The distinctive clinical features of toxic pulmonary edema are: Clinic of acute lung injuries caused by toxic substances

The entry of various aggressive substances into the body is fraught with the occurrence of a variety of health problems. The role of aggressors in this case can be drugs, poisons, salts of heavy metals, breakdown products of certain substances and toxins produced by the body itself in response to the development of some diseases. Such poisoning can lead to death or cause serious disruption of the functions of vital organs: heart, brain, liver, etc. Among such disorders is toxic pulmonary edema, the symptoms and treatment of which we will consider in a little more detail.

Toxic pulmonary edema can develop as a result of inhalation of certain aggressive substances, represented by nitric oxide, ozone, ammonia, chlorine, etc. It can be caused by certain infectious diseases, for example, pneumonia, leptospirosis and meningococcemia, as well as endotoxicosis, for example, sepsis, peritonitis, pancreatitis etc. In some cases, this condition is provoked by severe allergic diseases or poisoning.
Toxic pulmonary edema is characterized by a number of intense clinical manifestations, a particularly severe course and often an unfavorable prognosis.

Symptoms

If aggressive substances are inhaled, the patient may experience a slight cough, a feeling of tightness in the chest, a feeling of general weakness, headaches, and frequent shallow breathing. High concentrations of toxic elements provoke suffocation and cyanosis. It is impossible to prevent the likelihood of further pulmonary edema at this stage. After half an hour or an hour, the unpleasant symptoms completely disappear, and a period of hidden well-being may begin. But the progression of pathological processes leads to the gradual appearance of negative symptoms.

The initial sign of toxic pulmonary edema of any etiology is a feeling of general weakness and headache, a feeling of weakness, heaviness and tightness in the chest. The patient is bothered by a feeling of slight shortness of breath, coughing, breathing and pulse increase.

With sudden pulmonary edema, shortness of breath occurs abruptly, and with slow development it is of a constant progressive nature. Patients complain of a pronounced feeling of lack of air. Shortness of breath increases and turns into suffocation; it intensifies both in the lying position and with any movements. The patient tries to take a forced position: sitting and leaning forward, in order to make breathing at least a little easier.

Pathological processes cause a feeling of pressing pain in the chest area, they cause increased heart rate. The patient's skin becomes covered with cold sweat and turns bluish or gray.

The victim is bothered by a cough - initially dry, then with the release of foamy sputum, colored pink (due to the presence of blood streaks in it).

The patient's breathing becomes frequent, and as swelling increases, it becomes bubbling and audible at a distance. Developing edema causes dizziness and general weakness. The patient becomes frightened and agitated.

If pathological processes develop according to the type of “blue” hypoxemia, the victim begins to moan and rush about, he cannot find a place for himself and tries to greedily catch air with his mouth. Pinkish foam comes out of his nose and mouth. The skin turns blue, the blood vessels in the neck pulsate, and consciousness becomes darkened.

If pulmonary edema leads to the development of “gray” hypoxemia, the patient’s cardiovascular and respiratory system activity is sharply disrupted: collapse occurs, the pulse becomes weak and arrhythmic (may not be palpable), and breathing is rare. The skin turns earthy gray tones, the limbs become cold, and the facial features become pointed.

How is toxic pulmonary edema corrected, what is its effective treatment?

When symptoms of developing pulmonary edema appear, emergency medical care is immediately needed, the history of which contains many thousands of cases of saving patients. The victim should be kept at rest; sedatives and antitussives are indicated. As first aid, doctors can also inhale an oxygen-air mixture, passing it through defoamers (alcohol). To reduce blood flow to the lungs, they resort to bloodletting or the application of venous tourniquets to the limbs.

To eliminate toxic pulmonary edema that has begun, doctors administer steroidal anti-inflammatory drugs (usually prednisolone) and diuretics (most often furosemide) to the victim. Treatment also involves the use of bronchodilators (aminophylline), oncotically active agents (plasma or albumin), glucose, calcium chloride and cardiotonics. If progression of respiratory failure is observed, tracheal intubation and mechanical ventilation (artificial ventilation) are performed.

