Clinical stages of toxic pulmonary edema. Toxic pulmonary edema, symptoms, treatment
Pulmonary edema is the cause of the painful death of many patients. It occurs most often as a complication in the dysregulation of the volume of fluid that must circulate in the lungs.
At this moment, there is an active inflow of fluid from the capillaries into the pulmonary alveoli, which overflow with exudate and lose their ability to function and receive oxygen. The person stops breathing.
This is an acute pathological condition that carries a threat to life, requiring extremely urgent assistance, immediate hospitalization. The main characteristics of the disease are characterized by acute lack of air, severe suffocation and death of the patient in case of failure to provide resuscitation measures.
At this moment, there is an active filling of the capillaries with blood and the rapid passage of fluid through the walls of the capillaries into the alveoli, where so much of it is collected that it greatly impedes the supply of oxygen. IN respiratory organs disrupted gas exchange, tissue cells experience acute oxygen deficiency (hypoxia), the person suffocates. Often, suffocation occurs at night while sleeping.
Sometimes the attack lasts from 30 minutes to 3 hours, but often the excess accumulation of fluid in the extracellular tissue spaces grows with lightning speed, therefore resuscitation measures begin immediately in order to avoid death.
Classification, from what happens
The causes and types of pathology are closely related, subdivided into two basic groups.
| Hydrostatic (or cardiac) pulmonary edema | |
It happens during diseases, which are characterized by an increase in pressure (hydrostatic) inside the capillaries and the further penetration of plasma from them into the pulmonary alveoli. The reasons for this form are:
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| Non-cardiogenic pulmonary edema, which includes: | |
| Iatrogenic | There is:
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| Allergic, toxic (membranous) | It is provoked by the action of poisons, toxins that violate the permeability of the walls of the alveoli, when instead of air, liquid penetrates into them, filling almost the entire volume. Causes of toxic pulmonary edema in humans:
Often passes without characteristic signs. The picture becomes clear only when X-ray is taken. |
| Infectious | Develops:
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| Aspiration | It occurs when a foreign body, stomach contents penetrate into the lungs. |
| Traumatic | Happens with penetrating chest injuries. |
| Cancer | Occurs due to the failure of the functions of the pulmonary lymphatic system with difficulty in lymph outflow. |
| Neurogenic | Main reasons:
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Any attack of suffocation that occurs with such diseases is the basis for suspicion of a state of acute swelling of the respiratory system.
Under these conditions the alveoli become very thin, their permeability increases, and the integrity is disrupted, the risk of filling them with liquid increases.
At-risk groups
Since the pathogenesis (development) of pathology are closely related to concomitant internal diseases, at risk are patients with diseases or factors that provoke such a health and life threatening condition.
The risk group includes patients suffering from:
- disorders of the vascular system, heart;
- damage to the heart muscle with hypertension;
- , respiratory system;
- complex craniocerebral trauma, cerebral hemorrhages of various origins;
- meningitis, encephalitis;
- cancerous and benign neoplasms in the brain tissues.
- pneumonia, emphysema, bronchial asthma;
- and increased blood viscosity; there is a high probability of separation of a floating (floating) clot from the artery wall with penetration into the pulmonary artery, which is blocked by a thrombus, which causes thromboembolism.
Doctors have found that athletes who actively practice excessive loads have a serious likelihood of getting respiratory edema. These are scuba divers, climbers working at high altitudes (over 3 km), marathon runners, divers, long-distance swimmers. The risk of the disease is higher for women than for men.
Climbers experience this dangerous condition. when climbing quickly to a great height without pause on intermediate high-rise levels.
Symptoms: how it manifests itself and develops in stages
Classification and symptoms are related to the severity of the disease.
| Severity | The severity of symptoms |
| 1 - on the border of development | Revealed:
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| 2 - medium | Observed:
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| 3 - heavy | Explicit symptoms:
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| 4 degree - critical | The classic manifestation of a critical condition:
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First emergency first aid: what to do when it occurs
Before the ambulance arrives, relatives, friends, colleagues shouldn't waste a minute of time... To alleviate the patient's condition, do the following:
- Helps the person sit up or half-raise with their legs down
- If possible, they are treated with diuretics (they give diuretics - lasix, furosemide) - this removes excess fluid from the tissues, however, at low pressure, small doses of drugs are used.
- Organize the possibility of maximum oxygen access to the room.
- Suction of the foam is carried out and, if skillful, oxygen inhalations are performed through a solution of ethyl alcohol (96% of the pair - for adults, 30% of alcohol vapors for children).
- Prepare a hot foot bath.
- If skill is used, the imposition of harnesses on the limbs is appliednot too tightly pinching the veins in the upper third of the thigh. Leave the tourniquets for more than 20 minutes, while the pulse should not be interrupted below the places of application. This reduces blood flow to the right atrium and prevents tension in the arteries. When the tourniquets are removed, they do it carefully, loosening them slowly.
- Continuously monitor the patient's breathing and pulse rate.
- For pain, they give analgesics, if any, promedol.
- With high blood pressure, benzohexonium, pentamine are used, which promote the outflow of blood from the alveoli, nitroglycerin, which dilates blood vessels (with regular pressure measurement).
- At normal - small doses of nitroglycerin under the control of pressure indicators.
- If the pressure is below 100/50 - dobutamine, dopamine, which increase the function of myocardial contraction.
What is dangerous, forecast
Pulmonary edema is a direct threat to life... Without the adoption of extremely urgent measures that should be carried out by the patient's relatives, without subsequent urgent active therapy in the hospital, pulmonary edema is the cause of death in 100% of cases. The person is waiting for suffocation, coma, death.
Attention! When the very first signs of an acute pathological situation appear, it is important to provide qualified assistance at the hospital as soon as possible, therefore, an ambulance is called immediately.
Preventive measures
To prevent threats to health and life, the following measures are necessarily assumed, meaning elimination of factors contributing to this condition:
- In case of heart diseases (angina pectoris, chronic insufficiency), drugs are taken for their treatment and at the same time - for hypertension.
- With repeated edema of the respiratory system, an isolated blood ultrafiltration procedure is used.
- Prompt accurate diagnostics.
- Timely adequate treatment of asthma, atherosclerosis, and other internal disorders that can cause such pulmonary pathology.
- Isolation of the patient from contact with any kind of toxins.
- Normal (not excessive) physical and respiratory stress.
Complications
Even if the hospital quickly and successfully managed to prevent suffocation and death of a person, therapy continues. After such a critical condition for the whole body in patients serious complications often develop, most often in the form of persistently relapsing pneumonia that is difficult to treat.
Prolonged oxygen starvation has a negative effect on almost all organs. The most serious consequences are disorders of cerebral circulation, heart failure, cardiosclerosis, ischemic organ damage. These diseases pose a constant threat to life and do not do without intensive drug therapy.
These complications, despite the stopped acute pulmonary edema, are the cause of death of a large number of people.
The greatest danger of this pathology is its speed and panic state.into which the patient and the people around him fall.
