Toxic pulmonary edema is an organ damage that occurs as a result of inhalation of various pulmonary toxic chemicals. In this case, the integrity of the capillaries localized in the lungs is violated, that is, their permeability increases. This condition is quite dangerous for human life, because of this, oxygen starvation of the whole organism occurs.

Toxic edema is characterized by:

reflex period;
symptoms of a burn of the lungs and mucous membrane of the respiratory system;
signs from the action of a toxic substance - poison.

The mechanism of development of pathology

Toxic substances entering the lung tissue through the respiratory tract damage the alveolar-capillary barrier.. In this case, cell death occurs - alveocytes, endotheliocytes, etc. The alveoli are affected, fluid is accumulated in them (swelling). This condition causes a violation of the process of gas exchange in the lungs.

In the process of development of toxic edema, a change in the quality of the blood occurs. It thickens and becomes more viscous. And also all metabolic processes go astray, as there is an accumulation of acidic flora, respectively, and the pH shifts to the acid side.

Causes

The main cause of toxic pulmonary edema is the inhalation of various chemicals or drugs. Some medications can provoke the occurrence of such a dangerous condition. These include diuretics, cytostatics, non-steroidal anti-inflammatory drugs, narcotic analgesics, and radiopaque drugs.

Toxic edema from the above drugs does not occur in everyone, only in those who have an individual intolerance to some components.

Another toxic pulmonary edema occurs due to the inhalation of pulmonotoxins. They can be of an irritant nature, such as ammonia, hydrogen fluoride, concentrated acids. And also asphyxiating gases and vapors can be - chlorine, phosgene, diphosgene, nitrogen oxides, a large concentration of smoke from combustion. Also, substances that can provoke toxic edema can be glue and gasoline.

Toxic edema most often occurs due to non-compliance with safety regulations in enterprises with a technological process that includes the above chemicals. Another reason for such a dangerous condition may be an emergency situation at chemical enterprises. In wartime conditions, pulmonary edema can be provoked by various military poisons.

Additionally, lung damage can occur from:

excessive use of narcotic substances - methadone, heroin;
alcohol intoxication of the body, especially if alcoholic beverages are of poor quality;
hepatic or diabetic coma, uremia;
an allergic reaction to food or medications;
radiation exposure of the sternum.

Symptoms and signs

For toxic damage to the lungs, 4 periods are characteristic:

reflex disorders;
latent period - in this case, the symptoms subside;
pronounced swelling of the organ;
manifestation of complications.

Reflex disorders manifest themselves as symptoms of irritation of the mucous membranes. It can be cough, lacrimation, runny nose, discomfort in the throat and eyes. And also there is a feeling of pressure in the chest and pain, dizziness and weakness, these symptoms gradually increase. Breathing becomes difficult and even its reflex stop may occur.

Then the symptoms subside. This only means that the pathology passes into a latent period of the course. This stage can last from 4 to 24 hours. There are no symptoms, and if an examination is carried out at this time, bradycardia or emphysema will be diagnosed.

Pronounced pulmonary edema is already manifested by the next stage. And, as a rule, it fully develops in 24 hours. But quite often the symptoms begin to increase after 6 hours. Symptoms during this period include:

increase in body temperature;
cyanosis of the skin and mucous membranes;
respiratory rate reaches up to 50-60 times per minute;
breathing becomes heavy and can be heard at a distance, a bubbling sound is heard in the chest;
sputum with an admixture of blood is allocated.

It should be noted that the volume of sputum secreted can be quite large. The amount reaches 1 liter and even more.

"Blue" hypoxemia. And when "blue" hypoxemia develops, the patient exhibits panic behavior. That is, he begins to eagerly grab the air and at the same time is overexcited, constantly rushing about and cannot take a comfortable position of the body. At the same time, there is a pink discharge from the nose and mouth of a frothy nature. This condition got its name due to the fact that the skin turns blue.
"Gray" hypoxemia. In this period, "gray" hypoxemia may also develop, it usually proceeds in a severe form. In this case, the skin color becomes gray, and the limbs become cold. The severity of the condition lies in a weak pulse and a rapid drop in blood pressure to a critical state. Gray hypoxemia can lead to collapse.

