means a life”.
①Generalized cold injury is also called cold stiffness and is a frozen cold injury.
It is a large loss of body heat caused by prolonged exposure to low temperature and 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 of freezing cold injury caused by hypothermia, i.e., complete “freezing”, because of the rapid loss of body temperature, often before complete “freezing”, cardiac arrhythmia can occur and death can occur.
②The mortality rate of hypothermia is very high, and the clinical manifestation is like stroke or metabolic disorder.
(3) As the body temperature drops, the patient goes from fatigue, weakness, ataxia, emotional indifference and drowsiness to a state of acute psychosis.
When the body temperature drops to <32.2℃, it further develops into malaise and coma, hallucinations, aggressive behavior, refusal of assistance, etc. can also be seen. The hands, feet, and abdomen of hypothermic patients are cold to the touch; however, the absence of chills, shallow and slow breathing, slow pulse, and decreased blood pressure with atrial and ventricular arrhythmias are notable; the face may be puffy and peachy. In slightly less than 50% of hypothermic patients, the early ECG may show a characteristic J wave, a small positive wave that appears after the QRS group in the left heart leads. More commonly, the ECG shows baseline vibrations due to subtle rapid muscle tremors, which are often mistaken for electrical disturbances or patient-initiated actions; these subtle muscle tremors are usually not obvious, but in the hypothermic elderly, they may be physiologically equivalent to chills. Neurological signs such as tremors, ataxia, pathological reflexes and reflex inhibition, coma, seizures, and markedly increased muscle tone may occur. If the drop in temperature is not stopped, the patient often dies from cardiac arrest or ventricular fibrillation at temperatures between 24.9°C and 23.9°C. Even if the patient survives, the effects of hypoxia on systemic metabolism and tissue necrosis are inevitable. Hypothermia can delay the onset of many complications (the most common complications are pancreatitis, pulmonary edema, pneumonia, metabolic acidosis, renal failure, and gangrene of the limbs).
If a patient develops hypothermia, the temperature should be slowly raised to normal (≤0.6°C per hour). More rapid rewarming can often cause irreversible hypotension. In a warm room, the use of blankets or other higher-grade insulating substances can be used for the purpose of insulation. Careful monitoring of the patient and the ability to anticipate common complications are necessary for successful treatment.
6. rhabdomyolysis: “A turn over means a life”.
Patients who drink alcohol often fall asleep for a long time, and if the limb is inactive, prolonged compression of the site can also lead to ischemic necrosis of the muscles, 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 blocking the renal tubules often causes renal failure (acute renal failure), and the morbidity and mortality rate is high. Therefore, patients with acute alcoholism, must be turned regularly to prevent prolonged pressure on the limbs. “One turn means one life.”
Acute alcoholic myopathy mostly occurs in long-term alcoholics after a single heavy drinking session, and the main types are.
(1) Acute alcoholic myopathy with rhabdomyolysis.
It is most common among long-term heavy drinkers, especially among those who have been drinking lifelessly, and is caused by acute metabolic disorders of muscle cells caused by alcohol. Acute onset, muscle pain, muscle swelling, muscle spasm, ranging from tens of seconds to several hours, some with muscle weakness as the first symptom, muscle swelling, tightness, and severe pain on postural changes or compression. Sometimes it can appear in all muscles of the body, sometimes it is confined to some muscles. The dark brown color of urine is caused by myoglobin, and serum creatine kinase (CK) values are significantly elevated. Pathologically, swelling and necrosis of muscle fibers, cellular infiltration and phagocytosis are seen. Mild cases can recover in 1 to 2 weeks, while severe cases can lead to acute renal insufficiency due to myonecrosis and high myoglobinuria. In cases where the symptoms are limited to a portion of the muscle, it may be related to impaired muscle circulation due to prolonged pressure on one’s own weight during intoxication and sleep. CT and calcium isotope markers are needed to understand the extent of muscle lesions.
(2) Acute alcoholic myopathy with hypocalcemia.
Long-term heavy drinkers can suffer from hypocalcemia and its associated myopathy due to frequent diarrhea, vomiting, heavy work under high temperature, application of thiazide diuretics, taking licorice, etc., which can lead to calcium loss. It manifests as proximal weakness of the upper and lower extremities, low muscle strength of the anterior cervical flexor group, and difficulty in raising the head. Unlike acute myasthenia with rhabdomyolysis, muscle swelling, spontaneous pain, pressure pain, and myospasm are rare. Serum calcium values are markedly low, serum CK values are markedly elevated without myoglobinuria, and muscle biopsy reveals muscle fiber necrosis, vacuolation and cellular infiltration. Muscle strength returns to normal within a few days to 2-3 weeks after calcium supplementation.