Knowledge of the basic signs of the development of pulmonary edema, the causes, diseases and factors that can provoke it, as well as measures emergency care before the arrival of an ambulance can lead to a favorable outcome and lack of consequences even with such a serious threat to life.
Toxic pulmonary edema is a dangerous, acutely developing pathological condition caused by the intake of pulmonary toxic chemicals into the respiratory tract. Due to the effect of such substances, an increase in the permeability of the capillary wall is noted, which leads to an excessive accumulation of fluid in the pulmonary interstitium. This disease is characterized by the presence of several stages, which successively replace each other. In the event that medical assistance was not provided as soon as possible, there is a high probability of the death of a sick person due to progressive respiratory disorders.
Most often, pulmonary edema is the result of various disorders in the functional activity of the cardiovascular vascular system... The toxic form of this pathology accounts for no more than ten percent of all cases. This condition can be encountered by people of absolutely any age and gender. Toxic lung damage is the most severe form of exposure to poisons in the respiratory tract. Even if the condition of the sick person was stabilized and nothing threatens his life anymore, there is a risk of developing other, long-term complications. As an example, we can cite toxic emphysema, replacement of lung tissue with a connective tissue component, damage to the central nervous system, as well as various diseases of the liver and kidneys.
As we said earlier, the toxic lungs are based on the penetration of irritating or asphyxiant chemicals into the respiratory system. Such a pathological process is associated with ammonia, nitric oxide, carbon monoxide, hydrogen fluoride, and so on. Currently, this condition is most often found in people working in chemical industries, if they do not follow safety precautions. Previously, the overwhelming majority of cases of this violation were associated with man-made accidents or military actions.
The mechanism of development of toxic pulmonary edema is based on the primary damage to the alveolar-capillary barrier by pulmotoxic substances. Against this background, a number of complex biochemical processes are triggered, leading to the fact that alveocytes and endotheliocytes die. A large amount of fluid accumulates in the lumen of the alveoli, due to which the gas exchange process is disrupted. The oxygen level in the blood decreases and the concentration of carbon dioxide increases. As a result of the violations occurring, the rheological properties of the blood change and other internal organs suffer.
The classification of this disease includes three of its variants: complete, abortive and "mute". In classic cases, a complete version is encountered. In its development, several successive stages are distinguished, which differ on the basis of concomitant clinical manifestations. The abortive variant is characterized by an easier course, since it does not go through all the stages. Pulmonary edema, proceeding in a "silent" version, is established if the changes that have arisen can be detected only during radiography.
As we have already said, this pathological process begins sharply. When completed, everything starts with a reflex stage. It occurs almost immediately after contact respiratory tract with a toxic substance. Symptoms such as coughing, nasal discharge, discomfort and sore throat are present. A sick person complains of moderate pain in the chest, difficulty breathing, increased weakness and attacks of dizziness. As a rule, the above-described manifestations do not lead to a significant deterioration in the general condition of the patient; they gradually subside and pass into the second stage.
The duration of the second stage is from two to twenty four hours. It is called hidden. The patient feels relatively well and does not indicate any concerns about him. However, physical examination can reveal a number of abnormalities.
The next stage is characterized by an increase in the clinical picture. Symptoms such as severe attacks of shortness of breath, up to choking, blanching skin and cyanosis of the nasolabial triangle. Mandatory present. When coughing, a very large amount of foamy sputum is released. The patient indicates an increasing malaise with the addition of a headache. Chest pain syndrome also becomes more intense.
The fourth stage is accompanied by further progression of the disease. In some cases, the patient becomes agitated, greedily swallows air, rushes about the bed. From the respiratory tract, foamy masses with a pinkish color are released. The skin acquires a bluish tint, and consciousness is depressed. There is also a second option, in which the functional activity of not only the respiratory, but also the cardiovascular system is sharply disrupted. If medical assistance was not provided, the sick person dies at this stage.
With the right medical tactics, the final stage begins. It is manifested by the gradual subsiding of all the above symptoms and the normalization of the general condition of the patient.
This disease diagnosed on the basis of a general examination of a person, an auscultatory examination and radiography of the lungs. Blood tests are mandatory, in which a number of characteristic signs will be detected. To assess the state of the cardiovascular system, the purpose of electrocardiography is shown.
To date, the problem of toxic pulmonary edema is not well covered, in this regard, many issues of its diagnosis and treatment are little known to a wide range of doctors. Many doctors of different profiles, especially those working in multidisciplinary hospitals, very often deal with the symptom complex of acute respiratory failure.
This difficult clinical situation poses a serious danger to the patient's life. A lethal outcome can occur in a short time from the moment of occurrence, it directly depends on the correctness and timeliness of the provision medical care a doctor. Among the many causes of acute respiratory failure (atelectasis and collapse of the lung, massive pleural effusion and pneumonia involving large areas of the lung parenchyma, status asthmaticus, pulmonary embolism, etc.), doctors most often reveal pulmonary edema - a pathological process in which the interstitial lung tissue, and later in the alveoli themselves, excess fluid accumulates.
Toxic pulmonary edema is associated with damage, and in connection with this, an increase in the permeability of the alveolar-capillary membrane (in the literature, toxic pulmonary edema is denoted by the terms "shock lung", "non-coronary pulmonary edema", "adult respiratory distress syndrome or ARDS".
The main conditions leading to the development of toxic pulmonary edema are:
1) inhalation of poisonous gases and fumes (nitrogen oxide, ozone, phosgene, cadmium oxide, ammonia, chlorine, fluoride, hydrogen chloride, etc.);
2) endotoxicosis (sepsis, peritonitis, pancreatitis, etc.);
3) infectious diseases (leptospirosis, meningococcemia, pneumonia.);
4) severe allergic reactions;
5) heroin poisoning.
Toxic pulmonary edema is characterized by a high intensity of clinical manifestations, a severe course and a serious prognosis.
The causes of toxic pulmonary edema during hostilities can be extremely diverse. Most often it will be found during the destruction of chemical industries. Its development is also possible upon inhalation of toxic vapors of technical fluids in case of severe poisoning with various chemicals.
Diagnosis of toxic pulmonary edema should be based on a comparison of the history data with the results of a comprehensive objective medical examination. It is necessary first of all to establish whether the patient has had contact with OV or with other chemical agents and to assess the initial manifestations of the lesion.
The clinic for the development of toxic pulmonary edema can be divided into 4 stages or periods:
1). The initial reflex stage.
2). The stage of latent phenomena.
3). The stage of development of pulmonary edema.
4). Stage of outcomes and complications (reverse development).
1). It is known that after exposure to 0B asphyxiation or other irritating gases, there is a slight cough, a feeling of tightness in the chest, general weakness, headache, rapid shallow breathing with a distinct slowing down of the pulse. At high concentrations, suffocation and cyanosis appear due to reflex laryngo- and bronchospasm. The intensity of these symptoms can vary depending on the concentration of OV and the state of the body. It is practically difficult to determine in advance whether the poisoning will be limited to direct reactions or pulmonary edema will develop in the future. Hence, it becomes necessary to immediately evacuate those affected by irritating gases to the medical department or hospital, even in cases where the initial signs of poisoning seem harmless.
