Asphyxiating gases are those gaseous compounds that can directly impede the supply, ingestion, transportation, and utilization of oxygen. Excessive inhalation of asphyxiating gases can cause the body to suffer from hypoxia as the main link of the disease state, which is called asphyxiation gas poisoning.
First, suffocating gas
Asphyxial gas poisoning is the most common acute poisoning. According to statistics on national occupational disease incidence in 1988 , asphyxiating gas poisoning ranks first among acute poisonings; according to the analysis of 40 years of acute occupational poisoning deaths by the Ministry of Chemical Industry , the top priority is still asphyxiation. Gas poisoning, caused by the death toll actually accounted for 65 % of the total number of acute occupational poisoning deaths , showing the importance of such poisons. Based on the toxic effects of these asphyxiating gases, they can be roughly divided into three categories.
(1) Pure Asphyxiating Gas This type of gas has very low toxicity or is inert gas. However, if there is a lot of air, the oxygen content in the inhaled gas can be significantly reduced, leading to oxygen deficiency in the body. Under normal circumstances, the oxygen content in the air is about 20.96 %. If the oxygen content is < 16 %, it can cause breathing difficulties. If the oxygen content is < 10 %, it can cause coma or even death. Common asphyxiating gases belonging to this category are: nitrogen, methane, ethane, propane, ethylene, propylene, carbon dioxide, water vapor, and inert gases such as argon and helium.
(2) Blood asphyxiating gas Blood carries oxygen in a chemically bound manner, normally about 1.4 ml of oxygen per gram of hemoglobin , 15 g per 100 ml of blood The calculation of hemoglobin can carry about 21ml oxygen blood; the blood flow of the lung is about 5L /min , so the blood takes about 1000ml of oxygen from the lung every minute . The toxicity of blood asphyxiating gases is that they can significantly reduce the chemical binding capacity of hemoglobin to oxygen, and prevent hemoglobin from releasing oxygen that has been carried to the tissues, thus causing oxygen barriers to tissues. Therefore, such poisons are also called chemically asphyxiating gases. Common are: carbon monoxide, nitric oxide, benzene, nitro or amino compound vapors.
(3) Cell Asphyxiating Gases These toxicants mainly act on intracellular respiratory enzymes, inactivating them, thereby impeding the use of oxygen by cells, disrupting the process of biological oxidation, and creating hypoxic effects of cells. Since this type of hypoxia is essentially a "cell suffocation" or "internal asphyxiation," such poisons are also known as cytosolic poisons. Commonly hydrogen cyanide and hydrogen sulphide are known.
Second, toxic effects
The main toxicity of asphyxiating gases is that they can cause hypoxia in cells and tissues in the body. To study the mechanism of hypoxia-injury from the sub-cellular and even molecular levels, there are mainly two pathogenic links:
①anoxic anaerobic metabolism due to cell enhanced, so that the acidic metabolites within the cell increased significantly, resulting in metabolic acidosis. Intracellular H+ accumulation activates the H+-Na+ exchange mechanism to excrete too much H+ , but excess Na+ in the cell reactively activates the Na+-Ca2+ exchange system, prompting Ca2+ to enter the cell to drain excess Na+ . At this time, the lack of oxygen has caused the lack of ATP in the cells and is gradually depleted, so it is impossible to pump out excess Ca2+ in the cells, resulting in the imbalance of intracellular calcium homeostasis. One of the serious consequences of intracellular calcium overload is the activation of xanthine dehydrogenase invertase, which converts xanthine dehydrogenase to xanthine oxidase. Under normal circumstances, hypoxanthine degradation products of AMP without oxygen, can be oxidized under the catalysis of xanthine dehydrogenation to uric acid from the urine; in the absence of oxygen, ATP depletion, its degradation products AMP increased a lot, For the xanthine oxidase transformed from dehydrogenase to provide a large number of substrates, when the tissue is reperfusion, it can be metabolized to uric acid in the participation of O2 , and generate a large number of superoxide anions (O2-) , triggering lipid peroxidation. Reaction, damage to local tissue. It should be noted that suffocating gas poisoning is often treated with high-oxygen oxygen, and that the use of high-concentration oxygen for a long time will activate macrophages and neutrophils, causing a "breath burst," resulting in a large amount of reactive oxygen species. Injured tissue; In addition, hypoxia and excess free radicals generated in the body, all may make Fe3 + dislocation from the protein, this iron ion can generate large amounts of hydroxyl anion radicals ( · OH) through the Fenton reaction ; hemoglobin into high-speed iron Hemoglobin also produces reactive oxygen species such as O2- . These reactive oxygen species, through lipid peroxidation, destroy the biological structure, denature proteins, inactivate enzymes, and cause structural abnormalities in the nucleic acid, resulting in severe damage to tissue cells and constituting the molecular basis of asphyxial gas poisoning.