The main signs of toxic pulmonary edema are respiratory failure, the presence of shortness of breath and cough, pain in the chest and severe hypotension, which manifests itself along with tachycardia.

Acute toxic pulmonary edema is a condition that within 24-48 hours can provoke the death of the patient (as a complication of the condition). In addition, among other complications, secondary edema, pneumonia of a bacterial nature, myocardial dystrophy, and thrombosis of various localizations can be mentioned.

A complication of toxic pulmonary edema is often right ventricular heart failure. This is due to increased pressure in the pulmonary circulation.

Diagnostics

Diagnostic measures include a physical examination, laboratory tests, and x-rays. First, the doctor listens to the lungs. If there is toxic edema, then moist, finely bubbling rales will be heard, as well as crepitus.. If the edema is at the completion stage, then the wheezing will have a multiple character, while they are of different sizes. For a doctor, this is a fairly informative sign.

X-ray is an instrumental diagnostic method in which there will be fuzzy pulmonary edges in the picture, and the roots become expanded and fuzzy. With pronounced edema, the pulmonary pattern is more blurred, and spots may additionally be present. Foci of enlightenment may indicate emphysema.

From laboratory tests, you will need to donate blood. Toxic edema is evidenced by neutrophilic leukocytosis, an increase in hemoglobin. Also observed:

increased blood clotting;
hypoxemia;
hypercapnia or hypocapnia;
acidosis.

With toxic edema, additional diagnostics are also needed. To do this, you need to undergo an electrocardiogram and donate blood for liver tests.

First aid

When toxic pulmonary edema increases, a person needs urgent help, otherwise this condition will become more complicated. The first thing to do is to help the person sit up or take a position so that the legs can hang down and the upper body is raised. Blood pressure should be measured.

In the room where the patient is located, there must be an influx of fresh air. All this should be done before the ambulance arrives. It is recommended that the patient take diuretic drugs, but if the blood pressure is low, then the dosage should be low. In addition, with severe pain, a person can be given analgesics.

Medical therapy

Treatment of toxic pulmonary edema is aimed at eliminating the oxygen starvation of the body. This is achieved by restoring normal respiratory function and blood circulation. It is required to unload a small circle of blood circulation. Violations of metabolic processes in the lungs are important, they need to be restored, and in the presence of inflammatory processes, therapy is prescribed to eliminate them.

Patients admitted with toxic pulmonary edema are given oxygen inhalations.. These procedures will help to quickly remove arterial hypoxemia. But, besides this method, others are also used, since inhalations do not affect the saturation of venous blood.

To restore the normal respiratory process, a person needs to restore the patency of the respiratory tract. To do this, aspiration of the liquid is carried out, and in order to reduce foaming, inhalations with oxygen moistened with alcohol vapor are often prescribed.

Unloading of the pulmonary circulation is carried out only when the blood pressure is at a normal level. The easiest way is to apply tourniquets to the lower limbs. Additionally, diuretics are prescribed and sometimes even bloodletting is used. To unload the small circle, 200 ml of blood is required to be released. This procedure is carried out extremely rarely, as it can provoke re-edema.

Additionally, the following drugs are prescribed:

antihistamines;
glucocorticoids;
calcium preparations;
ascorbic acid.

The following types of drugs are also used in therapy:

Non-narcotic analgesics are administered to the patient in sufficiently large doses. They prevent breath excitation.
A glucose solution with insulin is also given to patients with toxic pulmonary edema. This is necessary to restore water-mineral metabolism and to combat acidosis.
In order to prevent recurrent toxic edema, novocaine blockades can be carried out., which are used for vagosympathetic nerve bundles localized on the neck or cervical nodes of the upper localization of the sympathetic type.
If a person has cardiac symptoms, then vasodilators, cardiac glycosides, and other antihypertensive drugs are required. Blood clots may also be needed. For example, in a hospital, heparin is administered subcutaneously.