2). After 30-60 minutes, the unpleasant subjective sensations of the initial period disappear and the so-called latent period, or a period of imaginary well-being. The shorter it is, the usually more severe the clinical course of the disease. The duration of this stage is on average 4 hours, but it can vary from 1-2 to 12-24 hours. It is characteristic that in the latent period, a thorough examination of the affected allows them to reveal a number of symptoms of an increase in oxygen starvation: moderate emphysema of the lungs, shortness of breath, cyanosis of the extremities, lability of the pulse. Poisonous substances with a tropism for lipids (nitric oxide, ozone, phosgene, cadmium oxide, monochloromethane, etc.) are deposited mainly in the alveoli, dissolving in the surfactant and diffuse through thin alveolar cells (pneumocytes) to the endothelium of the pulmonary capillaries, damaging them. The capillary wall responds to chemical damage by increased permeability with the release of plasma and blood cells into the interstitium, which leads to a significant (several times) thickening of the alveolar-capillary membrane. As a result, the "diffuse path" of oxygen and carbon dioxide significantly increases (stage interstitial pulmonary edema.)
3). As the pathological process progresses, the dilatation of the lung vessels increases, the lymph drainage is disturbed through the septal and prevascular lymphatic gaps, the edematous fluid begins to penetrate into the alveoli (alveolar stage of toxic edema). The resulting edematous foam fills and clogs the bronchioles and bronchi, further impairing lung function. This determines the clinic of severe respiratory failure until death (the lungs are drowned in edematous fluid).
Initial signs development of pulmonary edema are general weakness, headache, weakness, tightness and heaviness in the chest, mild shortness of breath, dry cough (coughing), increased breathing and heart rate. On the part of the lungs: lowering of the boundaries, percussion sound acquires a tympanic hue, the severity and emphysematosity of the lungs is determined radiographically. On auscultation - weakened breathing, and in the lower lobes - fine bubbly moist rales or crepitus. From the side of the heart: moderate tachycardia, expansion of the boundaries to the right, the accent of the second tone over the pulmonary artery - signs of stagnation in the pulmonary circulation. There is a slight cyanosis of the lips, nail phalanges, nose.
At the stage of clinically pronounced pulmonary edema, two different forms can be observed:
Blue form of hypoxia;
Gray form of hypoxia.
When edema occurs with "blue" hypoxemia, the main symptoms are: pronounced cyanosis, shortness of breath, in severe cases - noisy, "bubbling" breathing, cough with copious discharge of foamy sputum, sometimes pinkish or canary yellow. With percussion, dull tympanitis is determined over the lower posterior parts of the lungs, the boxed shade of percussion sound over the anterior and lateral parts of the chest, limitation of the mobility of the pulmonary margin. On auscultation - a large number of fine bubbly, sonorous moist rales. The pulse is usually quickened, but its filling and tension remains satisfactory. BP is normal or slightly higher, heart sounds are muffled. The body temperature can rise to 38 0 - 39 0 C. In the study of blood, pronounced neutrophilic leukocytosis with lymphopenia and eosinopenia is found, and in more severe cases - blood clotting, increased coagulation and viscosity.
Toxic pulmonary edema, proceeding according to the type of "gray" hypoxemia, is clinically characterized by a pale gray color of the skin and mucous membranes; small, frequent, sometimes threadlike pulse, low blood pressure, severity of pulmonary changes, low carbon dioxide content in the blood (hypocapnia); the respiratory center is suppressed.
Usually, the edema reaches full development by the end of the first day. Its pronounced signs are relatively stable for about a day. This period is the most dangerous, it falls on more deaths. Starting from the third day, the general condition of the patients improves markedly, the process enters the last phase - period of reverse development.
4). The onset of recovery is manifested by a decrease in shortness of breath, cyanosis, the number and prevalence of moist wheezing, normalization of body temperature, improvement in well-being, and the appearance of appetite. X-ray examination also indicates the reverse development of edema - large flocculent shadows are not visible. In peripheral blood, leukocytosis disappears, the number of neutrophils decreases with a simultaneous rise to normal amount lymphocytes, the normal blood gas composition is gradually restored.
Signs of advanced toxic pulmonary edema are quite characteristic and easily recognized. However, its severity ranges from minimal clinical and radiological symptoms to bubbling breathing with profuse frothy sputum.
Complications: often - secondary infectious pneumonia (in practice, it can be assumed that if after 3-4 days of illness the patient's condition does not improve, then it is almost unmistakable to diagnose pneumonia); less often - vascular thrombosis and embolism. Moreover, more often there are embolisms and pulmonary infarction, in which there are stabbing pains in the side and pure blood in the sputum. Pulmonary infarction is usually fatal. The development of a lung abscess is not excluded. In persons who have suffered severe damage, sometimes long-term consequences are noted in the form chronic bronchitis and pulmonary emphysema, interstitial pneumonia and pneumosclerosis.
Clinical forms defeat. Depending on the concentration of 0V and SDYAV vapors, exposure and the state of the body, there may be mild, moderate and severe lesions.
With mild lesions, the initial stage is weak, the latent period is longer. After this, the phenomenon of pulmonary edema is usually not detected, and only changes in the type of tracheobronchitis are noted. There is slight shortness of breath, weakness, dizziness, chest tightness, palpitations, and a slight cough. Objectively, a runny nose, hyperemia of the pharynx, hard breathing and occasional dry wheezing are noted. All these changes disappear in 3-5 days.
With a lesion of moderate severity after the latent stage, pulmonary edema develops, but it does not capture all the lobes or is more moderately expressed. Shortness of breath and cyanosis are moderate. Thickening of blood is insignificant. On the second day, resorption and improvement of the condition begins. But it must be borne in mind that in these cases complications are possible, mainly bronchopneumonia, and if the regime or treatment is violated, the clinic may become heavier with dangerous consequences.
The clinical picture of a severe lesion was described above. In addition, extremely severe lesions can occur when exposed to very high concentrations or prolonged exposures. In these cases, in the initial stage, the irritating effect of vapors is sharply expressed, there is no latent period and death occurs in the first hours after the defeat. Moreover, pulmonary edema is not very pronounced, and in some cases it does not have time to develop yet, but destruction and death of the epithelium of the pulmonary alveoli occurs as a result of the "cauterizing" action
Diagnostics.X-ray examination plays an important role in the diagnosis of toxic edema. The first X-ray changes are detected as early as 2-3 hours after the lesion, reaching a maximum by the end of the first - the beginning of the second day. The severity of changes in the lungs corresponds to the severity of the lesion. They are most significant at the height of intoxication and consist in a decrease in the transparency of the lung tissue, the appearance of large focal opacities of a confluent nature, usually recorded in both lungs, and also in the presence of emphysema in the supraphrenic areas. IN initial stages and with an abortive form of edema, the number and size of darkening is less. Later, as the pulmonary edema resolves, the intensity of focal darkening weakens, they decrease in size and disappear altogether. Other radiological changes also undergo reverse development.