2 The other serious consequence of the aforementioned intracellular calcium overload caused by hypoxia is the activation of the intracellular phospholipase A2 , which causes the phospholipid components of the biofilm to be largely decomposed to generate a large amount of free fatty acids, of which arachidonic acid can be Further conversion to thromboxane (TXA2) , prostaglandins (PG) , leukotrienes (LT) and the like. Thromboxane is an endogenous active substance that is known to cause the strongest microvascular vasospasm and can activate microplatelets to form microthrombi. Therefore, the production of trace thromboxanes can cause obvious hypoxia-ischemia in local tissues; arachidonic acid itself is also Can activate platelets, cause microthrombosis, aggravate ischemia and hypoxia; other metabolites are also inflammatory substances, can aggravate the inflammatory response and reactive oxygen species, strengthen the aforementioned process; ischemia and hypoxia then lead to more serious cell calcium Overloading leads to more reactive oxygen species and a vicious circle. Based on the above molecular damage mechanism, the most prominent pathological change caused by asphyxiating gas poisoning through the main link of hypoxia is brain edema. The brain is the organization with the highest oxygen consumption, although it only accounts for 2 % to 3 % of the body weight , but the oxygen consumption can account for 20 % to 25 % of the total body oxygen consumption , so it is most sensitive to hypoxia. Studies have shown that most nerve cells only have functional disturbances in the early days of hypoxia, and they can recover with proper treatment. If oxygen supply is further limited, the injury will become unrecoverable and even cause cell death. In other words, most of the fatal injuries of nerve cells are caused not directly by acute hypoxia, but by various evils caused by hypoxia. The most serious consequence is brain edema. The molecular damage mechanism of brain edema is the massive generation of reactive oxygen species and the intracellular calcium overload. The consequence of cerebral edema is the worsening of ischemic and hypoxic conditions in the brain tissue, and thus initiates a vicious cycle of hypoxic injury. The specific aspects of brain edema formation are roughly the following:
In addition cerebrovascular dilation reflex due to anoxia, causing swelling of the brain leads to blood stasis, hypoxia-induced cell permeability barriers and obstacles ATP production molecular mechanisms of hypoxia-induced cell damage caused by water can lead to a large number of intracellular sodium retention, The formation of a wide range of intracellular edema; hypoxic injury also makes the vascular endothelial permeability abnormalities, so that intravascular fluid infiltrated into the extracellular space, thereby causing intercellular edema of the brain cells; brain vascular endothelial cells can also be due to anoxic injury swelling , causing partial blood vessel narrowing or blockage. These changes will further reduce blood perfusion in the brain, increasing cerebral hypoxia; the other due to the fixed volume of the cranial volume, so a little increase in volume, which will cause a significant increase in intracranial pressure, but showed clinically severe symptoms.
Third, the clinical manifestations
1. Hypoxia performance
Hypoxia is a common pathogenic link of asphyxiating gas poisoning, so hypoxic symptoms are a common manifestation of various asphyxiating gas poisonings. Mild hypoxia mainly manifested as inattention, mental decline, disorientation, headache, dizziness, fatigue; severe hypoxia can have tinnitus, vomiting, lethargy, irritability, convulsions or convulsions, and even coma. However, the above symptoms are often disturbed or obscured by the unique toxicity of different asphyxiating gases, so it is not the same clinical manifestations of hypoxia caused by different pathogens. Timely treatment, so that the brain as soon as possible to improve oxygen deficiency, often avoid severe brain edema, otherwise it will lead to significant performance of acute intracranial hypertension.
