Hospital treatment - irritant gas poisoning

 

Hospital treatment is an indispensable link in the treatment of chemical accidents. If the emergency rescue of chemical accidents, on-the-spot first aid, and safe and rapid transit have a decisive effect on the life and death of critically ill patients, it is the basis of the next treatment treatment. Then hospital treatment is to prevent The key to further damage to vital organs and to ensure the maximum recovery of the body.

Irritant gases are mainly gaseous compounds that have direct stimulatory effects on the respiratory tract and alveolar epithelium due to their physicochemical properties. Excessive inhalation of irritant gas can cause respiratory tract irritation, inflammation, or pulmonary edema as the main manifestation of the disease state, known as irritating gas poisoning.

First, the main poison

The most common irritant gases can be roughly classified into the following categories.

(1) Acids and acid-forming compounds such as sulfuric acid, hydrochloric acid, nitric acid, hydrofluoric acid, etc.; acid oxides ( anhydrides ) - sulfur dioxide, sulfur trioxide, nitrogen dioxide, dinitrogen pentoxide, five Diphosphorus oxide, etc.; and such as acid hydride - hydrogen fluoride, hydrogen chloride, hydrogen bromide, hydrogen sulfide and so on.

(2) Ammonia and amine compounds such as ammonia, methylamine, ethylamine, ethylenediamine, vinylamine, and the like.

(3) Halogen and halogen compounds are most common with chlorine and chlorine-containing compounds ( such as phosgene ) , and organic fluoride poisoning has also increased in recent years, such as octafluoroisobutylene, dichlorochloromethane cracking gas, Freon, and PTFE. Pyrolysis gas and so on.

(4) Metal or metalloid compounds such as cadmium oxide, nickel carbonyl, vanadium pentoxide, and hydrogen selenide.

(5) Ester, aldehyde, ketone, ether and other organic compounds are particularly irritating, such as dimethyl sulfate and formaldehyde.

(6) Chemical weapons such as stimulants ( Phenethyl Chlorophenone, Adam's Gas, Xi'Aar ) , erosive agents ( mustard gas ), etc.

(7) Other ozone (O2) is also an important cause. It is often used as a disinfectant, bleach, and strong oxidant. Oxygen in the air can also be converted into ozone under high temperature or short-wave ultraviolet radiation, most commonly in argon arcs. Welding, X- ray machines, UV lamps, photocopying equipment, etc. High-molecular polymers have been widely used in modern building materials, furniture, and interior decoration. Therefore, fire smoke often contains a large number of irritating pyrolysis substances, such as nitrogen oxides, chlorine, hydrogen chloride, phosgene, ammonia, etc. Draw attention.

Second, toxic effects

The main toxicities of irritating gases are their irritation and damage to the respiratory tract and alveolar epithelium because they form acidic or alkaline substances with strong corrosive effects on the mucosal surface, such as acid or acid-forming compounds, ammonia or amines. Compounds, esters, phosgene, etc. These injuries can also cause damaged cells to release a variety of tissue factors, causing local leukocyte, macrophage accumulation, activation and respiratory burst, resulting in a large number of oxygen free radicals, resulting in lipid peroxidation, and further damage to the local tissue. A small amount of oxygen radicals can be rapidly cleared by the tissue's antioxidant system, and the peroxidic damage is halted; however, a large amount of oxygen radicals generated will deplete the local antioxidant potential, including various antioxidant enzymes [such as superoxide dismutase] (SOD), catalase (CAT), glutathione peroxidase (GSH - Px) and the like], and non-enzymatic antioxidants (e.g. VitC, vitE, GSH, mannitol, glucocorticoids, etc.), and The peroxidation reaction can fully exert its damaging effect.

Some irritating gas itself is a strong oxidant, such as ozone; Many compounds can also be directly generated oxygen free radical induced tissue, such as nitrogen oxide, selenium compounds, and vanadium pentoxide, which directly caused mainly. Chemical ( also known as toxic ) lung water is mainly caused by various compounds with strong stimulation or injury on the alveolar epithelium, stroma components, blood vessels, lymphatic vessels caused by the direct damage and destruction, such as alveolar surfactant is destroyed Or reduce the production, so that the alveolar hydrophobicity, surface tension increases, leading to increased water extravasation and atelectasis; alveolar epithelium, pulmonary interstitial blood vessels damaged, can make plasma and even cellular components from the blood vessels into the lung interstitial mass and Alveolar cavity; chemical irritation can also cause increased bronchospasm and secretion, and through pulmonary chemoreceptor reflex caused by pulmonary capillary and pulmonary lymphatic contraction, resulting in poor ventilation, increased pulmonary vascular hydrostatic pressure, Poor quality of drainage, increase pulmonary edema. This complex pathogenic link, complex exudate composition, combined with the pathological basis of organizational structure damage, so that treatment needs more comprehensive consideration, can not be ignored.

