The hallmark clinical features of toxic pulmonary edema are. Clinic of acute lung damage by toxic substances

The intake of various aggressive substances in the body is fraught with the occurrence of a variety of health problems. In this case, drugs, poisons, heavy metal salts, decay products of certain substances and toxins produced by the body itself in response to the development of some diseases can act as aggressors. Such poisoning can be fatal or cause a serious violation of the functions of vital organs: the heart, brain, liver, etc. Among these disorders is toxic pulmonary edema, the symptoms and treatment of which will be considered 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 some infectious lesions, for example, pneumonia, leptospirosis and meningococcemia, as well as endotoxicosis, for example, sepsis, peritonitis, pancreatitis etc. In some cases, such a condition is provoked by severe allergic diseases or poisoning.
Toxic pulmonary edema is characterized by a number of intense clinical manifestations, especially severe course and often poor 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 possibility of further pulmonary edema at this stage. After half an hour or an hour, the unpleasant symptoms completely disappear, a period of latent 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 disturbed by a feeling of slight shortness of breath, coughing, breathing and pulse become more frequent.

With a sharp pulmonary edema, shortness of breath occurs abruptly, and with a 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 supine position and with any movements. The patient tries to take a forced position: sitting with an inclination forward, in order to at least slightly ease breathing.

Pathological processes cause a feeling of pressing pain in the chest area, they cause an increase in heart rate. The patient's skin is covered with cold sweat and is painted in cyanotic or gray tones.

The victim is worried about coughing - at first dry, after - with the separation of frothy sputum, colored pink (due to the presence of blood streaks in it).

The patient's breathing becomes frequent, and as the 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. A pinkish foam comes out of his nose and mouth. The skin turns blue, blood vessels pulsate in the neck, and consciousness becomes clouded.

If pulmonary edema leads to the development of "gray" hypoxemia, the patient's activity of the cardiovascular and respiratory systems is sharply disrupted: a collapse occurs, the pulse becomes weak and arrhythmic (may not be felt), and breathing is rare. The skin becomes 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 keeps many thousands of cases of saving patients. The victim should be kept calm, he is shown sedatives and antitussives. As a first aid, doctors can also inhale an oxygen-air mixture by passing it through defoamers (alcohol). To reduce blood flow to the lungs, they resort to bloodletting or the imposition of venous tourniquets on the limbs.

To eliminate the onset of toxic pulmonary edema, doctors administer to the victim steroidal anti-inflammatory drugs (usually prednisone), as well as diuretics (most often furosemide). Also, treatment involves the use of bronchodilators (aminophylline), oncotic active agents (plasma or albumin), glucose, calcium chloride and cardiotonic drugs. If progression of respiratory failure is observed, tracheal intubation and mechanical ventilation (artificial ventilation of the lungs) are carried out.

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

The prognosis and survival of toxic pulmonary edema depends on the factor that provoked this disorder, on the severity of the edema, and on 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 the cause of disability.

Additional Information

Patients who have had toxic pulmonary edema can benefit from a variety of herbal and home remedies. They can be used for recreational purposes and only after consulting a doctor.

So an excellent effect is given by treatment with oats, recipes for which (some) have already been given earlier. Brew a glass of such raw materials with half a liter of milk and evaporate on a fire of minimum power until the volume of the broth is reduced by half. At the same time, do not forget to stir the prepared medicine from time to time. Then wipe the oats through a sieve. Drink the resulting mixture at one time before a meal. Take it three times a day.

The feasibility of using traditional medicine should be discussed with the doctor without fail.

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 an increase in the permeability of capillary membranes, which, apparently, can be facilitated by damage to the sulfhydryl groups of lung tissue proteins. The increase in permeability is carried out with the participation of histamine, active globulins and other substances released or formed in the tissue under the action of stimuli on it. Important in the regulation of capillary permeability belongs to the nervous mechanisms. So, for example, in the experiment it was shown 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 pathoanatomical 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 are ahead of cellular infiltration.

The development of pulmonary edema causes a violation of gas exchange in the lungs. At the height of the 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 supply of tissues with oxygen - hypoxia. Acidic metabolic products accumulate in tissues, reserve alkalinity decreases and pH shifts to the acid side.

Clinically distinguish 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) hidden period; 3) the period of increase in edema; 4) the period of completed edema; 5) reverse development of edema.