With toxic pulmonary edema, the prognosis is unfavorable. Positive results of treatment can be achieved if a person takes diuretics in large doses. But not everyone is recommended such therapy, for some people it is simply contraindicated.

Actually toxic pulmonary edema is associated with damage by toxicants to cells involved in the formation of the alveolar-capillary barrier. Military-grade toxicants capable of causing toxic pulmonary edema are called asphyxiant HIT.

The main cause of disorders of many functions of the body in case of poisoning with pulmonotoxicants is oxygen starvation. Oxygen starvation that develops when affected by asphyxiating substances can be characterized as a mixed type of hypoxia: hypoxic (impaired external respiration), circulatory (disturbance of hemodynamics), tissue (disturbance of tissue respiration).

Hypoxia underlies severe disorders of energy metabolism. At the same time, organs and tissues with a high level of energy consumption (nervous system, myocardium, kidneys, lungs) suffer the most. Violations on the part of these organs and systems underlie the clinic of intoxication with asphyxiating OVTV.

Chlorine

Chlorine was the first substance used in the war as an agent. On April 22, 1915, near the city of Ypres, the German units released it from cylinders (about 70 tons), directing a stream of gas driven by the wind towards the positions of the French troops. This chemical attack caused the death of more than 7,000 people. Later, the substance was widely used on the fronts of the 1st World War, and therefore the clinic of the lesion is well studied.

At present, chlorine is not considered as an OM. Nevertheless, millions of tons of substances are produced annually and used for technical needs: water purification (2 - 6%), bleaching of cellulose and fabrics (up to 15%), chemical synthesis (about 65%), etc. Chlorine is the most common cause of accidents at work.

Physicochemical characteristics. Toxicity

Chlorine is a yellowish-green gas with a characteristic suffocating odor, about 2.5 times heavier than air. Spreading in the contaminated atmosphere, it follows the terrain, flowing into pits and shelters. It is well adsorbed by activated carbon. Chemically very active. Chlorine is neutralized with an aqueous solution of hyposulfite. It is stored and transported in liquefied form under high pressure. In the event of accidents at production, storage, transportation and use facilities, mass injury to people is possible.

The mechanism of the damaging effect of chlorine on the cells of the respiratory system is associated with its high oxidative activity, the ability to form hydrochloric acid (a sharp change in the pH of the medium and denaturation of macromolecules) and hypochlorous acid when interacting with water. Hypochlorous acid forms chloramines in the cytosol of cells, which have a sufficiently high biological activity, can interact with unsaturated fatty acid bonds of phospholipids and form peroxides, block sulfhydryl groups of oligopeptides and proteins. Data have been obtained that in the reactions of hypochlorous acid with biomolecules, a superoxide radical is formed - the initiator of the process of free radical oxidation in cells.

The main manifestations of intoxication

In rare cases (with inhalation of extremely high concentrations), death can occur already at the first breaths of contaminated air. The cause of death is a reflex stop of breathing and cardiac activity. Another cause of rapid death of victims (within 20 - 30 minutes after inhalation of the substance) is lung burns. In these cases, the color of the skin of the victim acquires a greenish tint, clouding of the cornea is observed.

More often, in cases of severe poisoning, at the time of exposure, the victims felt a sharp burning sensation in the area of the eyes and upper respiratory tract, and shortness of breath. The poisoned person seeks to ease breathing by tearing the collar of his clothes. At the same time, extreme weakness is noted, the poisoned fall and are unable to leave the affected area. Almost from the beginning of exposure, a hysterical, painful cough appears, later shortness of breath joins, and additional respiratory muscles participate in breathing. The affected person tries to take a position that facilitates breathing. Speech is impossible. Sometimes there is vomiting.

Some time after leaving the affected area, some relief may occur (latent period), but more often (unlike phosgene damage), complete remission does not occur: coughing, pain along the trachea and in the diaphragm region persist.