2. Acute intracranial hypertension performance
1 headache. Is the main symptoms of the early, full headache, particularly forehead, the degree is very dramatic, any increase in intracranial pressure factors such as coughing, sneezing, bowel movements, and even a sudden turn of the head can significantly increase the headache;
2 vomiting. Is a common symptom of increased intracranial pressure, mainly due to pressure in the vomiting center of the medulla oblongata, but the brain edema caused by asphyxiating gas poisoning is mainly intracellular edema, the degree of intracranial pressure rise is not heavy, so jet vomiting and Rare;
3 convulsions. Frequent epilepsy-like seizures are mainly caused by ischaemia and hypoxia or edema compression in the cerebral cortex; if the brain stem is also involved in the reticular formation, paroxysmal or persistent limb rigidity may occur.
4 papilledema. Asphyxial gas poisoning is mainly based on intracellular edema, and the intracranial pressure rises slowly and to a lesser extent. Therefore, it is difficult to detect papilledema in the early stage. It usually appears gradually after 2 to 3 days, so the early stage of poisoning cannot be detected. Seeing papilledema does not exclude the presence of brain edema;
5 Changes in the cardiovascular system. Early increase in blood pressure, slow pulse, is the medulla cardiovascular movement center due to edema compression and ischemia and hypoxia compensatory effect; if medullary failure, you can see a sharp drop in blood pressure, pulse is also weak, rapid;
6 Breathing changes. The early manifestation of deep breathing is also the compensatory response of the medulla oblongata; if the respiratory center is depleted, the breathing turns to shallow, irregular, or sigh-like breathing, and severe respiratory arrest may occur;
7 other performance. Stimulating the vestibular labyrinth, and intracranial hypertension, can cause tinnitus, vertigo; abducens nerve compression can cause abducens nerve palsy; medullary sympathetic ganglia stimulation, may result in excessive shrinkage peripheral, pulmonary stasis of blood flow, a so-called brain occurs Pulmonary Edema;
8 cerebral palsy. Asphyxiating gas poisoning caused by cerebral palsy is not much, if found that symptoms of increased intracranial pressure suddenly increased, coma, increased body temperature, both sides of the pupil is not the same size, limb spasms, decerebrate rigidity and other performance, should be alert to ditch back ( also said canopy hernia) possible; see if there is then dilated pupil to narrow, fixed, respiratory depression or even a sudden stop, drop in blood pressure, neck stiffness was forced head position, positive bilateral pyramidal syndrome, muscle tension and deep reflexes such as performance, the Should consider the possibility of cerebellar tonsil hernia. Computer tomography (CT), magnetic resonance imaging (NMR) help to identify early brain edema, conditions can be used in time.
3. Particular manifestations of different asphyxiating gas poisoning
1 Symptoms caused by large amounts of nitrogen inhalation are most similar to the hypoxia symptoms mentioned above, but at a slightly higher concentration can often cause extreme excitement, awkward expression, and unsteady gait, such as drunkenness, known as “nitrogen deficiencyâ€. Inhalation of very high concentrations of nitrogen can quickly stun the patient and cause death, known as "nitrogen asphyxia."
2 Carbon dioxide is also a pure asphyxiating gas, but due to CO2 retention, respiratory acidosis, and hyperkalemia, the brain edema manifests itself often and lastingly. Inhalation at high concentrations can quickly become unconscious and die within seconds.
3 Carbon monoxide is a blood-asphyxial gas. After inhalation, it can rapidly combine with hemoglobin to form carboxyhemoglobin (HbCO) . Therefore, blood HbCO measurement is an important basis for diagnosing CO poisoning. HbCO > 10 % in blood may cause acute CO poisoning. Because HbCO is bright red, the skin and mucous membrane of the patient is cherry-red at the beginning of poisoning, which is obviously different from that of general hypoxic patients. It is one of its clinical features. In addition, the general malaise is very obvious, even after soaking, although it is still awake, It is difficult to act and cannot save itself. The rest of the symptoms are similar to normal hypoxia.
4 Benzene amino or nitro compounds ( such as aniline, nitroaniline, nitrobenzene, etc. ) vapors are also blood asphyxiating gases, and the hypoxia symptoms caused by the poisons are mainly due to normal Hb being converted to methemoglobin (MtHb) . Loss of oxygen carrying capacity . MtHb is blue-purple, and its amount exceeding 15 % of total Hb can cause purpura and become characteristic manifestation of degenerative hemoglobinemia. MtHb is also an important evidence for the poisoning of such compounds. Unresolved methemoglobinemia, which has not been corrected, can cause hemolytic anemia due to the formation of Heinz bodies in erythrocytes . In addition, toxic liver and kidney damage are common manifestations of such compounds.