(3) Acute alcoholic myopathy with hypokalemia.
It is caused by vomiting, diarrhea, heavy physical labor in a hot environment, or loss of potassium by taking potassium-removing diuretics. It is characterized by weakness of the limbs, with the proximal limbs heavier than the distal limbs, and difficulty in lifting the neck due to weakness of the neck muscles. Blood potassium is measured to be significantly low, serum CK is significantly elevated, there is usually no myoglobinuria, and muscle strength generally recovers within days or 2 weeks after potassium supplementation.
The pathogenesis of acute alcoholic myopathy is unclear, and it is speculated that it may be related to the following factors.
① alcohol and acetaldehyde decrease glycolytic enzyme activity and inhibit the metabolism of sugars.
② alcohol and the metabolite acetaldehyde have toxic effects on myocytes causing toxic damage to myosin membranes and mitochondria and mitochondrial dysfunction; or blocking actin and myoglobin kinases and preventing troponin binding; thus damaging cell structure and affecting cellular transport leading to myocyte damage.
(iii) causing major oxidative substrates of skeletal muscle
(iv) The presence of metabolic abnormalities such as hypokalemia, hyponatremia, hypophosphorus, hypocalcemia and hypomagnesia, as well as vitamin B deficiency, resulting in secondary muscle damage.
⑤ Patients with alcoholism who have seizures, tremors, delirium and hyperthermia can increase somatic activity and myocyte metabolism, leading to myocyte damage; seizures and limb compression can induce rhabdomyolysis. Pathological manifestations are muscle necrosis, with or without inflammatory response muscle fiber regeneration, type I fiber atrophy.
7, hypotonicity after gastric lavage: “A detail that means a life”.
In the first aid of alcohol poisoning, emetic, gastric lavage, and catheterization can have a certain effect on the removal of residual ethanol in the gastrointestinal tract; however, active gastric lavage is not advocated. The main reason is that alcohol is absorbed quickly, so gastric lavage is not very meaningful, and there is an increased risk of accidental aspiration, and gastric lavage may cause more irritation to the gastric mucosa than alcohol. However, in some special cases where gastric emptying is required, such as full meals and simultaneous administration of other toxic substances, gastric lavage is still necessary. At present, most hospitals use hypotonic water for gastric lavage, which can enter the blood in large quantities, thus causing a hypotonic state in the body, and hypotonic cerebral edema can occur. Since the patient is in a comatose state, clinical signs such as cerebral edema are easy to ignore, and once brain herniation occurs, sudden death can occur. Therefore, after massive gastric lavage, the preventive application of some drugs to prevent the occurrence of hypotonic state, such as diuretics, glucocorticoids, mannitol, etc., may prevent the occurrence of this type of sudden death. “A detail that means a life”.
Secondly, alcohol intoxication itself can also cause ischemia or even cerebral edema in brain tissue. The mechanisms by which this occurs may be.
(1) Platelet hyperfunction and blood hypercoagulability: Alcohol intoxication can cause an exponential increase in platelet rebound, as well as a decrease in fibrinolysis and a significant prolongation of fibrin spontaneous lysis. Heavy alcohol consumption can also induce platelet aggregation and an increase in 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.
(2) After 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, resulting in further impairment of blood supply to the cerebral circulation.
8. Cardiac emergencies: “A check-up means a life”.
Drinking alcohol can induce acute myocardial infarction, and this point needs no elaboration. In emergency work, alcoholic patients need an ECG, especially the elderly and those with underlying pathologies such as diabetes. Acute myocardial infarction in a drowsy drinker is relatively insidious and can be asymptomatic. “A test that means a life.”
In addition, acute alcohol intoxication itself can cause heart damage. Among patients with acute alcohol intoxication, some cases have abnormal electrocardiograms and myocardial enzymatic changes, and the degree of acute alcohol damage to the heart is directly proportional to the time and degree of intoxication.
9. Cerebral hemorrhage: “An experience that means a life”.
A patient was rushed to the hospital for rescue due to deep alcohol intoxication. The doctor diagnosed acute alcohol intoxication and gave appropriate active treatment in 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 brain hemorrhage. It is estimated that 110,000 people die each year in China from brain hemorrhage caused by alcohol poisoning, accounting for 1.3 percent of the total mortality rate. “One experience means one life”.
In short, there are at least eight ways to die from acute alcoholism, and once you know the “why”, which means understanding its pathophysiology, it is clear how to deal with alcoholism.