Pathological changes in case of death: the lungs are sharply increased in volume. Their weight is also increased and reaches 2-2.5 kg instead of 500-600 g in the norm. The surface of the lungs has a characteristic spotty (marbled) appearance due to the alternation of pale pink protruding areas of emphysema, dark red depressed areas of atelectasis and cyanotic areas of edema.
On the incision, an abundant amount of serous frothy fluid is released from the lungs, especially when pressed.
The trachea and bronchi are filled with edematous fluid, but their mucous membrane is smooth and shiny, slightly hyperemic. Microscopic examination in the alveoli reveals an accumulation of edematous fluid, which azure-eosin turns pink.
The heart is moderately dilated, with dark blood clots in its cavities. The parenchymal organs are congestively full-blooded. Meninges and the substance of the brain is full-blooded, in places there are punctate hemorrhages, sometimes vascular thrombosis and foci of softening.
In case of a later death (3-10 days), the lungs take a picture of confluent bronchopneumonia, in the pleural cavities there is a small amount of serous-fibrinous fluid. Flabby heart muscle. Other organs are congestively full-blooded.
The mechanism of occurrence and development of toxic pulmonary edema.
The development of toxic pulmonary edema is a very complex process. The chain of cause-and-effect relationships consists of the main links:
Violation of the basic nervous processes in the reflex arc (receptors vagus nerve lungs, hypothalamus-sympathetic nerves of the lungs);
Inflammatory trophic disorders in the lung tissue, increased vascular permeability;
Accumulation of fluid in the lungs, displacement of the mediastinal organs, stagnation of blood in the vessels of the pulmonary circulation;
Oxygen starvation: the stage of "blue hypoxia" (with compensated blood circulation) and "gray hypoxia" (in the case of collapse).
Treatment of toxic pulmonary edema.
Pathogenetic and symptomatic therapy is used, aimed at reducing pulmonary edema, combating hypoxia and relieving other symptoms, as well as combating complications.
1. Providing maximum rest and warming - the body's need for oxygen decreases and the body's oxygen deprivation is facilitated. In order to relieve neuropsychic arousal, phenazepam or seduxen is given in tablets.
2. Pathogenetic and symptomatic therapy:
A) funds that reduce the permeability of the pulmonary capillaries;
B) dehydration agents;
C) cardiovascular drugs;
D) oxygen therapy.
A) Glucocorticoids: IV prednisolone at a dose of 30-60 mg or drip at a dose of up to 150-200 mg. Antihistamines (pipolfen, diphenhydramine). Ascorbic acid (5% solution 3-5 ml). Calcium chloride or gluconate 10 ml of 10% solution IV in the first hours, during the period of increasing edema.
B) 20-40 mg of lasix (2-4 ml of 1% solution) is injected intravenously. Intravenous furosemide (lasix) 2-4 ml of a 1% solution is injected under the control of the acid-base state, the level of urea and electrolytes in the blood, 40 mg initially after 1-2 hours, 20 mg after 4 hours during the day;
IN). When tachycardia, ischemia appear, sulfocamphokaine, korglikon or strophanthin, aminophylline are administered to reduce stagnation in the pulmonary circulation. With a decrease in blood pressure - 1 ml of 1% mezaton solution. With the phenomena of blood thickening - heparin (5000 U), you can use trental.
D) Inhalation of an oxygen-air mixture containing 30-40% oxygen is effective for 15-30 minutes, depending on the patient's condition. When foaming the edematous fluid, anti-foaming surface active agents (ethyl alcohol) are used.
With pulmonary edema, sedatives (phenazepam, seduxen, elenium). The administration of adrenaline is contraindicated, which can increase edema, morphine, which depress the respiratory center. It may be advisable to introduce an inhibitor of proteolytic enzymes, in particular kininogenases, which reduce the release of bradykinin, trasilol (contrycal) 100,000 - 250,000 IU in isotonic glucose solution. With severe pulmonary edema, in order to prevent secondary infectious pneumonia, especially with an increase in body temperature, antibiotics are prescribed.
When gray form of hypoxia therapeutic measures are aimed at removing from the collaptoid state, stimulating the respiratory center and ensuring airway patency. Shows the introduction of korglikon (strophanthin), mezaton, lobelin or cytiton, inhalation of carbogen (a mixture of oxygen and 5-7% carbon dioxide). To thin the blood, an isotonic 5% glucose solution is injected with the addition of mesaton and vitamin C 300-500 ml intravenously drip. If necessary, intubation, suction of fluid from the trachea and bronchi and transfer of the patient to controlled breathing.
First aid and assistance at the stages of medical evacuation.
First and first aid... The affected person is freed from the restraining uniforms and equipment, provided maximum rest (any movements are strictly prohibited), placed on a stretcher with a raised head end, and protect the body from cooling. The respiratory tract is freed from the accumulated fluid by giving the victim an appropriate position, with a gauze swab to remove fluid from the oral cavity. With anxiety, fear, especially with combined lesions (pulmonary edema and chemical burns), an analgesic agent is administered from an individual first-aid kit. In case of reflex cessation of breathing, artificial ventilation of the lungs is done using the mouth-to-mouth method. With shortness of breath, cyanosis, severe tachycardia, oxygen is inhaled for 10-15 minutes using an inhaler, cardiovascular agents (caffeine, camphor, cordiamine) are administered. The victim is transported on a stretcher. The main requirement is to deliver the victim to the WFP as soon as possible under conditions of a calm situation.
First aid. If possible, do not disturb or shift the patient. Inspection is performed, pulse and number of breaths are counted, blood pressure is determined. Assign peace, warmth. With the rapid development of toxic pulmonary edema through a soft rubber catheter, foamy liquid is aspirated from the upper respiratory tract. Oxygen inhalation with defoamers, bloodletting (200 - 300 ml) are used. Intravenous inject 40 ml of a 40% glucose solution, strophanthin or korglikon; subcutaneously - camphor, caffeine, cordiamine.
After carrying out the first medical aid measures, the affected person should be taken to the medical department or hospital as soon as possible, where he will be provided with qualified and specialized therapeutic assistance.
Qualified and specialized medical care.
In the medb (hospital), the efforts of doctors should be aimed at eliminating the phenomena of hypoxia. In this case, it is required to determine the sequence in carrying out a complex of therapeutic measures affecting the leading mechanisms of edema
Violation of the airway patency is eliminated by giving the patient a posture in which their drainage is facilitated due to the natural outflow of the transudate, in addition, fluid is sucked from the upper respiratory tract and anti-foaming agents are used. Ethyl alcohol is used as antifoaming agents (30% solution in unconscious patients and 70-90% in unconscious patients) or 10% alcohol solution of antifomsilan.
Continue the administration of prednisolone, furosemide, diphenhydramine, ascorbic acid, korglikon, euphyllin and other agents, depending on the patient's condition. Persons with severe symptoms of edema within 1-2 days are considered non-transportable and require constant medical supervision and treatment.
In the therapeutic hospital, specialized medical care is provided in full until recovery. After stopping dangerous symptoms of pulmonary edema, reducing shortness of breath, improving cardiac activity and general condition, the main attention is paid to preventing complications and full recovery all body functions. In order to prevent secondary infectious pneumonia with an increase in body temperature, antibiotic therapy is prescribed, periodic administration of oxygen. In order to prevent thrombosis and embolism - control over the blood coagulation system, according to indications heparin, trental, aspirin (a weak anticoagulant).