Abortive form characterized by a change of four periods: 1) initial phenomena; 2) hidden 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 phenomena 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. 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 voiced fine bubbling wet 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 dilated, have fuzzy 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 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, pronounced cyanosis of the skin and mucous membranes is noted, pronounced shortness of breath - up to 50-60 breaths per minute. In the distance, bubbling breathing is heard. Cough with large amounts of frothy sputum, often containing blood. During auscultation, a mass of different-sized wet rales is found throughout the lung fields. Tachycardia is noted, blood pressure remains normal or even slightly increased. When examining blood, its significant thickening is revealed: the content of hemoglobin increases. Coagulation is enhanced. The arterialization of blood in the lungs is disturbed, which is manifested by a deficiency in arterial blood oxygen saturation with a simultaneous increase in carbon dioxide content (hypercapnic hypoxemia). Compensated gaseous 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. Face covered with cold sweat. The limbs 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 content of carbon dioxide (hypoxemia with hypocapnia). The coefficient of oxygen utilization and its arteriovenous difference decrease. The state of "gray hypoxemia" may be preceded by a period of "blue hypoxemia". Sometimes the process begins immediately according to the type of "gray hypoxemia". This can be facilitated by physical activity, 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 an overload of the "acute pulmonary heart" type, as well as myocardial ischemia and vegetative changes. Regardless of the type of edema in the stage of completed edema, an increase in the blurring of the lung pattern and the appearance in the lower and middle sections of small (2-3 mm) spotted shadows at first, which later increase in size due to the merging of individual foci, form fuzzy contoured shadows resembling "flakes of melting snow" Areas of darkening alternate with enlightenments due to emerging foci of bullous emphysema. The roots of the lungs become even wider with fuzzy contours.

The transition of the period of increasing to expanded pulmonary edema often occurs very quickly, characterized by a rapidly progressive course. Severe forms of pulmonary edema can be fatal in 24-48 hours. In milder cases and with timely intensive care, a period of regression of pulmonary edema occurs.

During the reverse development of edema, coughing and the amount of sputum discharge gradually decrease, shortness of breath subsides. Cyanosis decreases, weaken, and then wheezing in the lungs disappears. X-ray studies indicate the disappearance of first large and then small focal shadows, only the fuzziness of the lung 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 - 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 of subsiding of the clinical manifestations of edema and improvement of the general condition, usually on the 3rd-4th day after poisoning, there is a rise in temperature to 38-39 ° C, coughing again intensifies with mucopurulent sputum. In the lungs, areas of finely bubbling wet rales appear or increase. In the blood, leukocytosis increases and an acceleration of ESR appears. Radiologically, small pneumonic foci of the type of small-focal pneumonia are noted. Another serious complication of toxic edema is the so-called "secondary" pulmonary edema, which can develop at the end of the 2nd - the middle of the 3rd week, as a result of the onset of acute heart failure. In the long-term follow-up after toxic pulmonary edema, toxic pneumosclerosis and pulmonary emphysema may develop. An exacerbation of previously latent pulmonary tuberculosis and other chronic infections may occur.

In addition to changes in the lungs and the cardiovascular system, changes in the nervous system are often found in toxic pulmonary edema. The victims complain of headache, dizziness. Relatively often, instability in the neuro-emotional sphere is revealed: irritability, anxiety, the predominance of depressive-hypochondriac 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 vegetative disorders is possible.

At the height of toxic edema, diuresis sometimes decreases, up to anuria. In the urine, traces of protein, hyaline and granular cylinders, erythrocytes are found. These changes are associated with the possibility of developing toxic kidney damage due to general vascular changes.
With pulmonary edema, liver damage is often noted - a slight increase in the organ, a change in functional liver tests by the type of toxic hepatitis. These changes in the liver 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 sweating of blood plasma, as a result of which pulmonary gas exchange is disturbed and acute oxygen starvation develops, pulmonary hypoxia with a sharp violation of all body functions. Toxic pulmonary edema also develops in case of poisoning with other toxic and irritating substances (nitrogen oxides, nitric acid vapors, sulfuric acid, ammonia, lewisite, etc.).

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

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

Biochemical;

Nervous reflex;

Hormonal.

Biochemical. In pulmonary edema, inactivation of the surfactant system of the lungs plays a certain role. 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. The surfactant reduces the surface tension forces in the alveoli at the air-water interface, thus preventing alveolar atelectasis and exudation of fluid into the alveoli.

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

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 a center located in the brain stem; The efferent pathway is the sympathetic division of the nervous system. At the same time, pulmonary edema is considered as a protective physiological reaction aimed at washing off the irritating agent.

Under the action of phosgene, the neuroreflex 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 vapors of phosgene and other substances of this group.