To prevent pneumonia, doctors use broad-spectrum antibiotics in the usual dosage, and to prevent thromboembolic complications they use anticoagulants. The total duration of therapy can reach one and a half months.

The prognosis and survival rate for toxic pulmonary edema depend on the factor that provoked this disorder, the severity of the edema, and how quickly and professionally medical care was provided. Toxic pulmonary edema at the acute stage of development often causes death, and in the long term often becomes a cause of disability.

Additional Information

Patients who have suffered toxic pulmonary edema can benefit from various herbal and improvised remedies. They can be used for health purposes and only after consulting a doctor.

Thus, treatment with oats gives an excellent effect, recipes for which (some) have already been given earlier. Brew a glass of such raw materials with half a liter of milk and simmer over low heat until the volume of the decoction is reduced by half. At the same time, do not forget to stir the prepared medicine from time to time. Then rub the oats through a sieve. Drink the resulting mixture in one dose before meals. Take it three times a day.

The advisability of using traditional medicine should be discussed with your doctor.

This is the most severe form of lung toxicity.

The pathogenesis of toxic pulmonary edema cannot be considered definitive. The leading role in the development of toxic pulmonary edema belongs to the increase in the permeability of capillary membranes, which, apparently, can be facilitated by damage to the sulfhydryl groups of lung tissue proteins. Increased permeability is carried out with the participation of histamine, active globulins and other substances released or formed in the tissue when irritants act on it. Nervous mechanisms play an important role in the regulation of capillary permeability. For example, the experiment showed that vagosympathetic novocaine blockade can reduce or even prevent the development of pulmonary edema.

Based on the clinical picture of toxic edema with the presence of leukocytosis and temperature reaction, as well as pathological data indicating the presence of confluent catarrhal inflammation in the absence of microbial flora, some researchers consider pulmonary edema as one of the variants of toxic pneumonia, in which exudation processes precede cellular infiltration.

The development of pulmonary edema causes a violation of gas exchange in the lungs. At the height of edema, when the alveoli are filled with edematous fluid, the diffusion of oxygen and carbon dioxide is possible only due to the solubility of gases. At the same time, hypoxemia and hypercapnia gradually increase. At the same time, there is a thickening of the blood, an increase in its viscosity. All these factors lead to insufficient oxygen supply to tissues - hypoxia. Acidic metabolic products accumulate in tissues, reserve alkalinity decreases and the pH shifts to the acidic side.

Clinically distinguished two forms of toxic pulmonary edema: developed, or completed, and abortive.

At developed form There is a consistent development of five periods: 1) initial phenomena (reflex stage); 2) latent period; 3) period of swelling increase; 4) the period of completed edema; 5) reverse development of edema.

Abortive form characterized by a change of four periods: 1) initial phenomena; 2) latent period; 3) increase in edema; 4) reverse development of edema.

In addition to the two main ones, another form of acute toxic pulmonary edema is distinguished - the so-called " silent swelling”, which is detected only by X-ray examination of the lungs, while the clinical manifestations of pulmonary edema are practically absent.

The period of initial effects develops immediately after exposure to a toxic substance and is characterized by mild symptoms of irritation of the mucous membranes of the respiratory tract: a slight cough, sore throat, chest pain. As a rule, these mild subjective disorders do not have a significant effect on the well-being of the victim and soon disappear.

The latent period follows the subsidence of irritation and can have a different duration (from 2 to 24 hours), more often 6-12 hours. During this period, the victim feels healthy, but with a thorough examination, the first symptoms of increasing oxygen deficiency can be noted: shortness of breath, cyanosis , pulse lability. It has been experimentally proven that in this "hidden" period from the very beginning it is possible to detect histological changes corresponding to edema of the interstitial tissue of the lung, so the absence of clear clinical manifestations does not yet indicate the absence of an emerging pathology.