Third, the clinical manifestations

Irritant gas poisoning can be divided into the following three manifestations according to its clinical characteristics.

1. Chemical ( or toxic ) respiratory inflammation

The irritant gas is mainly responsible for the direct irritative damage to the respiratory tract mucosa. The more water-soluble irritant gas, the stronger the damage to the upper respiratory tract, and the less amount it enters deep lung tissue, such as chlorine, Ammonia, sulfur dioxide, various kinds of acid mist and so on. In this case, see also rhinitis, pharyngitis, trachea, bronchi and performance go far ocular irritation symptoms such as sneezing, runny nose, tearing, photophobia, eye pain, pharynx on, sore throat, hoarseness, cough, expectoration Such as severe, may have blood stasis and shortness of breath, chest tightness, chest pain and other symptoms; inhalation of high concentrations of irritating gas due to laryngeal edema caused by significant hypoxia, cyanosis, and sometimes even cause laryngeal fistula, resulting in suffocation and death. Heavier chemical respiratory infections may present with systemic symptoms such as headache, dizziness, fatigue, palpitations, and nausea. Physical examination revealed nasal, pharyngeal mucosal hyperemia, edema, and even erosion. Severe fashion can be seen uvula edema, laryngeal edema; the lungs only heard breath sounds rough, even can hear dry rales. Laboratory tests and X- ray examinations were found to have no abnormalities. Most of these are mildly irritating gas poisoning, or early performance when inhaled with high concentrations of irritating gases. Timely disengagement, can be quickly recovered after appropriate treatment.

2. Chemical ( toxic ) pneumonia

Mainly due to the irritant gas into the deep respiratory tract on bronchioles and alveolar epithelial stimulating damage caused by the pathological examination can be seen mainly bronchial, bronchial mucosal hyperemia, edema, degeneration, loss, pulmonary capillary dilatation and congestion, pulmonary interstitial obvious Out and a large number of polymorphonuclear cells, macrophage infiltration, alveolar effusion may also have. In addition to clinical symptoms of upper respiratory tract irritation, the main manifestations are more obvious chest tightness, chest pain, shortness of breath, cough, phlegm, and even hemoptysis; body temperature is moderately elevated, with more obvious systemic symptoms, such as Headaches, chills, fatigue, nausea, vomiting, etc., generally last 3 to 5 days. The examination was mainly for the two lungs and scattered in small blisters; laboratory tests showed that the total number of white blood cells and the proportion of neutrophils were increased; X -ray showed thick lung texture, the edge is not clear, the two lungs scattered scattered irregular shadows, many Distribution along the bronchus, bilateral asymmetry, no significant changes in hilar. This type of performance can be considered moderately irritating gas poisoning, which is mostly caused by a longer inhalation of a higher concentration of irritating gas, but the prognosis is better. Healing can still be achieved after appropriate treatment , although the required recovery time is slightly longer. However, sometimes this type of performance is a manifestation of toxic early pulmonary edema, it should be given great attention, because once the progress of pulmonary edema, the prognosis is much more severe.

3. Chemical ( toxic ) pulmonary edema

Pulmonary edema is the most serious clinical manifestation after the inhalation of irritant gas. Because it occurs as a result of chemical substances acting on the lung tissue and causing damage, it requires a certain evolution time and is called clinically the "induction period" of lung cancer. The length of the induction period and the physicochemical properties of the irritating gas itself and the strength of the action have a peroxidative damage, ie, the lipid peroxidation destroys the cell structure.

The damage described above occurs in the respiratory tract and can cause irritation. Severe cases can lead to chemical inflammation, edema, congestion, hemorrhage, and even mucosal necrosis. In the alveoli, it can cause chemical pulmonary edema. This type of chemical pulmonary edema is more complicated than the various types of pulmonary edema that are common in medicine. Caused by internal medicine pulmonary edema such as acute left cardiac insufficiency, excessive over-infusion, or even kidney disease or malnutrition caused by hypoproteinemia, poor lymphatic drainage, etc., the increase of pulmonary capillary hydrostatic pressure is caused by this class mainly acute pulmonary edema, pulmonary structural damage rarely present, it is more simple, direct relationship __ moisture seeping in, the stronger the toxicity or the greater the intensity, the shorter the induction period, the more severe pulmonary edema. Inhalation of high concentrations of irritant gases can cause severe pulmonary edema in the short term, but under normal circumstances, chemical pulmonary edema is mostly evolved from chemical airway inflammation or even chemical pneumonia. At this time, the aforementioned inflammatory processes are It can be considered as the "stimulus period" of pulmonary edema, and also the "induction period" of pulmonary edema.