Excitation efferently spreads to the sympathetic branches of the lungs, as a result of a violation of the trophic function of the sympathetic nervous system and the local damaging effect of phosgene, swelling and inflammation of the lung membrane and a pathological increase in permeability in the vascular membrane of the lungs occur. Thus, there are two main links 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 neuroreflex mechanism, neuroendocrine reflexes, among which antisodium And antidiuretic reflexes occupy a special place. Under the influence of acidosis and hypoxemia, chemoreceptors are irritated. The slowing down of blood flow in the small circle contributes to the expansion of the lumen of the veins and irritation of volumenreceptors that respond to changes in the volume of the vascular bed. Impulses from chemoreceptors and volumenreceptors reach the midbrain, the response of which is the release of aldosterone-tropic factor, neurosecretate, into the blood. In response to its appearance in the blood, the secretion of aldosterone is stimulated in the adrenal cortex. The mineral corticoid aldosterone is known to promote the retention of sodium ions 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, lingering in the lung tissue, cause an imbalance in osmotic balance. This first phase of neuroendocrine responses is called antisodium reflex.

The second phase of neuroedocrine reactions begins with the excitation of lung osmoreceptors. The impulses sent by them reach the hypothalamus. In response to this, the posterior 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 through 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 in pulmonary edema, which is called the antidiuretic reflex.

Thus, the following main links of the pathogenetic chain in pulmonary edema can be distinguished:

1) violation 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 stagnation of blood in the pulmonary circulation;

4) oxygen starvation of the blue and gray types.

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Doctors of various specialties, especially those working in multidisciplinary hospitals, constantly observe the symptom complex of acute respiratory failure, the development of which can be due to a number of reasons. The dramatic nature 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 with involvement of large areas of the lung parenchyma in the process, status asthmaticus, pulmonary embolism, etc.), pulmonary edema is most often detected - a pathological process in which in the interstitium of the lung tissue, and later in the alveoli themselves, fluid accumulates in excess.

Pulmonary edema can be based on various pathogenetic mechanisms, depending on which it is necessary to distinguish between two groups of pulmonary edema (Table 16).

Etiology and pathogenesis

Despite the unequal mechanisms of development of pulmonary edema, doctors often do not distinguish them by pathogenesis and carry out the same type of treatment of 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 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, 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 an increase in the permeability of the alveolar-capillary membrane due to its damage. Such pulmonary edema is called toxic. In the literature, it is also referred to by the terms "shock lung", "non-coronary (non-cardiac) pulmonary edema", "adult respiratory distress syndrome (ARDS)".

Toxic pulmonary edema occurs when one or another damaging factor (substance, agent) directly affects the alveolar-capillary membrane. Such a substance can reach the alveolar-capillary membrane aerogenically by inhalation of toxic gases or fumes, or hematogenously with the blood stream (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) that enter the bloodstream. The pathogenesis of ARDS in endotoxicoses 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 mediator systems of the body.

Endotoxins interact with sensitive cells and cause them to release large amounts of histamine, serotonin and other vasoactive compounds. 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 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 secrete the so-called tumor necrosis factor, which has a direct damaging effect on endothelial cells, causing pronounced disturbances in both their permeability and microcirculation. Of certain importance are various enzymes released during the massive breakdown of neutrophils: elastase, collagenase and non-specific proteases that destroy glycoproteins of the interstitium and the main membrane of cell walls.

As a result of all this, damage to the alveolar-capillary membrane occurs during sepsis, which is confirmed by the results of microscopic examination: edema 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.

Similar in pathogenesis are toxic pulmonary edema in other endotoxicoses and infectious diseases (peritonitis, leptospirosis, meningococcal and non-clostridial anaerobic infections) and pancreatitis, although, perhaps, in the latter, the direct effect of proteases on the endothelial cells of the pulmonary capillaries is also of great importance.

The development of toxic pulmonary edema by 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 related 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 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 slightly different damaging effect. They dissolve in the bronchial secretion of the airways, exerting a pronounced irritating effect.

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

With toxic pulmonary edema of different etiologies 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 impact 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.

In parallel, occurring microcirculation disorders in the form of blood stasis in paralytically dilated pulmonary capillaries also significantly impair gas exchange. During this period, ARDS the patient begins to notice shortness of breath with increased respiration, as in a healthy person after exercise. 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 a diffuse enhancement of the pulmonary pattern due to the vascular component is detected during radiography, and a decrease in the partial pressure of oxygen in capillary blood (less than 80 mm Hg) is detected in a laboratory study. 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 follow in ARDS caused by the 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 thrombosis, a sharp dilatation of blood vessels and a violation of lymph drainage through the septal and perivascular membranes, which leads to 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 liquid.

As a result of damage to type II pneumocytes (which is most pronounced in persons whose lungs were 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 wet rales appear above the lungs, breathing becomes bubbling, and an x-ray examination reveals a decrease in pneumatization of the lung tissue according to the "snow storm" type (intra-alveolar stage of pulmonary edema).