5 Aspergillus hydrogen cyanide gas, its poisoning is clinically characterized by symptoms of hypoxia is very obvious, inhalation at a slightly higher concentration can cause extreme dyspnea, severe systemic sacral spasm can occur; very high concentrations of HCN can be in minutes Causes respiratory heartbeat to stop and die. Due to the strong inhibitory effect of HCN on cellular respiratory enzymes, the cells almost lose the ability to use oxygen, resulting in venous blood is still full of sufficient oxygen to show the bright red of oxygenated hemoglobin (HbO2) , so the mucosal skin color of patients with early poisoning is redder, Become another clinical feature of hydrogen cyanide poisoning. 6 Hydrogen sulfide is also a cytosolic gas, but it also has stimulatory effects and should be noted. There are three clinical features:
1 After inhaling a high concentration of breath, the respiratory heartbeat stops immediately and a so-called "lightning-type" death occurs;
2 Because H2S can form blue-violet vulcanized degeneration hemoglobin in blood, a small amount (4 % to 5 % ) can cause purpura, so the color of patients with H2S poisoning is mostly blue-gray;
3 exhaled breath and clothing with a strong odor smell; respiratory tract and lungs may produce chemical inflammation or pulmonary edema. The clinical manifestations of common asphyxiating gases are summarized in Table 5-1 for reference.
Fourth, treatment
1. The principle of treatment
The operation of the acute asphyxiation gas group poisoning treatment can refer to the irritant gas poisoning section, but the suffocation gas poisoning condition is even more urgent. Therefore, various measures, especially detoxification and oxygen therapy, should be carried out as soon as possible. Specific details are as follows.
2. Pathogen treatment
Asphyxiating gas poisoning significant dose - response relationship, the more the number of poison invade the body, the greater the harm, and because the disease is also more acute weight, so as soon as possible with particular emphasis interrupt poison intrusion, lift the body of toxic poisons. The sooner the rescue measures begin, the smaller the damage to the body, and the fewer complications and sequelae.
(1) Patients who continue to invade into the hospital after the interruption of poisons have been removed from the site, but care should be taken to remove clothing and skin contamination sources. Patients with hydrogen sulfide poisoning should remove contaminated work clothes; if there is liquid such as hydrocyanic acid, aniline, and nitrobenzene splashed on the body, the contaminated skin should be thoroughly cleaned. Critically ill patients are prone to central respiratory and circulatory failure and should be highly vigilant. In such cases, cardiopulmonary resuscitation should be performed immediately.
(2) Detoxification measures There are no special antidotes for asphyxiating gases such as nitrogen, but respiratory stimulants can be used for CO2 inhalation. In severe cases, mechanical hyperventilation can be used to excrete excess CO2 in the body . This is considered a "detoxification" measure. Nothing is wrong. In blood asphyxiating gases, there is no special detoxification drug for CO , but oxygen can be inhaled to accelerate the dissociation of HbCO , which can also be considered as a detoxification measure. The denaturalized hemoglobin formed by the poisoning of benzene's amino or nitro compounds is still reduced to the best detoxification treatment with methylene blue. In cell-asphyxiating gases, HCN is usually driven by sodium nitrite - sodium thiosulfate therapy;
In China, 4 -dimethylaminophenol (4-DMAP) is also used instead of sodium nitrite, which also has better effects. Methylene blue can also replace sodium nitrite, but the dose should be large. In theory, H2S poisoning can also use HCN antidote, but H2S conversion rate in the body is very fast, and the above measures will generate a considerable amount of MtHb and reduce the blood carrying oxygen, so unless immediately after poisoning, it may be more disadvantageous than Lee.
3. Etiology treatment
As mentioned above, asphyxiating gases cause organisms to suffer from hypoxia and even cause "injury." In the course of pathogen treatment, anti-hypoxia and anti-brain hypoxia measures should be implemented as soon as possible.