The period of increasing edema is clinically manifested, which is associated with the accumulation of edematous fluid in the alveoli and a more pronounced violation of the respiratory function. The victims have an increase in breathing, it becomes superficial and is accompanied by paroxysmal excruciating cough. Objectively, slight cyanosis is noted. In the lungs, ringing, fine, moist rales and crepitus are heard. During X-ray examination in this period, one can note fuzziness, blurring of the pulmonary pattern, small ramifications of blood vessels are poorly differentiated, some thickening of the interlobar pleura is noted. The roots of the lungs are somewhat expanded and have unclear contours.

Identification of signs of increasing toxic pulmonary edema is very important for appropriate therapeutic and preventive measures to prevent the development of edema.

The period of completed edema corresponds to 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, pronounced cyanosis of the skin and mucous membranes and pronounced shortness of breath are observed - up to 50-60 breaths per minute. In the distance, bubbling breathing can be heard. Cough producing large amounts of foamy sputum, often mixed with blood. Upon auscultation, a mass of different-sized moist rales is detected throughout the pulmonary fields. Tachycardia is noted, blood pressure remains normal or even increases slightly. When examining the blood, its significant thickening is revealed: the hemoglobin content increases. Coagulability increases. The arterialization of blood in the lungs is impaired, which is manifested by a deficiency in arterial blood oxygen saturation with a simultaneous increase in carbon dioxide content (hypercapnic hypoxemia). Compensated gas acidosis develops.

With the “gray” type of toxic edema, the clinical picture is more severe due to the addition of pronounced vascular disorders. The skin becomes pale gray in color. The face is covered with cold sweat. Extremities are cold to the touch. The pulse becomes frequent and small. There is a drop in blood pressure. The gas composition of the blood in these cases is characterized by a decrease in oxygen saturation and a low carbon dioxide content (hypoxemia with hypocapnia). The coefficient of oxygen utilization and its arteriovenous difference decreases. The state of “gray hypoxemia” may be preceded by a period of “blue hypoxemia”. Sometimes the process begins immediately, like “gray hypoxemia.” This can be facilitated by physical activity and long-term transportation of the victim.

Disorders of the cardiovascular system in toxic pulmonary edema are caused by impaired blood flow in the pulmonary circulation with overload of the “acute cor pulmonale” type, as well as myocardial ischemia and autonomic shifts. Regardless of the type of edema, in the stage of completed edema, an increase in blurring of the pulmonary pattern and the appearance in the lower and middle sections of initially small (2-3 mm) spotty shadows, which subsequently increase in size due to the merging of individual foci, forming vaguely contoured shadows resembling "flakes of melting snow." Areas of darkening alternate with clearing caused by developing foci of bullous emphysema. The roots of the lungs become even wider with unclear contours.

The transition from the period of increasing to full-blown pulmonary edema often occurs very quickly, characterized by a rapidly progressing course. Severe forms of pulmonary edema can lead to death after 24-48 hours. In milder cases and with timely intensive therapy, a period of reverse development of pulmonary edema begins.

During the reverse development of edema, the cough and the amount of sputum produced gradually decrease, and shortness of breath subsides. Cyanosis decreases, wheezing in the lungs weakens and then disappears. X-ray studies indicate the disappearance of first large and then small focal shadows, only the vagueness of the pulmonary pattern and the contours of the roots of the lungs remains, and after a few days the normal X-ray morphological picture of the lungs is restored, the composition of the peripheral blood is normalized. Recovery can have significant variability in terms of time - from several days to several weeks.

The most common complication of toxic pulmonary edema is the addition of infection and the development of pneumonia. During the period when the clinical manifestations of edema subside and the general condition improves, usually on the 3-4th day after poisoning, the temperature rises to 38-39 ° C, the cough intensifies again with the release of mucopurulent sputum. Areas of fine-bubbly moist rales appear or increase in the lungs. Leukocytosis increases in the blood and ESR accelerates. X-rays reveal small pneumonic foci of the type of small focal pneumonia. Another serious complication of toxic edema is the so-called “secondary” pulmonary edema, which can develop at the end of the 2nd to the middle of the 3rd week, as a consequence of advancing acute heart failure. In long-term follow-up after toxic pulmonary edema, the development of toxic pneumosclerosis and pulmonary emphysema is possible. An exacerbation of previously latent pulmonary tuberculosis and other chronic infections may occur.