In contrast to hemodynamic pulmonary edema, copious, frothy, pink-colored sputum is rarely observed in adult respiratory distress syndrome. Damage to the mucous membrane opens the way for a 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 and Pseudomonas aeruginosa, Proteus, Klebsiella and Staphylococcus aureus.

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 other infectious diseases, ARDS often occurs at the height of the development of infectious-toxic (septic) shock, significantly aggravating the already serious condition of the patient. 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 joins 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 type 1 allergic reactions.

Inhalation of toxic aerosols, industrial gases, as well as fumes generated in large quantities during a fire, immediately causes a paroxysmal cough, a feeling of rawness in the nasopharynx, and laryngo-bronchospasm may be observed. 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 when inhaling fumes - up to 2-3 days.

However, in the future, the condition of the victim deteriorates sharply: cough intensifies, dyspnea increases in intensity, clinical manifestations of expanded pulmonary edema are noted. When inhaled nitrogen dioxide in high concentrations, methemoglobinemia develops simultaneously with pulmonary edema. When the victim is in the fire zone, along with fumes 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 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 of 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 diagnosis of the latter is carried out on the basis of 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 pulmonary capillary wedge pressure, normal borders 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). At the same time, it is necessary to carry out short courses of treatment with glucocorticoid drugs (no more than 24-48 hours), since with a longer use they significantly increase the risk of secondary, often fatal pulmonary purulent-inflammatory complications.

It is justified, especially in the case of the development of respiratory distress syndrome in adults 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 in the treatment of ARDS is adequate oxygen therapy. It begins with inhalation of 100% humidified oxygen through a nasal catheter (6-10 l/min), creating a positive end-expiratory pressure, which increases lung compliance and straightens atelectatic areas. With an increase in the phenomena of hypoxemia (partial pressure of oxygen less than 50 mm Hg), it is necessary to transfer the patient to artificial ventilation of the lungs.

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 pressure of the blood, it is necessary to create an excess gradient. For this purpose, 200-400 ml of a 10-20% albumin solution is re-introduced per day. In case of ARDS due to endotoxicosis, detoxification therapy by extraorganic detoxification methods (hemofiltration, hemosorption, plasmapheresis) is mandatory.

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 low 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 (kontrykal, Gordox), blocking plasma and leukocyte proteolysis.

It is difficult and ambiguous to resolve the issue of antibiotic therapy tactics in patients with adult respiratory distress syndrome that occurs with endotoxicosis of infectious origin, 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 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 beginning 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 with a high protein content accumulates in the alveoli, which is a favorable environment for the reproduction of microflora.

All this forces the use of antibacterial drugs in average therapeutic doses in the treatment of 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 stabilization of hemodynamic parameters) 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 (drugs) to prevent the development and stopping 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 leads to a high incidence 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

This is the most severe form of lung toxicity. Clinically, two forms of toxic pulmonary edema are distinguished: developed, or completed, and abortive.

With a developed form, a consistent development of five periods is observed: 1) initial phenomena (reflex stage); 2) hidden period; 3) the period of increase in edema; 4) period of completion of edema; 5) reverse development of edema.

The period of initial phenomena 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, pass quickly, and upon contact with compounds that are poorly soluble in water, they may be completely absent.

The latent period follows the subsidence of the irritation phenomena and can have a different duration (from 2 to 24 hours), more often than 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 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, pronounced cyanosis of the skin and mucous membranes is noted, pronounced shortness of breath - 50-60 breaths per minute. In the distance, bubbling breathing is heard. Cough with large amounts of frothy sputum, often containing blood. Auscultation reveals a mass of various wet rales throughout the lung fields. tachycardia is noted, blood pressure remains normal or even slightly increased. The arterialization of blood in the lungs is disturbed, 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 unsharply excited, 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, as a rule, is lethargic, adynamic, poorly answers questions. The skin becomes pale gray in color. Face covered with cold sweat. The limbs 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).

During the reverse development of edema, the cough and the amount of sputum discharge gradually decrease, shortness of breath subsides. Cyanosis decreases, weaken, and then wheezing in the lungs disappears. X-ray studies indicate the disappearance of 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 result 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 giving of antitussives is shown.

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. Shown bed rest, intermittent oxygen therapy. 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.

The 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 aminofillin, cardiovascular agents and analeptics (corglicon, cordiamine, camphor preparations).

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

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

Previously commonly used bloodletting is now rarely used due to possible complications (collapse). It is most expedient to carry out the so-called. "bloodless bloodletting" - the imposition of tourniquets on 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 hospitalized in poison control centers or intensive care units.