After some time (from several hours to a day), the condition worsens again, coughing and shortness of breath increase (up to 40 respiratory acts per minute), the face becomes cyanotic (blue type of hypoxia), and in extremely severe cases, ashy color. Wheezing is heard over the lungs. The victim constantly expectorates a foamy yellowish or reddish liquid (more than 1 liter per day). Severe headaches are observed, body temperature drops. The pulse is slow. Blood pressure drops. The victim loses consciousness and dies with symptoms of acute respiratory failure. If pulmonary edema does not lead to death, then after a few hours (up to 48), the condition begins to improve. However, in the future, the disease gradually passes into the next period - complications, during which the phenomena of bronchopneumonia usually develop.

Pulmonary edema is the cause of the painful death of many patients. It occurs most often as a complication of dysregulation of the amount of fluid that must circulate in the lungs.

At this moment, there is an active influx of fluid from the capillaries into the pulmonary alveoli, which overflow with exudate and lose the ability to function and take in oxygen. The person stops breathing.

This is an acute pathological condition that threatens life, requiring extremely urgent care, immediate hospitalization. The main characteristics of the disease are characterized acute lack of air, severe suffocation and death of the patient when no resuscitation measures are provided.

At this moment, there is an active filling of the capillaries with blood and the rapid passage of fluid through the walls of the capillaries into the alveoli, where there is so much of it that it greatly complicates the supply of oxygen. IN respiratory organs, gas exchange is disturbed, tissue cells experience acute oxygen deficiency(hypoxia), the person suffocates. Often choking occurs at night during sleep.

Sometimes the attack lasts from 30 minutes to 3 hours, but often the excess accumulation of fluid in the extracellular tissue spaces increases at lightning speed, so resuscitation begins immediately to avoid death.

Classification, from what happens

The causes and types of pathology are closely related, divided into two basic groups.

Toxic pulmonary edema causes clinic first aid. Causes and consequences of pulmonary edema: this knowledge can save a life

1996 0

Doctors of various specialties, especially those working in multidisciplinary hospitals, constantly observe the symptom complex of acute respiratory failure, the development of which 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 involving large areas of the lung parenchyma, asthmatic status, pulmonary embolism, etc.), pulmonary edema is most often detected - a pathological process in which excess fluid accumulates in the interstitium of the lung tissue, and later in the alveoli themselves.

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 the left atrium (mitral valve disease, 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. 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 adult respiratory distress syndrome when inhaling fumes and toxic substances, inhalation of glucocorticoids in high 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 the metered-dose inhaler is completely empty, designed for 200-2 50 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, the patient's condition almost immediately improves in most cases, treatment of toxic edema is a rather difficult task due to the variety of pathogenetic mechanisms and the lack of effective methods (drugs) to prevent the development and stop the violation of the permeability of the alveolar-capillary membrane.

The most difficult to treat is toxic pulmonary edema, which develops in a patient with multiple organ failure of various nature (against the background of sepsis or peritonitis). All this 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

Pulmonary edema

A characteristic form of damage by pulmonotoxicants is pulmonary edema. The essence of the pathological condition is the release of blood plasma into the wall of the alveoli, and then into the lumen of the alveoli and the respiratory tract. Edematous fluid fills the lungs - a condition develops, previously referred to as "drowning on land."

Pulmonary edema is a manifestation of a violation of the water balance in the lung tissue (the ratio of the fluid content inside the vessels, in the interstitial space and inside the alveoli). Normally, blood flow to the lungs is balanced by its outflow through the venous and lymphatic vessels (the rate of lymphatic drainage is about 7 ml/hour).

The water balance of fluid in the lungs is provided by:

Regulation of pressure in the pulmonary circulation (normally 7-9 mm Hg; critical pressure - more than 30 mm Hg; blood flow rate - 2.1 l / min).

The barrier functions of the alveolar-capillary membrane, which separates the air in the alveoli from the blood flowing through the capillaries.

Pulmonary edema can occur as a result of a violation of both regulatory mechanisms, and each separately.