The length of this period is related to the toxicity and intensity of inhaled gas, but also related to the patient's physical load, cardiopulmonary function, individual sensitivity, joint pathogenic factors, treatment status and other factors, because these factors can be carried out by human intervention, so Making full use of the “induction period” and actively taking measures to reduce or even prevent the occurrence of pulmonary edema are important for improving the prognosis. In general, this induction period is 1 to 24 hours. The clinical features of pulmonary edema are based on the respiratory tract stimuli, or after a period of remission, sudden and shortness of breath, severe chest tightness, severe coughing, large amounts of foam phlegm, respiratory rate of 30 to 40 beats / minute or more, and accompanied by Clear cyanosis, irritability, sweating, can not lie. Auscultation can be heard in both lungs with wet rales, and the heart rate increases. In severe cases, complications such as shock and acute renal failure may occur, and moderate fever may occur. Laboratory tests showed that peripheral blood leukocyte counts increased significantly, the proportion of neutrophils were more than 0.9 ; blood gas analysis showed significant hypoxemia, early often due to hyperventilation and CO2 partial pressure decreased, late can be due to ventilation Obstruction causes CO2 retention. Chest X- ray examination, often seen in the early morning, the translucency of the two lungs generally decreased, the lung texture increased, the reticular structure was obvious, the hilum expanded, suggesting the existence of pulmonary interstitial edema; after the formation of alveolar edema, the two lungs appeared scattered irregular Flake shadows, unclear edges, and serious ones can be merged into large pieces. The X- ray appearance of pulmonary edema is often earlier than the clinical symptoms and signs, so early examination of the film helps early diagnosis, and should be repeated several times in order to determine the condition. Generally, the most dramatic change occurs at the beginning of the 24th hour. If there are no other factors, the development peak of chemical pulmonary edema is often around 36 hours.

The recovery period of pulmonary edema depends on the cause and condition, and treatment conditions. Under normal circumstances, the signs of pulmonary edema can generally subside after 3 to 5 days after treatment , but it usually takes 1 to 2 weeks for the X- ray to be normal, and it takes 1 to 3 months for ventilation and ventilation to recover gradually. Most chemical pulmonary edema does not leave sequelae after cure; but some irritant gases such as phosgene, nitrogen oxides, organic fluoropyrolytic gas, chloropicrin ( triclosan ), and other pulmonary edema, after recovery 2 From 6 weeks onwards, cough, fever, difficulty in breathing, and even death from acute respiratory failure may occur, mainly due to fibroproliferative bronchiolitis caused by the exudation of bronchioles; there are also some compounds, Such as chlorine, ammonia, etc. can be due to bronchial mucosal scars and hypertrophy, leading to chronic obstructive pulmonary disease; organofluorine compounds, modern building fire smoke can cause pulmonary interstitial fibrosis.

Fourth, treatment

1. Operation of group irritant gas poisoning hospital treatment

When receiving relevant departments' notice and preparing to receive a group of patients, they should immediately report the leadership of the hospital for unified command and coordination of the strength of the hospital. The Occupational Disease Unit or any consulting department should immediately prepare the bed, and if necessary, transfer the light patient or transfer to the office or conference room, or transfer the hospital bed from the hospital to the emergency room.

2 Based on the preliminary understanding of the scale and severity of the accident, make preparations for medicines, equipment and special inspections, special inspections, and liaise with the relevant brothers' offices to assist in handling the patient.

3 According to the data transmitted with the patient, the wards should be arranged according to the disease condition and be adjusted at any time according to the progress of the disease after admission. Patients at all levels should conduct uniform visits , division of labor, close observation, and timely disposal. In principle, anyone who has a history of acute irritant gas inhalation should stay for at least 24 hours.

4 strict ward sterile concept and isolation and disinfection system, the observation period and critically ill patients should decline to visit, to ensure that the ward quiet and clean treatment environment.

2. Early ( induction period ) treatment

1 All patients, including those who stayed at the clinic, should be examined as soon as possible with X -ray examinations to record the amount of fluid in and out and rest in bed.

2 actively improve the symptoms. For example, cough suppressants can be given as antitussives, including appropriate central antitussive agents; restless sedatives such as diazepam and phenazine; bronchial spasm available as isoproterenol aerosols. Inhalation or intravenous injection of aminophylline; neutrotic aerosol inhalation to help relieve respiratory irritation, including glucocorticoids, procaine, aminophylline and other effects better.

3 moderate oxygen. Use nasal congestion or masks, oxygen concentration into the lungs should be < 55 %; use positive oxygen pressure mechanically, so as not to induce airway necrosis tissue blockage, mediastinal emphysema, pneumothorax and so on.