(1) Oxygen therapy studies have shown that increasing oxygen tension not only improves tissue cells
Table 5-1 Common Asphyxiating Gases
Oxygen uptake ability, but also have an activating effect on poisoned respiratory enzymes, so oxygen therapy has become one of the main routine measures for rescue of acute asphyxial gas poisoning. High concentrations ( > 55 % ) of oxygen should be given rapidly after poisoning . Commonly used masks, masks, valve flaps, balloon or oxygen traps, and ventilators should be used for oxygen administration. Hyperbaric oxygen therapy can also be used under certain conditions. You can use the "inner oxygen" method to inject intravenous 0.3 % hydrogen peroxide ( see detoxification and special treatment section ) .
(2) artificial low temperature hibernation ( see detoxification and special treatment section ) to avoid care, rewarming process is too difficult, the temperature does not have to be too low, the rectal temperature can be maintained at about 34 °C ; time does not have to be too long, generally maintain 2 ~
After 3 days, gradually warm up.(3) The main measures for improving brain perfusion are as follows.
1 Maintain adequate cerebral perfusion pressure. The main point is to maintain the blood pressure at normal or slightly higher levels, so any reason for low blood pressure is promptly corrected, but it should also prevent the sudden increase in blood pressure too much, so as not to cause a sudden increase in intracranial pressure. Emergency situations available 4 ~ 10 ℃ saline or dextran (300 ~ 500ml / 0.5h) direct bolus through the carotid artery, in order to achieve cooling, and then through the microcirculation purposes.
2 correct intracranial "theft of blood." Moderate mechanical hyperventilation can be used to correct. Due to the decrease of PaCO2 , the blood vessels in the region less affected by hypoxia can be reflexively contracted and the blood can be reinfused into the severe hypoxic region to improve the shunt in the brain and correct the purpose of "theft of blood." PaCO2 is generally maintained at 4kPa (30mmHg) can be, PaCO2 too low may lead to excessive cerebral vasoconstriction, in addition to increased cerebral hypoxia.
3 Improve microcirculation conditions. It may be administered with a low molecular weight (MW2 ~ 4 million) dextran, help improve the plasma colloid osmotic pressure, recovering extracellular water, lower blood viscosity, prevention and elimination of micro-thrombosis, and may be rapidly excreted by glomerular having Diuretic effect; generally can be used within 24 hours with 1000 ~ 1500ml .
Molecular mechanisms of cell intervention hypoxic injury (4) injury hypoxic mainly two: the generation of active oxygen and intracellular calcium overload, so that the current interventions for these two cells, the primary object of Injury Repress at the subcellular level and do not progress to cell and tissue damage.
1 antioxidants. It has obvious anti-scavenging effect on reactive oxygen species including oxygen free radicals and their damaging effects ( see Detoxification and Special Treatment Sections ) .
2 calcium channel blockers. Because it can prevent Ca2+ from translocating into cells and directly block the damaging effects of thromboxane, it has been widely used in various ischemic and hypoxic conditions ( see Detoxification and Special Treatment Section ) .
4. Prevention and treatment of brain edema
Brain edema is the most serious consequence of hypoxia and the most important cause of asphyxial gas poisoning death. Therefore, it is the key to successfully rescue acute asphyxial intoxication; its main point is early prevention and treatment, so that brain edema does not occur or make it happen. Lighter. The above is the basic measure for prevention and treatment of hypoxic cerebral edema. In addition, there are other measures, as described below.
(1) Use ATP or energy mixture to improve brain cell ion pump function and reduce intracellular sodium and water retention; ATP still has the function of expanding microvessels, and can promote cell metabolism, which is beneficial to the recovery of brain cells. Usually 20 ~ 40mg ATP intramuscular or intravenous, can also be formulated as a static energy mixture.
(2) Diuresis dehydration Because of hypoxic brain edema, there is also extracellular edema, so it is also necessary for urine dehydration, but it needs to be well-controlled, because diuretic dehydration does not solve the problem of intracellular edema, but it causes blood volume reduction and blood pressure drop. The best. Usually furosemide (20 ~ 40mg , intramuscular or intravenous ) or sodium thiourea (20 ~ 50mg intravenous infusion ) 2 times / day, the latter can still inhibit cerebrospinal fluid secretion, reduce cerebral edema; acetazolamide also diuresis and reduce Cerebrospinal fluid secretion, can be 0.25 ~ 0.5g Oral, 2 to 3
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