Medical rehabilitation is to restore the functions of organs and systems. In severe cases of poisoning, it may be necessary to determine the group of disabilities and recommendations for employment.
Toxic pulmonary edema (TOL) is a symptom complex that develops in severe inhalation poisoning with asphyxiant and irritating poisons. TOL develops with inhalation poisoning: BOV (phosgene, diphosgene), as well as when exposed to SDYA, for example, methyl isocyanate, sulfur pentafluoride, CO, etc. TOL easily occurs when inhaled caustic acids and alkalis (nitric acid, ammonia) and is accompanied by a burn upper respiratory tract. This dangerous pathology of the lungs often occurs in emergency conditions, so any practitioner can face a similar serious complication of many inhalation poisoning in his work. Future doctors should know well the mechanism of development of toxic pulmonary edema, clinical picture and treatment of TOL in many pathological conditions.
Differential diagnosis hypoxia.
| No. p p | Indicators | Blue uniform | Gray shape |
| 1. | Coloring of the skin and visible mucous membranes | Cyanosis, blue-purple color | Pale, blue-gray or ash-gray |
| 2. | Breathing state | Dyspnea | Severe shortness of breath |
| 3. | Pulse | The rhythm is normal or moderately rapid, satisfactory filling | Filiform, frequent, weak filling |
| 4. | Arterial pressure | Normal or slightly increased | Sharply lowered |
| 5. | Consciousness | Retained, sometimes the phenomena of excitement | Often unconscious, no arousal |
| Content in arterial and venous blood | Oxygen deficiency with excess in the blood (hypercapnia) | Severe failure with a decrease in blood levels (hypocapnia) |
Measures in the outbreak and at the stages of medical evacuation with the defeat of OS and SDYAV of a suffocating effect.
| Type of medical assistance | Normalization of the main nervous processes | Normalization of metabolism, elimination of inflammatory changes | Unloading the pulmonary circulation, reducing vascular permeability | Elimination of hypoxia by normalizing blood circulation and respiration |
| First aid | Putting on a gas mask; inhalation of ficilin under a gas mask | Shelter from the cold, warm with a cape, medical and other means | Stretcher evacuation of all casualties with head-up or in a sitting position | Artificial respiration with reflex cessation of breathing |
| First aid | Inhalation of ficilin, rinsing the eyes, mouth and nose with water; promedol 2% w / m; phenazepam 5 mg orally | Warming | Tourniquets for limb vein compression; evacuation with raised head end of stretcher | Removing the gas mask; inhalation of oxygen with alcohol vapor; cordiamine 1 ml / m |
| First aid | Barbamil 5% 5 ml / m; 0.5% solution of dikain, 2 drops per eyelids (according to indications) | Diphenhydramine 1% 1 ml / m | Bloodletting 200-300 ml (with a blue form of hypoxia); lasix 60-120 mg iv; vitamin C 500 mg orally | Suction of fluid from the nasopharynx using DP-2 inhalation of oxygen with alcohol vapor; strophanthin 0.05% solution 0.5 ml in glucose solution iv |
| Qualified assistance | Morphine 1% 2 ml subcutaneously, anaprilin 0.25% solution 2 ml / m (with blue form of hypoxia) | Hydrocortisone 100-150 mg / m, diphenhydramine 1% 2 ml / m, penicillin 2.5-5 million units per day, sulfadimethoxine 1-2 g / day. | 200-400 ml of 15% solution of mannitol i.v., 0.5-1 ml of 5% solution of pentamine i.v. (with blue form of hypoxia) | Aspiration of liquid from the nasopharynx, inhalation of oxygen with alcohol vapors, 0.5 ml of 0.05% solution of strophanthin intravenous drip in a glucose solution, inhalation of carbogen. |
| Specialized assistance | A complex of diagnostic, therapeutic and rehabilitation measures carried out in relation to the affected with the use of complex techniques, the use of special equipment and equipment in accordance with the nature, profile and severity of the lesion | |||
| Medical rehabilitation | A complex of medical and psychological measures to restore combat and working capacity. |
Physical properties of SDYAV, features of the development of toxic pulmonary edema (TOL).
| Name | Physical properties | Routes of entry of poison | Production where there may be contact with poison | LC 100 | The peculiarity of the PPE clinic. |
| Isocyanates (methyl isocyanate) | Liquid b / tsv. with a pungent odor T bp \u003d 45 ° C | Inhalation ++++ Ch / k ++ | Paints, varnishes, insecticides, plastics | May cause HCN-type instant death | Irritating to eyes, top. breath. paths. Latent period up to 2 days, decreased body t. There is only an insulating gas mask in the hearth. |
| Sulfur pentafluoride | Liquid b / color | Inhalant. +++ Ch / k- V / gkt- | By-product of sulfur production | 2.1 mg / l | The development of TOL by the type of phosgene poisoning, but with a more pronounced cauterizing effect on lung tissue. Protects the filter gas mask |
| Chloropicrin | Liquid b / color with a pungent odor. t bale \u003d 113 ° С | Inhalant. ++++ Ch / c ++ V / LCt ++ | Educational OV | 2 g / m 3 10 minutes | Sharp eye irritation, vomiting, shortened latency period, formation of methemoglobin, weakness of the cardiovascular system. Protects the filtering gas mask. |
| Phosphorus trichloride | B / color liquid with a strong odor. | Inhalant. +++ B / C ++ Eyes ++ | Receiving | 3.5 mg / l | Irritation of skin, eyes, shortened latency period in TOL. Exceptionally insulated. mask. Skin protection is a must. |
This is the most severe form of lung toxicity. Clinically, two forms of toxic pulmonary edema are distinguished: developed, or complete, and abortive.
With a developed form, the sequential development of five periods is observed: 1) initial phenomena (reflex stage); 2) latent period; 3) the period of increasing edema; 4) the period of completion of the edema; 5) reverse development of edema.
The period of initial symptoms develops immediately after exposure to a toxic substance and is characterized by mild irritation of the mucous membranes of the respiratory tract: a slight cough, sore throat, chest pain. All these phenomena are not very pronounced, they pass quickly, and upon contact with compounds that are poorly soluble in water, they may be absent altogether.
The latent period begins after the symptoms of irritation subside and may have a different duration (from 2 to 24 hours), more often 6-12 hours during this period, the victim feels healthy, but upon careful examination, the first symptoms of increasing oxygen deficiency can be noted: shortness of breath, cyanosis, lability of the pulse.
The period of increasing edema manifests itself clinically, which is associated with the accumulation of edematous fluid in the alveoli and a more pronounced violation of respiratory function. There is a slight cyanosis, in the lungs, voiced fine-bubbling moist rales and crepitus are heard.