In addition to changes in the lungs and cardiovascular system, changes in the nervous system are often found with toxic pulmonary edema. Victims complain of headaches and dizziness. Relatively often, instability in the neuro-emotional sphere is detected: irritability, anxiety, the predominance of depressive-hypochondriacal reactions, in some victims - agitation and convulsions, and in severe cases - stupor, drowsiness, adynamia, loss of consciousness. In the future, the addition of asthenoneurotic and autonomic disorders is possible.

At the height of toxic edema, diuresis sometimes decreases, up to anuria. Traces of protein, hyaline and granular casts, and red blood cells are found in the urine. These changes are associated with the possibility of developing toxic kidney damage caused by general vascular changes.
With pulmonary edema, liver damage is often observed - some enlargement of the organ, changes in functional liver tests like toxic hepatitis. These liver changes can persist for quite a long time, often combined with functional disorders of the gastrointestinal tract.

The essence of pulmonary edema is that the pulmonary alveoli are filled with edematous fluid (transudate) due to the exudation of blood plasma, as a result of which pulmonary gas exchange is disrupted and acute oxygen starvation and pulmonary hypoxia develop with a sharp disruption of all body functions. Toxic pulmonary edema also develops in case of poisoning with other toxic and irritating substances (nitrogen oxides, vapors of nitric acid, sulfuric acid, ammonia, lewisite, etc.).

Most researchers consider the main cause of toxic pulmonary edema to be an increase in the permeability of the pulmonary capillaries and alveolar epithelium, a violation of their microstructure, which has now been proven using electron microscopy.

Many theories have been put forward regarding the development of toxic pulmonary edema. They can be divided into three groups:

Biochemical;

Nervous reflex;

Hormonal.

Biochemical. Inactivation of the pulmonary surfactant system plays a role in pulmonary edema. Lung surfactant is a complex of phospholipid substances with surface activity, located in the form of a submicroscopic film thickness on the inner surface of the alveoli. Surfactant reduces the surface tension forces in the alveoli at the air-water interface, thus preventing alveolar atelectasis and fluid leakage into the alveoli.

With pulmonary edema, capillary permeability first increases, swelling and thickening of the alveolar interstitium appears, then an increase in the permeability of the alveolar walls and alveolar pulmonary edema occur.

Nervous reflex.

The basis of toxic pulmonary edema is a neuro-reflex mechanism, the afferent path of which is the sensory fibers of the vagus nerve, with the center located in the stem part of the brain; efferent pathway - sympathetic division of the nervous system. In this case, pulmonary edema is considered as a protective physiological reaction aimed at washing away the irritating agent.

Under the action of phosgene, the neuro-reflex mechanism of pathogenesis is presented in the following form. The afferent link of the neurovegetative arc is the trigeminal nerve and vagus, the receptor endings of which are highly sensitive to phosgene vapor and other substances of this group.

Excitation by the efferent route spreads to the sympathetic branches of the lungs; as a result of disruption of the trophic function of the sympathetic nervous system and the local damaging effect of phosgene, swelling and inflammation of the pulmonary membrane and a pathological increase in permeability in the vascular membrane of the lungs occur. Thus, two main links arise in the pathogenesis of pulmonary edema: 1) increased permeability of the pulmonary capillaries and 2) swelling, inflammation of the interalveolar septa. These two factors cause the accumulation of edematous fluid in the pulmonary alveoli, i.e. leads to pulmonary edema.

Hormonal.

In addition to the neuro-reflex mechanism, important neuroendocrine reflexes, among which antinatriuric And antidiuretic reflexes occupy a special place. Under the influence of acidosis and hypoxemia, chemoreceptors are irritated. Slowing down the blood flow in the pulmonary circulation contributes to the expansion of the lumen of the veins and irritation of volume receptors that respond to changes in the volume of the vascular bed. Impulses from chemoreceptors and volume receptors reach the midbrain, the response of which is the release of aldosterontropic factor - neurosecretate - into the blood. In response to its appearance in the blood, the secretion of aldosterone is stimulated in the adrenal cortex. The mineralcorticoid aldosterone is known to promote sodium ion retention in the body and enhance inflammatory reactions. These properties of aldosterone are most easily manifested in the “place of least resistance,” namely in the lungs damaged by a toxic substance. As a result, sodium ions, retaining in the lung tissue, cause an imbalance in osmotic balance. This first phase of neuroendocrine reactions, called antisodium reflex.