In this regard, there are three types of pulmonary edema:

- toxic pulmonary edema, developing as a result of a primary lesion of the alveolar-capillary membrane, against the background of normal, in the initial period, pressure in the pulmonary circulation;

- hemodynamic pulmonary edema, which is based on an increase in blood pressure in the pulmonary circulation, due to toxic damage to the myocardium and a violation of its contractility;

- mixed pulmonary edema when the victims have both a violation of the properties of the alveolar-capillary barrier and the myocardium.

The main toxicants causing the formation of pulmonary edema of various types are presented in Table 4.

The mechanism of damage to lung tissue cells by asphyxiating OVTV is not the same (see below), but the processes that develop after that are quite close.

Damage to cells and their death leads to an increase in the permeability of the barrier and disruption of the metabolism of biologically active substances in the lungs. The permeability of the capillary and alveolar parts of the barrier does not change simultaneously. Initially, the permeability of the endothelial layer increases, and the vascular fluid leaks into the interstitium, where it temporarily accumulates. This phase of development of pulmonary edema is called interstitial. During the interstitial phase, it is compensatory, about 10 times faster lymph flow. However, this adaptive reaction is insufficient, and the edematous fluid gradually penetrates through the layer of destructively altered alveolar cells into the cavities of the alveoli, filling them. This phase of the development of pulmonary edema is called alveolar and is characterized by the appearance of distinct clinical signs. “Switching off” part of the alveoli from the process of gas exchange is compensated by stretching of intact alveoli (emphysema), which leads to mechanical compression of the capillaries of the lungs and lymphatic vessels.

Cell damage is accompanied by the accumulation of biologically active substances such as norepinephrine, acetylcholine, serotonin, histamine, angiotensin I, prostaglandins E1, E2, F2, kinins in the lung tissue, which leads to an additional increase in the permeability of the alveolar-capillary barrier, impaired hemodynamics in the lungs. The rate of blood flow decreases, the pressure in the pulmonary circulation increases.

The edema continues to progress, fluid fills the respiratory and terminal bronchioles, and due to the turbulent movement of air in the airways, foam is formed, stabilized by the washed-out alveolar surfactant. In addition to these changes, for the development of pulmonary edema, systemic disorders are of great importance, which are included in the pathological process and intensify as it develops. Among the most important are: violations of the gas composition of the blood (hypoxia, hyper- and then hypocarbia), changes in the cellular composition and rheological properties (viscosity, clotting ability) of the blood, hemodynamic disorders in the systemic circulation, impaired renal function and central nervous system.

Characteristics of hypoxia

The main cause of disorders of many functions of the body in case of poisoning with pulmonotoxicants is oxygen starvation. So, against the background of developing toxic pulmonary edema, the oxygen content in arterial blood decreases to 12 vol.% or less, at a rate of 18-20 vol.%, venous - up to 5-7 vol.%, at a rate of 12-13 vol.%. The CO2 tension in the first hours of the development of the process increases (more than 40 mm Hg). In the future, as the pathology develops, hypercapnia is replaced by hypocarbia. The occurrence of hypocarbia can be explained by a violation of metabolic processes under hypoxic conditions, a decrease in CO2 production and the ability of carbon dioxide to easily diffuse through the edematous fluid. The content of organic acids in the blood plasma at the same time increases to 24-30 mmol/l (at a rate of 10-14 mmol/l).

Already in the early stages of the development of toxic pulmonary edema, the excitability of the vagus nerve increases. This leads to the fact that a smaller, compared to normal, stretching of the alveoli during inhalation serves as a signal to stop inhalation and start exhalation (Hering-Breuer reflex). At the same time, breathing becomes more frequent, but its depth decreases, which leads to a decrease in alveolar ventilation. The release of carbon dioxide from the body and the supply of oxygen to the blood are reduced - hypoxemia occurs.

A decrease in the partial pressure of oxygen and a slight increase in the partial pressure of CO2 in the blood leads to a further increase in dyspnea (a reaction from the vascular reflex zones), but, despite its compensatory nature, hypoxemia not only does not decrease, but, on the contrary, increases. The reason for the phenomenon is that although in conditions of reflex shortness of breath the minute volume of breathing is preserved (9000 ml), alveolar ventilation is reduced.