The period of completed edema corresponds to the further progression of the pathological process. During toxic pulmonary edema, two types are distinguished: « blue hypoxemia "and" gray hypoxemia ". With the "blue" type of toxic edema, there is a pronounced cyanosis of the skin and mucous membranes, severe shortness of breath - 50-60 breaths per minute. A bubbling breath is heard in the distance. Cough with a large amount of frothy expectoration, often bloody. Auscultation reveals a mass of moist rales of various sizes throughout the pulmonary fields. tachycardia is noted, blood pressure remains normal or even rises slightly. Arterialization of blood in the lungs is impaired, which is manifested by a deficiency in the saturation of arterial blood with oxygen with a simultaneous increase in carbon dioxide content (hypercapnic hypoxemia).
With the "blue" type of toxic edema, the patient is mildly agitated, inadequate to his condition. A picture of acute hypoxemic psychosis may develop.
With the "gray" type of toxic edema, the clinical picture is distinguished by a greater degree of severity due to the addition of pronounced vascular disorders. The patient, as a rule, is lethargic, adynamic, and does not answer questions well. The skin becomes pale gray in color. The face is covered with cold sweat. The limbs are cold to the touch. The pulse becomes fast and small. There is a drop in blood pressure. The gas composition of the blood in these cases is characterized by a decrease in carbon dioxide (hypoxemia with hypocapnia).
During the reverse development of edema, the cough and the amount of sputum separated gradually decrease, shortness of breath subsides. Cyanosis decreases, weakens, and then wheezing in the lungs disappears. X-ray studies indicate the disappearance of first large, and then small focal tissues .. Recovery may occur in a few days or a few weeks.
Another dangerous complication of toxic edema is the so-called secondary edema, which can develop at the end of the 2nd - the middle of the 3rd week of illness, as a consequence of the onset of acute heart failure.
Treatment of acute intoxication.
First aid consists in the immediate cessation of contact with a toxic substance - the victim is taken out of the gaseous atmosphere into a warm, well-ventilated room or into fresh air, freed from clothing that is restricting breathing. If a toxic substance comes into contact with the skin, wash the contaminated areas thoroughly with soap and water. In case of contact with eyes, immediately rinse the eyes with plenty of water or 2% sodium bicarbonate solution, then drip 0.1-0.2% dicaine, 30% sodium sulfacyl solution, apply anti-inflammatory eye ointment (0.5% synthomycin, 10 % sulfacyl).
In case of damage to the upper respiratory tract, rinse or warm-wet inhalations with a 2% solution of sodium bicarbonate, mineral waters or herbal infusions are prescribed. Giving antitussives is shown.
If the larynx is damaged, a mode of silence is necessary, drinking warm milk with sodium bicarbonate, Borjomi. With the phenomena of reflex spasm, antispasmodics (atropine, no-shpa, etc.) and antihistamines are shown.
In cases of severe laryngospasm, tracheotomy and intubation have to be used.
To prevent infection, anti-inflammatory drugs are prescribed. Patients with manifestations in the form of bronchobronchiolitis require inpatient treatment. Shown bed rest, intermittent oxygen therapy. The therapeutic complex includes bronchodilators (teopec, berotek, atrovent, aminophylline, etc.) in combination with secretolytics and expectorants (bromhexine, lasolvon, etc.), antihistamines. In the early stages, active antibiotic therapy is prescribed.
Treatment of toxic pulmonary edema requires the greatest attention. Even if toxic edema is suspected, it is necessary to create complete rest for the patient. Transportation to medical institution carried out on a stretcher, and in the hospital, bed rest and observation is required for at least 12 hours after contact with a toxic substance.
At the first manifestations of the clinic of edema, long-term oxygen therapy with heated, humidified oxygen is indicated. Antifoaming agents are prescribed at the same time: most often it is ethyl alcohol. For the same purposes, inhalations of antifomsilan in 10% alcohol solution can be used for 10-15 minutes repeatedly.
For the purpose of dehydration of lung tissue, saluretics are prescribed: lasix or 30% urea solution intravenously.
In the early stages, corticosteroid drugs are used intravenously up to 150 ml in terms of prednisolone per day and broad-spectrum antibiotics.
The complex of therapy includes antihistamines, intravenous aminophylline, cardiovascular agents and analeptics (korglikon, cordiamine, camphor preparations).
In order to increase the oncotic blood pressure, 10-20% albumin 200-400 mg / day is injected intravenously.
To improve the processes of microcirculation, heparin and antiproteases (contrikal) can be used under the control of hematocrit.
The previously commonly used phlebotomy is now rarely used due to possible complications (collapse). It is most advisable to conduct the so-called "Bloodless bloodletting" - the imposition of tourniquets on the limbs.
In the case of a severe course of pulmonary edema, intensive care methods are used - intubation with suction of secretions, mechanical ventilation, hemosorption and plasmaphoresis are used for detoxification.
Treatment of patients with toxic edema is most effective when these patients are admitted to poison control centers or intensive care units.
1996 0
Doctors of various specialties, especially those working in multidisciplinary hospitals, constantly observe the symptom complex of acute respiratory failure, the development of which may be due to a number of reasons. The drama of this clinical situation is that it poses a direct threat to life. The patient can die in a short period of time from the moment of its occurrence. The outcome depends on the correctness and timeliness of assistance.
Of the many causes of acute respiratory failure (atelectasis and collapse of the lung, massive pleural effusion and pneumonia involving large areas of the lung parenchyma, status asthmaticus, pulmonary embolism, etc.), pulmonary edema is most often revealed - a pathological process in which in the interstitium of the pulmonary tissue, and later in the alveoli themselves, excess fluid accumulates.
The basis of pulmonary edema can be a variety of pathogenetic mechanisms, depending on which it is necessary to distinguish between two groups of pulmonary edema (Table 16).
Etiology and pathogenesis
Despite the different mechanisms of development of pulmonary edema, doctors often do not distinguish between them by pathogenesis and carry out the same type of treatment for fundamentally different conditions, which adversely affects the fate of patients.The most common pulmonary edema associated with a significant increase in hemodynamic (hydrostatic) pressure in the pulmonary capillaries on the basis of a significant increase in diastolic pressure in the left ventricle (aortic heart disease, systemic hypertension, cardiosclerosis or cardiomyopathy, arrhythmia, hypervolemia due to the infusion of large amounts of fluid or renal failure) or left atrium (mitral valve defects, myxoma of the left atrium).
In such cases, as a result of a significant increase in the pressure gradient, the fluid passes through the alveolar-capillary barrier. Since the permeability of the alveolar epithelium is lower than that of the endothelium of the pulmonary capillaries, a widespread edema of the pulmonary interstitium first develops and only subsequently intraalveolar extravasation occurs. The ability of an intact vascular wall to retain blood proteins determines the accumulation of fluid with a low protein content in the alveoli.
Table 16. Major diseases (conditions) leading to the development of pulmonary edema
Pulmonary edema may be associated with an increase in the permeability of the alveolar-capillary membrane due to its damage. This pulmonary edema is called toxic. In the literature, it is also denoted by the terms "shock lung", "non-coronary (noncardiac) pulmonary edema", "adult respiratory distress syndrome (ARDS)".