The second phase of neuroedocrine reactions begins with stimulation of the osmoreceptors of the lungs. The impulses sent by them reach the hypothalamus. In response to this, the posterior lobe of the pituitary gland begins to produce antidiuretic hormone, the “fire-fighting function” of which is to urgently redistribute the body’s water resources in order to restore osmotic balance. This is achieved due to oliguria and even anuria. As a result, the flow of fluid to the lungs is further enhanced. This is the second phase of neuroendocrine reactions during pulmonary edema, which is called the antidiuretic reflex.

Thus, we can distinguish the following main links in the pathogenetic chain for pulmonary edema:

1) disruption of the main nervous processes in the neurovegetative arc:

pulmonary branches of the vagus, brain stem, sympathetic branches of the lungs;

2) swelling and inflammation of the interalveolar septa due to metabolic disorders;

3) increased vascular permeability in the lungs and blood stagnation in the pulmonary circulation;

4) oxygen starvation of the blue and gray type.

1996 0

Doctors of various specialties, especially those working in multidisciplinary hospitals, constantly observe a symptom complex of acute respiratory failure, the development of which may be due to a number of reasons. The drama of this clinical situation lies in the fact that it poses a direct threat to life. The patient may die within 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, asthmatic status, pulmonary embolism, etc.), the most often detected is pulmonary edema - a pathological process in which in the pulmonary interstitium tissue, and subsequently in the alveoli themselves, excess fluid accumulates.

Pulmonary edema may be based on 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 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 is pulmonary edema associated with a significant increase in hemodynamic (hydrostatic) pressure in the pulmonary capillaries due to a significant increase in diastolic pressure in the left ventricle (aortic heart defects, 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, left atrial myxoma).

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 epithelium of the alveoli is lower than that of the endothelium of the pulmonary capillaries, widespread edema of the pulmonary interstitium develops at first and only later does intraalveolar extravasation occur. 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. Main diseases (conditions) leading to the development of pulmonary edema

Pulmonary edema may be associated with increased permeability of the alveolar-capillary membrane due to its damage. Such pulmonary edema is called toxic. In the literature it is also referred to as “shock lung”, “non-coronarogenic (non-cardiac) pulmonary edema”, "adult respiratory distress syndrome (ARDS)".

Toxic pulmonary edema occurs in cases where one or another damaging factor (substance, agent) directly affects the alveolar-capillary membrane. Such a substance can reach the alveolar-capillary membrane aerogenously by inhaling toxic gases or fumes, or hematogenously through the bloodstream (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 occur when the endothelium of the pulmonary capillaries is directly exposed to toxic substances and allergens (immune complexes) entering the bloodstream. 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 occurrence 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. Due to the active participation of the lungs in the metabolism of these substances (the so-called non-respiratory function of the lungs), pronounced changes occur in this organ.

Electron microscopy revealed that high concentrations of histamine are created in the area of alveolar capillaries, 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 release 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 the various enzymes released during the massive breakdown of neutrophils: elastase, collagenase and nonspecific proteases, which 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 during sepsis, which is confirmed by the results of a microscopic examination: swelling of pneumocytes, microcirculation disorders in the alveolar capillaries with structural disorders in endothelial cells and signs of increased vascular permeability are detected in the lung tissue.

Toxic pulmonary edema is similar in pathogenesis to other endotoxicosis and infectious diseases (peritonitis, leptospirosis, meningococcal and non-clostridial anaerobic infections) and pancreatitis, although, perhaps, with the latter, the direct effect of proteases on the endothelial cells of the pulmonary capillaries is of great importance.