So, under normal conditions, at a respiratory rate of 18 per minute, alveolar ventilation is 6300 ml. Tidal volume (9000 ml: 18) - 500 ml. Dead space volume - 150 ml. Alveolar ventilation: 350 ml x 18 = 6300 ml. With an increase in breathing to 45 and the same minute volume (9000), the tidal volume decreases to 200 ml (9000 ml: 45). Only 50 ml of air (200 ml -150 ml) enters the alveoli with each breath. Alveolar ventilation per minute is: 50 ml x 45 = 2250 ml, i.e. decreases by about 3 times.

With the development of pulmonary edema, oxygen deficiency increases. This is facilitated by an ever-increasing violation of gas exchange (difficulty in the diffusion of oxygen through an increasing layer of edematous fluid), and in severe cases - a hemodynamic disorder (up to collapse). Developing metabolic disorders (decrease in the partial pressure of CO2, acidosis, due to the accumulation of incompletely oxidized metabolic products) impair the process of oxygen utilization by tissues.

Thus, the oxygen starvation that develops when affected by asphyxiating substances can be characterized as a mixed type of hypoxia: hypoxic (impaired external respiration), circulatory (disturbance of hemodynamics), tissue (disturbance of tissue respiration).

Violation of the composition of peripheral blood

Significant changes in pulmonary edema are observed in peripheral blood. As edema increases and vascular fluid enters the extravascular space, the content of hemoglobin increases (at the height of edema, it reaches 200–230 g/l) and erythrocytes (up to 7–9.1012/l), which can be explained not only by thickening of the blood, but also by the release of formed elements from the depot (one of the compensatory reactions to hypoxia). The number of leukocytes increases (9-11.109/l). Significantly accelerated blood clotting time (30-60 s instead of 150 s under normal conditions). This leads to the fact that the affected have a tendency to thrombosis, and in case of severe poisoning, intravital blood clotting is observed.

Hypoxemia and thickening of the blood exacerbate hemodynamic disturbances.

Violation of the activity of the cardiovascular system

The cardiovascular system, along with the respiratory system, undergoes the most severe changes. Already in the early period develops bradycardia (excitation of the vagus nerve). As hypoxemia and hypercapnia increase, tachycardia develops and the tone of peripheral vessels increases (compensation reaction). However, with a further increase in hypoxia and acidosis, the contractility of the myocardium decreases, the capillaries expand, and blood is deposited in them. Blood pressure drops. At the same time, the permeability of the vascular wall increases, which leads to tissue edema.

Violation of the nervous system

The role of the nervous system in the development of toxic pulmonary edema is very significant.

The direct effect of toxic substances on the receptors of the respiratory tract and lung parenchyma, on the chemoreceptors of the pulmonary circulation can be the cause of the neuro-reflex impairment of the permeability of the alveolar-capillary barrier. The dynamics of the development of pulmonary edema is somewhat different when affected by various substances of asphyxiating action. Substances with a pronounced irritant effect (chlorine, chloropicrin, etc.) cause a more rapidly developing process than substances that practically do not cause irritation (phosgene, diphosgene, etc.). Some researchers refer to substances of "fast action" mainly those that damage mainly the alveolar epithelium, "slow action" - affecting the endothelium of the capillaries of the lungs.

Usually (with phosgene intoxication), pulmonary edema reaches a maximum 16 to 20 hours after exposure. It stays at this level for a day or two. At the height of the edema, the death of the affected is observed. If death does not occur in this period, then from 3 to 4 days the reverse development of the process begins (liquid resorption by the lymphatic system, increased outflow with venous blood), and on days 5 to 7 the alveoli are completely freed from fluid. Mortality in this formidable pathological condition is usually 5-10%, and about 80% of the total number of deaths die in the first 3 days.

Complications of pulmonary edema are bacterial pneumonia, the formation of pulmonary infiltrate, thromboembolism of the main vessels.