4 strictly to avoid any increase in heart and lung load activities, such as physical workload, emotional excitement, cough, defecation difficulties, too fast excessive infusion, etc., if necessary, can be administered drugs for control, and appropriate diuretic dehydration.

5 The early dose of glucocorticoids may be slightly larger. For example, the daily dose of dexamethasone should not be less than 40 mg ( intravenous or intravenous drip ). The first day should have a larger impact; the amount of aerosolized inhaled hormone can be reduced. The effect seems more obvious.

6 Early administration of calcium gluconate, vitamin C and other drugs to enhance blood vessel density;

0.5 % procaine 40ml was added intravenously to the glucose solution to relieve pulmonary vasospasm.

7 anti-infection. Can be used penicillin, streptomycin, and then adjusted according to drug sensitivity test at any time.

8 The use of oxygen radical quenchers and calcium channel blockers to cut off the occurrence of pulmonary edema at the subcellular level , see Detoxification and special treatment section.

3. Treatment of pulmonary edema

The key to prevention and treatment of pulmonary edema is to grasp the treatment of the induction period, in order to prevent the occurrence of pulmonary edema or to reduce the degree, because once the occurrence of pulmonary edema, the difficulty of treatment and prognosis are much different from before. After the occurrence of pulmonary edema, the treatment points are as follows.

1 Keep the airway open. The most commonly used defoamers remove viscous foam from the airways, such as 1 % dimethyl silicone aerosol, 30 % ethanol into an oxygen humidifier bottle to inhale its vapor; also available alpha - chymotrypsin, N- acetylcysteine Intramuscular injection or atomization inhalation, tracheal instillation, etc., to thin the sputum; excess sputum or coma patient feasible tracheotomy and suction; mucosa necrosis and drop off when the airway can be removed with the help of the tracheoscope Blockage.

2 reasonable oxygen therapy. Generally recommended to be used when inverse ratio ventilation or mechanical ventilation; oxygen addition to the foregoing methods, the use of high frequency jet ventilation may be posted or oxygen, the former do not too fast jetting frequency (100 times / min or can), so as not to affect the CO2 emission Positive end-expiratory pressure (PEEP) does not advocate hyperbaric oxygen therapy.

3 adequate use of glucocorticoids, such as daily dexamethasone 60 ~ 80mg intramuscular injection, 3 to 5 days after the withdrawal.

4The use of cholinergic blockers, such as anisodamine or 654-2 , can be used 10 to 20mg intravenous injection, repeated 20 to 30 minutes, to maintain atropine after intravenous infusion, to shunt the blood flow in the lung, reduce Pulmonary vascular hydrostatic pressure reduces pulmonary edema.

5 diuretic dehydration should be controlled, should be based on the amount of liquid intake to avoid hypovolaemia shock.

6 Do a good job of anti-infective treatment, especially in the case of large doses of hormones and antibiotics to prevent fungal infection.

7 Critically ill patients can be given artificial low temperature hibernation, cooling should not be too low, the rectal temperature is maintained at about 34 °C , 2 to 3 days, the phase of pulmonary edema can be gradually removed, not long-term maintenance.

8 Common complications are handled as follows.

a. Hypovolemic shock: patients with pulmonary edema have seen venous collapse, loose skin, decreased urine ( < 20 ml/h) , increased urine density ( > 1.020) , increased hematocrit ( > 0.5) , and decreased central venous pressure.

( < 0.588kPa , or < 60mmH2O) or persistently low pulmonary artery clamping pressure ( < 1.07kPa , or < 8mmHg) , more suggestive of hypovolaemia may be possible, should be rehydration, crystal fluid is appropriate; after the replacement of the aforementioned indicators to improve The blood pressure is still not rising or the heart rate is very fast. We should consider whether there is any problem of heart failure.

b. acid-base balance disorders: mild metabolic acidosis can not be corrected; significant metabolic acidosis fundamental corrective measures lie in changing oxygen, and the other can be based on the carbon dioxide binding force or base residual value, enter the appropriate amount of sodium bicarbonate solution. Respiratory alkalosis can use air bags to collect the patient's exhaled breath to re-inhale to increase the blood CO2 level; the key to the treatment of respiratory acidosis is to improve the ventilation function, available respiratory stimulants, and if necessary, use mechanical ventilation.

c. Mediastinal emphysema and spontaneous pneumothorax: In addition to avoiding cough and breath-holding movements, mediastinal emphysema may be taken from a sitting position to introduce gas slowly into the neck and subcutaneously; when the pneumothorax is light, it can be absorbed by itself, and the person with severe pneumothorax can evacuation or Intubation for closed drainage.

d. Adult Respiratory Distress Syndrome: See Rescue Day of Critically Ill Patients.

This article is edited and compiled by China Rescue Equipment Network. Please indicate the link.