The development of toxic pulmonary edema has been studied in most detail when inhaling highly toxic substances in the form of their vapors and aerosols, as well as fumes. These substances are deposited on the mucous membranes of the respiratory tract and lead to disruption of their integrity. The nature of the damage depends primarily on what part of the respiratory tract and lung tissue is affected, which is mainly due to the solubility of the chemical 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 are the ones that dissolve in the surfactant and easily diffuse through thin pneumocytes to the endothelium of the capillaries, 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 slightly different damaging effect. They dissolve in the bronchial secretions of the airways, producing a pronounced irritant effect.

Clinically, this manifests itself in the form of laryngospasm, swelling of the vocal cords and toxic tracheobronchitis with persistent painful cough up to reflex respiratory arrest. Only in the case of inhalation of very high concentrations of toxic substances can alveolar-capillary barriers be involved in the pathological process.

With toxic pulmonary edema of different etiology and pathogenesis, the same cycle of changes occurs in the lung tissue, causing the two-phase clinical symptoms of respiratory distress syndrome in adults. Thus, the wall of the pulmonary capillary responds to the influence 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, the diffusion of oxygen through it suffers, as a result of which hypoxemia develops.

Parallel microcirculatory disturbances 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. During a physical examination, pathological changes in the lungs are usually not detected in cases where there is no independent pathological process in the lung tissue; only during radiography, a diffuse increase in the pulmonary pattern due to the vascular component is detected, and during a laboratory study - a decrease in the partial pressure of oxygen in capillary blood (less than 80 mm Hg). Art.).

This stage of pulmonary edema is called interstitial. It most often occurs 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 in 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 lymph drainage 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 fluid.

As a result of damage to type II pneumocytes (which is most pronounced in individuals whose lungs have been exposed to toxic 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” (intra-alveolar stage of pulmonary edema).

In contrast to hemodynamic pulmonary edema, the production of copious, frothy, pink sputum is rarely observed in adult respiratory distress syndrome. 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 - Escherichia coli and Pseudomonas aeruginosa, Proteus, Klebsiella and staphylococci.

It is possible to note some features of the clinical course of toxic pulmonary edema in various diseases and conditions. In sepsis, leptospirosis and a number of other infectious diseases, ARDS often occurs at the height of the development of infectious-toxic (septic) shock, significantly aggravating the patient’s already serious condition. Cases have been described in which allergic reactions to drugs (primarily 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 in severe allergic reactions (primarily to drugs administered intravenously - plasma expanders, antibiotics, etc.). In these cases, acute respiratory failure is added to skin manifestations, hypotension, hyperthermia, but it is not based on total bronchospasm, but on pulmonary edema with damage to the pulmonary endothelium by immune complexes and biologically active substances (histamine, serotonin, slow-reacting substance of anaphylaxis, allergens, etc. .), formed during allergic reactions of type 1.

When inhaling toxic aerosols, industrial gases, as well as smoke generated in large quantities during a fire, a paroxysmal cough, a feeling of rawness in the nasopharynx, and laryngo-bronchospasm may immediately occur. After cessation of contact (leaving the contaminated area or premises, putting on a gas mask), a period of imaginary well-being begins, which can last several hours, and if fumes are inhaled, up to 2-3 days.

However, subsequently the victim’s condition worsens sharply: The cough intensifies, shortness of breath increases in intensity, and clinical manifestations of full-blown pulmonary edema are noted. When nitrogen dioxide is inhaled in high concentrations, methemoglobinemia develops simultaneously with pulmonary edema. When a victim is in a fire zone, along with smoke and toxic products of incomplete combustion, carbon monoxide enters the lungs, 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 treatment of toxic pulmonary edema largely depends on the speed of its recognition and 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 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) development of acute respiratory failure against the background of a disease or pathological condition accompanied by endotoxicosis or exposure to toxic substances on the lungs;
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 pulmonary capillary wedge pressure, normal boundaries of cardiac dullness and the 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 in the treatment of toxic pulmonary edema is the use of a set of drugs 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 nature are glucocorticoid drugs, which, due to the variety of mechanisms of action (anti-inflammatory, reduced histamine production, increased metabolism, etc.), reduce the initially high permeability of the alveolar membrane.