Hydrostatic (or cardiac) pulmonary edema
It happens during diseases that are characterized by an increase in pressure (hydrostatic) inside the capillaries and further penetration of plasma from them into the pulmonary alveoli. The reasons for this form are: vascular defects, heart; myocardial infarction; acute insufficiency of the left ventricle,; stagnation of blood in hypertension, cardiosclerosis; with the presence of difficulty in heart contractions; emphysema, bronchial asthma.
Non-cardiogenic pulmonary edema, which includes:
iatrogenic	Occurs: at an increased rate of drip injection into a vein of large volumes of saline or plasma without actively forcing urine output; with a low amount of protein in the blood, which is often detected with cirrhosis of the liver, nephrotic kidney syndrome; during a period of prolonged rise in temperature to high numbers; during fasting; with eclampsia of pregnant women (toxicosis of the second half).
Allergic, toxic (membranous)	It is provoked by the action of poisons, toxins that violate the permeability of the walls of the alveoli, when liquid penetrates into them instead of air, filling almost the entire volume. Causes of toxic pulmonary edema in humans: inhalation of toxic substances - glue, gasoline; an overdose of heroin, methadone, cocaine; poisoning with alcohol, arsenic, barbiturates; drug overdose (Fentanyl, Apressin); penetration into the cells of the body of nitric oxide, heavy metals, poisons; extensive deep burns of lung tissue, uremia, diabetic coma, hepatic food allergy, medicinal; radiation damage to the sternum; poisoning with acetylsalicylic acid with prolonged use of aspirin in large doses (more often in adulthood); metal carbonate poisoning. Often passes without characteristic signs. The picture becomes clear only when X-rays are taken.
Infectious	Develops: when an infection enters the bloodstream, causing pneumonia, sepsis; in chronic diseases of the respiratory organs - emphysema, bronchial asthma, (clotting of an artery with a clot of platelets - an embolus).
aspiration	Occurs when a foreign body enters the lungs, the contents of the stomach.
Traumatic	Occurs with penetrating chest trauma.
Cancer	Occurs due to a malfunction of the functions of the pulmonary lymphatic system with difficulty in the outflow of lymph.
neurogenic	Main reasons: intracranial hemorrhage; intense convulsions; accumulation of exudate in the alveoli after brain surgery.

Any asthma attack that occurs with such diseases is the basis for suspecting a state of acute swelling of the respiratory system.

Under these conditions alveoli become very thin, their permeability increases, integrity is broken, increases the risk of filling them with liquid.

At-risk groups

Since the pathogenesis (development) of pathology closely associated with comorbid internal diseases, at risk are patients with diseases or factors provoking such a life-threatening condition.

The risk group includes patients suffering from:

disorders of the vascular system, heart;
damage to the heart muscle with hypertension;
, respiratory systems;
complex craniocerebral injuries, cerebral hemorrhages of various origins;
meningitis, encephalitis;
cancerous and benign neoplasms in brain tissues.
pneumonia, emphysema, bronchial asthma;
and increased blood viscosity; there is a high probability of separation of a floating (floating) clot from the wall of the artery with penetration into the pulmonary artery, which is blocked by a thrombus, which causes thromboembolism.

Doctors have found that athletes who actively practice excessive exercise have a serious chance of getting respiratory edema. These are scuba divers, climbers working at high altitudes (more than 3 km), marathon runners, divers, swimmers for long distances. For women, the risk of the disease is higher than for men.

Climbers have such a dangerous condition happens during rapid ascent to high altitude without pausing at intermediate levels.

Symptoms: how it manifests itself and develops in stages

Classification and symptoms are related to the severity of the disease.