Toxic pulmonary edema occurs when one or another damaging factor (substance, agent) acts directly on the alveolar-capillary membrane. Such a substance can reach the alveolar-capillary membrane aerogenically by inhalation of toxic gases or fumes, or hematogenously with blood flow (endotoxins, allergens, immune complexes, heroin, etc.). The pathogenetic mechanisms underlying this pathological condition depend on the disease (condition) on the basis of which ARDS develops.
Toxic pulmonary edema can appear when the endothelium of the pulmonary capillaries is directly exposed to toxic substances and allergens (immune complexes) supplied with the blood stream. The pathogenesis of ARDS in endotoxicosis has been studied in detail using the example of sepsis. In such cases, the most important role in the development of toxic pulmonary edema is played by endotoxins, which have both a direct damaging effect on the endothelial cells of the pulmonary capillaries, and indirectly, due to the activation of the body's mediator systems.
Endotoxins interact with cells sensitive to them and cause the release of large amounts of histamine, serotonin and other vasoactive compounds from them. In connection with the active participation of the lungs in the metabolism of these substances (the so-called non-respiratory function of the lungs), pronounced changes occur precisely in this organ.
Electron microscopy revealed that in the area of \u200b\u200balveolar capillaries high concentrations of histamine are created, tissue basophils accumulate and degranulation occurs in them, which is accompanied by damage to both endothelial cells and type 1 pneumocytes.
In addition, under the influence of toxins, macrophages secrete the so-called tumor necrosis factor, which has a direct damaging effect on endothelial cells, causing severe disturbances in both their permeability and microcirculation. Of particular importance are various enzymes released during the massive disintegration of neutrophils: elastase, collagenase and nonspecific proteases that destroy the glycoproteins of the interstitium and the main membrane of the cell walls.
As a result of all this, damage to the alveolar-capillary membrane occurs in sepsis, which is confirmed by the results of microscopic examination: edema of pneumocytes, microcirculation disorders in alveolar capillaries with structural disorders in endothelial cells and signs of increased vascular permeability are revealed in the lung tissue.
Toxic pulmonary edema is similar in pathogenesis in other endotoxicosis and infectious diseases (peritonitis, leptospirosis, meningococcal and non-clostridial anaerobic infections) and pancreatitis, although, possibly, in the latter, the direct effect of proteases on endothelial cells of pulmonary capillaries is also of great importance.
The development of toxic pulmonary edema upon inhalation of highly toxic substances in the form of their vapors and aerosols, as well as fumes, has been studied in most detail. These substances are deposited on the mucous membranes of the respiratory tract and lead to a violation of their integrity. The nature of the damage depends primarily on which part of the respiratory tract and lung tissue is affected, which is mainly associated with solubility chemical substance in lipids and water.
The development of toxic pulmonary edema is caused mainly by toxic substances that have a tropism for lipids (nitric oxide, ozone, phosgene, cadmium oxide, monochloromethane, etc.). They dissolve in the surfactant and easily diffuse through thin pneumocytes to the capillary endothelium, damaging them.
Substances that are highly soluble in water (ammonia, calcium oxide, hydrogen chloride and fluoride, formaldehyde, acetic acid, bromine, chlorine, chloropicrin, etc.) have a somewhat different damaging effect. They dissolve in the bronchial secretions of the airways, providing a pronounced irritant effect.
Clinically, this manifests itself in the form of laryngospasm, edema of the vocal cords and toxic tracheobronchitis with persistent painful cough up to reflex cessation of breathing. Only in the case of inhalation of very high concentrations of toxic substances can the alveolar-capillary barriers be involved in the pathological process.
With toxic pulmonary edema different in etiology and pathogenesis, the same cycle of changes occurs in the lung tissue, which determines the biphasic nature of the clinical symptoms of adult respiratory distress syndrome. Thus, the wall of the pulmonary capillary responds to the effect of a damaging factor with metabolic and structural changes with an increase in its permeability and the release of plasma and blood cells into the interstitium, which leads to a significant thickening of the alveolar-capillary membrane.
As a result, the diffusion path of oxygen and carbon dioxide through the alveolar-capillary membrane is lengthened. First of all, oxygen diffusion through it suffers, as a result of which hypoxemia develops.
In parallel, disturbances of microcirculation in the form of blood stasis in paralytically dilated pulmonary capillaries also significantly impair gas exchange. During this period of ARDS, the patient begins to notice shortness of breath with increased breathing, as in a healthy person after physical activity... On physical examination, pathological changes in the lungs are usually not detected in cases of the absence of an independent pathological process in the lung tissue, only with X-ray diffuse enhancement of the pulmonary pattern due to the vascular component is detected, and in laboratory research - a decrease in the partial pressure of oxygen in the capillary blood (less than 80 mm Hg. Art.).
This stage of pulmonary edema is called interstitial. It is most common in pancreatitis, leptospirosis, severe allergic reactions and some forms of sepsis and can last from 2 to 12 hours. It is difficult to trace in ARDS caused by inhalation of toxic substances and fumes, as well as with peritonitis and aspiration of acidic gastric contents.
In these cases, as well as with the progression of the pathological process in the lung tissue, gross changes in the microvasculature of the lungs occur with intravascular thrombus formation, sharp dilatation of blood vessels and impaired drainage of lymph through the septal and perivascular membranes, which leads to the accumulation of fluid in the alveoli and blockage of the bronchioles. Due to damage to the vascular endothelium, large amounts of protein enter the alveolar cavity along with the fluid.
As a result of damage to type II pneumocytes (which is most pronounced in persons whose lungs were exposed to poisonous gases and fumes), the synthesis of surfactant is disrupted and the alveoli collapse. All this leads to an even greater disruption of gas exchange in the lungs with the development of severe respiratory failure. Scattered moist rales appear over the lungs, breathing becomes bubbling, and X-ray examination reveals a decrease in pneumatization of the lung tissue like a "snow storm" (intraalveolar stage of pulmonary edema).
In contrast to hemodynamic pulmonary edema in adult respiratory distress syndrome, the separation of copious, foamy pink sputum is rarely observed. Damage to the mucous membrane opens the way for bacterial infection, which, along with the accumulation of protein-rich fluid in the alveoli, contributes to the occurrence of purulent bronchitis and pneumonia. The most common causative agents of the inflammatory process are opportunistic microbes - E. coli and Pseudomonas aeruginosa, Proteus, Klebsiella and Staphylococcus.
Some features of the clinical course of toxic pulmonary edema in various diseases and conditions can be noted. With sepsis, leptospirosis and a number of others infectious diseases ARDS often occurs at the height of the development of infectious-toxic (septic) shock, significantly aggravating the patient's already grave condition. Cases are described when allergic reactions to drugs (primarily to antibiotics) served as one of the factors in the development of ARDS in patients with endotoxicosis, including sepsis.
Toxic pulmonary edema can also be observed with a severe allergic reaction (primarily to drugs administered intravenously - plasma substitutes, antibiotics, etc.). In these cases, acute respiratory failure is associated with skin manifestations, hypotension, hyperthermia, but it is not based on total bronchospasm, but pulmonary edema with damage to the pulmonary endothelium by immune complexes and biologically active substances (histamine, serotonin, slowly reacting substance of anaphylaxis, allergens, etc. .), formed during allergic reactions of type 1.