Prednisolone is usually 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 longer use they significantly increase the risk of secondary, often fatal pulmonary pyoinflammatory complications.

It is justified, especially in the case of the development of adult respiratory distress syndrome when inhaling fumes and toxic substances, inhalation of glucocorticoids in large doses according to the following method: 4-5 inhalations of a metered-dose aerosol of auxilozone (dexamethasone isonicotinate) or becotide (becometasone dipropionate) every 10 minutes until completely empty metered dose inhaler, designed 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- and mutual assistance when the victim is in a contaminated atmosphere, and even more so when the first symptoms of toxic pulmonary edema develop.

The most important pathogenetic direction of treatment of ARDS is adequate oxygen therapy. It begins with inhalation of 100% humidified oxygen through a nasal catheter (6-10 l/min), creating positive end-expiratory pressure, which helps to increase lung compliance and straighten atelectatic areas. If hypoxemia increases (partial pressure of oxygen is less than 50 mm Hg), it is necessary to transfer the patient to artificial ventilation.

Treatment of toxic pulmonary edema includes infusion therapy. In order to direct fluid flow from the interstitium into the lumen of the vessel by increasing the oncotic pressure of the blood, it is necessary to create an excess gradient. For this purpose, 200-400 ml of 10-20% albumin solution is re-introduced per day. In case of ARDS due to endotoxemia, it is necessary to carry out detoxification therapy using extraorgan detoxification methods (hemofiltration, hemosorption, plasmapheresis).

The high efficiency of repeated hemofiltration sessions is due not only to the convertible transfer of large quantities of medium molecules involved in the formation of endotoxemia and disorders of vascular permeability, 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 helps prevent the progression of hemocoagulation disorders in the vessels of the lungs, and protease inhibitors (contrical, gordox), which block plasma and leukocyte proteolysis.

The issue of antibacterial therapy tactics in patients with adult respiratory distress syndrome arising from endotoxicosis of infectious origin is difficult and ambiguous, since without adequate use of antibacterial drugs it is impossible to stop the infectious process. However, active therapy with properly selected antibacterial agents naturally leads to the destruction of microorganisms, increasing toxemia due to the release of large quantities of endotoxins. This contributes to the progression (development) of infectious-toxic shock and toxic pulmonary edema.

There are often cases when the development of toxic pulmonary edema coincides with the start of antibacterial therapy, which is especially typical for patients with severe forms of leptospirosis. In addition, it should be taken into account that with ARDS, unlike hemodynamic pulmonary edema, fluid with a high protein content accumulates in the alveoli, which is a favorable environment for the proliferation of microflora.

All this forces the use of antibacterial drugs in medium therapeutic doses when treating patients with toxic pulmonary edema. At the same time, as practice shows, in cases of development of ARDS at the height of infectious-toxic shock with leptospirosis, sepsis and meningococcal infection, it is necessary to temporarily (at least until hemodynamic parameters stabilize) to significantly reduce single doses of antibiotics.

Unlike hemodynamic pulmonary edema, in which after the administration of peripheral vasodilators and diuretics in most cases the patient’s condition almost immediately improves, with toxic edema treatment is a rather difficult task due to the variety of pathogenetic mechanisms and the lack of effective methods (medicines) to prevent the development and relieving impaired 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 natures (against the background of sepsis or peritonitis). All this causes a high incidence of deaths in these complex clinical situations and requires further development of approaches to the treatment of toxic pulmonary edema.

V.G. Alekseev, V.N. Yakovlev

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, a sequential development of five periods is observed: 1) initial phenomena (reflex stage); 2) latent period; 3) period of swelling increase; 4) period of completion of edema; 5) reverse development of edema.

The period of initial effects develops immediately after exposure to a toxic substance and is characterized by mild symptoms of irritation of the mucous membranes of the respiratory tract: a slight cough, sore throat, chest pain. All these phenomena are mild, pass quickly, and upon contact with compounds that are poorly soluble in water, they may be completely absent.