Severity	Severity of symptoms
1 - on the border of development	Revealed: mild shortness of breath; violation of the heart rate; often there is bronchospasm (a sharp narrowing of the walls of the bronchi, which causes difficulties with the flow of oxygen); anxiety; whistling, individual wheezing; dry skin.
2 - medium	Observed: wheezing that can be heard at a short distance; severe shortness of breath, in which the patient is forced to sit, leaning forward, leaning on outstretched arms; throwing, signs of neurological stress; perspiration appears on the forehead; severe pallor, cyanosis in the lips, fingers.
3 - heavy	Explicit symptoms: bubbling, seething rales are heard; there is a pronounced inspiratory dyspnea with a difficult breath; dry paroxysmal cough; the ability to only sit (because the cough increases in the supine position); constricting pressure pain in the chest caused by oxygen deficiency; the skin on the chest is covered with profuse sweat; pulse at rest reaches 200 beats per minute; intense anxiety, fear.
4 degree - critical	The classic manifestation of a critical condition: severe shortness of breath; cough with copious pink frothy sputum; severe weakness; far audible coarse bubbling rales; painful attacks of suffocation; swollen neck veins; bluish, cold extremities; fear of death; profuse sweat on the skin of the abdomen, chest, loss of consciousness, coma.

First aid first aid: what to do if it occurs

Before the arrival of the ambulance, relatives, friends, colleagues don't waste a minute of time. To alleviate the patient's condition, do the following:

Helping a person to sit up or half rise with their legs down
If possible, they are treated with diuretics (they give diuretics - lasix, furosemide) - this removes excess fluid from the tissues, however, at low pressure, small doses of drugs are used.
Organize the possibility of maximum access of oxygen to the room.
The foam is sucked off and, if skillful, oxygen inhalations are performed through a solution of ethyl alcohol (96% of a couple - for adults, 30% alcohol vapor - for children).
Prepare a hot foot bath.
With skill - apply the imposition of tourniquets on the limbs, not too tightly pinching the veins in the upper third of the thigh. Leave tourniquets longer than 20 minutes, while the pulse should not be interrupted below the application sites. This reduces blood flow to the right atrium and prevents tension in the arteries. When the tourniquets are removed, it is done carefully, slowly loosening them.
Continuously monitor the patient's breathing and pulse rate.
For pain, give analgesics, if there is - promedol.
With high blood pressure, benzohexonium, pentamine are used, which promote the outflow of blood from the alveoli, nitroglycerin, which dilates blood vessels (with regular measurement of pressure).
In normal - small doses of nitroglycerin under the control of pressure indicators.
If the pressure is below 100/50 - dobutamine, dopmin, which increase the function of myocardial contraction.

What is dangerous, the forecast

Pulmonary edema is a direct threat to life. Without taking extremely urgent measures, which should be carried out by the patient's relatives, without subsequent urgent active therapy in a hospital, pulmonary edema is the cause of death in 100% of cases. A person is waiting for suffocation, coma, death.

Attention! When the very first signs of an acute pathological situation appear, it is important to provide qualified assistance on the basis of a hospital as soon as possible, so an ambulance is called immediately.

Preventive measures

To prevent a threat to health and life, the following measures are necessarily assumed, meaning elimination of factors contributing to this condition:

In case of heart diseases (angina pectoris, chronic insufficiency), they take funds for their treatment and at the same time - hypertension.
With repeated edema of the respiratory organs, the procedure of isolated blood ultrafiltration is used.
Prompt accurate diagnosis.
Timely adequate treatment of asthma, atherosclerosis, and other internal disorders that can cause such pulmonary pathology.
Isolation of the patient from contact with any kind of toxins.
Normal (not excessive) physical and respiratory stress.

Complications

Even if the hospital promptly and successfully managed to prevent suffocation and death of a person, therapy continues. After such a critical condition for the whole organism in patients often develop serious complications, most often in the form of constantly recurring pneumonia, difficult to treat.

Prolonged oxygen starvation has a negative effect on almost all organs. The most serious consequences are cerebrovascular accidents, heart failure, cardiosclerosis, ischemic organ damage. These diseases are a constant threat to life and can not do without intensive drug therapy.

These complications, despite the stopped acute pulmonary edema, are the cause of the death of a large number of people.

The greatest danger of this pathology is its speed and panic state. into which the patient and the people around him fall.

Knowledge of the basic signs of the development of pulmonary edema, the causes, diseases and factors that can provoke it, as well as emergency measures before the ambulance arrives, can lead to a favorable outcome and no consequences even with such a serious threat to life.