Inhalation of toxic aerosols, industrial gases, as well as fumes generated in large quantities during a fire, immediately there is a paroxysmal cough, a sore feeling in the nasopharynx, and laryngo-bronchospasm may occur. After the termination of contact (leaving the contaminated area or from the premises, putting on a gas mask), a period of imaginary well-being begins, which can last several hours, and if smoke is inhaled, up to 2-3 days.
However, in the future, the victim's condition deteriorates sharply:cough increases, shortness of breath appears increasing in intensity, clinical manifestations of expanded pulmonary edema are noted. When nitrogen dioxide is inhaled in high concentrations, methemoglobinemia develops simultaneously with pulmonary edema. When the victim is in the fire zone, carbon monoxide enters the lungs along with smoke and toxic products of incomplete combustion, which leads to a significant increase in the level of carboxyhemoglobin in the blood.
Such changes lead to significant disturbances in gas exchange and oxygen transport, and therefore the degree of oxygen starvation of tissues in adult respiratory distress syndrome increases significantly.
Treatment
The effectiveness of the treatment of toxic pulmonary edema largely depends on the speed of its recognition and the timely initiation of adequate therapy. Despite the fact that ARDS and hemodynamic pulmonary edema are based on fundamentally different pathogenetic mechanisms, doctors often consider them as a single symptom complex and carry out the same type of treatment for these fundamentally different conditions.The patient is prescribed drugs that reduce the hydrostatic pressure in the pulmonary capillaries (peripheral vasodilators, diuretics and cardiac glycosides), which adversely affects his condition. In this regard, it is important to distinguish between hemodynamic and toxic pulmonary edema.
The latter is diagnosed based on the following criteria:
1) the development of acute respiratory failure against the background of a disease or pathological condition, accompanied by the phenomena of endotoxicosis or exposure to the lungs of toxic substances;
2) clinical and radiological manifestations of the interstitial or intraalveolar stage of pulmonary edema;
3) the course of pulmonary edema against the background of normal central venous pressure and the pressure of pulmonary capillary wedging, normal borders of cardiac dullness and absence of effusion in the pleural cavities (if there are no severe concomitant diseases of the heart and lungs).
Having established the diagnosis of ARDS, you should immediately begin active complex therapy:treatment of the underlying disease and relief of toxic pulmonary edema. The main direction of the treatment of toxic pulmonary edema is the use of a complex of agents and therapeutic measures in order to normalize the impaired permeability of the alveolar-capillary membrane and prevent its further damage.
Currently, the drugs of choice in the prevention and treatment of toxic pulmonary edema of various natures are glucocorticoid drugs, which, due to a variety of mechanisms of action (anti-inflammatory, decrease in histamine production, increase in its metabolism, etc.), reduce the initially high permeability of the alveolar membrane.
Usually, prednisolone is administered up to 1.2-2 g per day intravenously (repeated intravenous bolus injections every 2-3 hours). In this case, it is necessary to carry out short courses of treatment with glucocorticoid drugs (no more than 24-48 hours), since with a longer use of them, the risk of secondary, often fatal pulmonary purulent-inflammatory complications increases significantly.
It is justified, especially in the case of the development of respiratory distress syndrome in adults when inhaling fumes and toxic substances, inhalations of glucocorticoids in large doses according to the following method: 4-5 inhalations of metered aerosol of auxilozone (dexamethasonisonicotinate) or becotide (becomethasone) every 10 min. metered dose inhaler for 200-250 doses.
Due to their sufficient effectiveness in these situations in a number of European countries, the equipment of rescue teams and firefighters includes the drug "Auxiloson" (firm "Thomae", Germany) in an individual package. It is used to provide self-help and mutual assistance when the victim is in an infected atmosphere, and even more so when the first symptoms of toxic pulmonary edema develop.
The most important pathogenetic direction of ARDS treatment is adequate oxygen therapy... It begins with the inhalation of 100% humidified oxygen through a nasal catheter (6-10 L / min), creating a positive pressure at the end of exhalation, which helps to increase lung compliance and straighten the atelectasized areas. With an increase in the phenomena of hypoxemia (the partial pressure of oxygen is less than 50 mm Hg), it is necessary to transfer the patient to artificial ventilation.
Treatment for toxic pulmonary edema includes infusion therapy... In order to direct the flow of fluid from the interstitium into the lumen of the vessel by increasing the oncotic blood pressure, an excessive gradient must be created. For this purpose, 200-400 ml of 10-20% albumin solution is re-injected per day. With ARDS on the basis of endotoxicosis, it is necessary to carry out detoxification therapy by methods of extraorgan detoxification (hemofiltration, hemosorption, plasmapheresis).
The high efficiency of repeated hemofiltration sessions is due not only to the convertible transfer of large amounts of medium molecules involved in the formation of endotoxicosis and vascular permeability disorders, but also to the removal of excess extravascular fluid. The treatment program also includes the use of heparin in small doses (10,000-20,000 units per day subcutaneously), which prevents the progression of hemocoagulation disorders in the vessels of the lungs, and protease inhibitors (counterkal, gordox), which block plasma and leukocyte proteolysis.
The question of the tactics of antibiotic therapy in patients with adult respiratory distress syndrome arising from endotoxicosis of an infectious genesis is difficult and ambiguous, since the infectious process cannot be stopped without adequate use of antibacterial drugs. However, active therapy with correctly selected antibacterial agents naturally leads to the destruction of microorganisms, increasing toxemia due to the release of large amounts of endotoxins. This contributes to the progression (development) of infectious-toxic shock and toxic pulmonary edema.
There are frequent cases when the development of toxic pulmonary edema coincides with the initiation of antibiotic therapy, which is especially typical for patients with severe forms of leptospirosis. In addition, it should be taken into account that in ARDS, in contrast to hemodynamic pulmonary edema, fluid accumulates in the alveoli with high content protein, which is a favorable environment for the reproduction of microflora.
All this makes the use of antibacterial drugs in moderate therapeutic doses in the treatment of patients with toxic pulmonary edema. At the same time, as practice shows, in cases of the development of ARDS at the height of infectious-toxic shock in leptospirosis, sepsis and meningococcal infection, it is necessary to temporarily (at least until the hemodynamic parameters stabilize) significantly reduce single doses of antibiotics.
Unlike hemodynamic pulmonary edema, in which, after the introduction of peripheral vasodilators and diuretics, in most cases, the patient's condition improves almost immediately, with toxic edema, treatment is a rather difficult task due to the variety of pathogenetic mechanisms and the lack of effective methods (medicines) prevention of the development and relief of violations of the permeability of the alveolar-capillary membrane.
The most difficult to treat is toxic pulmonary edema, which develops in a patient with multiple organ failure of various nature (against the background of sepsis or peritonitis). All this determines the high frequency of deaths in these difficult clinical situations and requires further development of approaches to the treatment of toxic pulmonary edema.
V.G. Alekseev, V.N. Yakovlev