The latent period occurs after the subsidence of the irritation phenomena and can have a different duration (from 2 to 24 hours), usually 6-12 hours during this period the victim feels healthy, but with a thorough examination the first symptoms of increasing oxygen deficiency can be noted: shortness of breath, cyanosis, pulse lability.

The period of completed edema corresponds to 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, pronounced cyanosis of the skin and mucous membranes and pronounced shortness of breath are observed - 50-60 breaths per minute. In the distance, bubbling breathing can be heard. Cough producing large amounts of foamy sputum, often mixed with blood. Upon auscultation, a mass of moist rales of various sizes is detected throughout the pulmonary fields. tachycardia is noted, blood pressure remains normal or even slightly increases. The arterialization of blood in the lungs is impaired, which is manifested by a deficiency in arterial blood oxygen saturation with a simultaneous increase in carbon dioxide content (hypercapnic hypoxemia).

With the “blue” type of toxic edema, the patient is mildly excited and inadequate to his condition. A picture of acute hypoxemic psychosis may develop.

With the “gray” type of toxic edema, the clinical picture is more severe due to the addition of pronounced vascular disorders. The patient is usually lethargic, adynamic, and does not answer questions well. The skin becomes pale gray in color. The face is covered with cold sweat. Extremities are cold to the touch. The pulse becomes frequent 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).

Another dangerous complication of toxic edema is the so-called secondary edema, which can develop at the end of the 2nd to the middle of the 3rd week of illness, as a consequence of the onset of acute heart failure.

Treatment of acute intoxications.

First aid consists in immediately stopping contact with a toxic substance - the victim is taken out of the polluted atmosphere into a warm, well-ventilated room or into fresh air, freed from clothing that restricts breathing. If a toxic substance comes into contact with the skin, thoroughly wash the contaminated areas with soap and water. In case of contact with eyes, immediately rinse eyes with plenty of water or 2% sodium bicarbonate solution, then drip 0.1-0.2% dicain, 30% sodium sulfacyl solution, apply anti-inflammatory eye ointment (0.5% synthomycin, 10 % sulfacyl).

In case of damage to the upper respiratory tract, rinsing or warm-moist inhalations with a 2% solution of sodium bicarbonate, mineral waters or herbal infusions are prescribed. The administration of antitussives is indicated.

If the larynx is affected, a silence regime is necessary, drinking warm milk with sodium bicarbonate, Borjomi. With the phenomena of reflex spasm, antispasmodics (atropine, no-shpa, etc.) and antihistamines are indicated.

In cases of severe laryngospasm, tracheotomy and intubation have to be resorted to.

Anti-inflammatory drugs are prescribed to prevent infection. Patients with manifestations in the form of bronchobronchio- litis need inpatient treatment. Bed rest and intermittent oxygen therapy are indicated. The treatment complex includes bronchodilators (teopec, berotek, atrovent, eufillin, 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 a medical institution is carried out on a stretcher, and in a hospital, bed rest and observation for at least 12 hours after contact with a toxic substance are required.

At the first manifestations of the edema clinic, long-term oxygen therapy with heated, humidified oxygen is indicated. At the same time, defoamers are prescribed: most often it is ethyl alcohol. For the same purposes, antifomsilan inhalations in a 10% alcohol solution can be used for 10-15 minutes repeatedly.

In order to dehydrate the lung tissue, saluretics are prescribed: lasix or 30% urea solution intravenously.

In the early stages, intravenous corticosteroids up to 150 ml in terms of prednisolone per day and broad-spectrum antibiotics are used.

The complex of therapy includes antihistamines, intravenous aminophylline, cardiovascular drugs and analeptics (korglykon, cordiamine, camphor preparations).

In order to increase the oncotic pressure of the blood, 10-20% albumin 200-400 mg/day is administered intravenously.

To improve microcirculation processes, heparin and antiproteases (contrical) can be used under the control of hematocrit.

Previously frequently used, bloodletting is now rarely used due to possible complications (collapse). It is most expedient to carry out the so-called. “bloodless bloodletting” - applying tourniquets to the limbs.

In the case of severe pulmonary edema, intensive therapy methods are used - intubation with secretion suction, 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.