Toxic pulmonary edema blue hypoxemia. Toxic pulmonary edema: causes of development. Urgent medical care for pulmonary edema

This is the most severe form toxic damage lungs.

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

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

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

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

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

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

In addition to the two main ones, there is another form of acute toxic pulmonary edema - the so-called “ silent swelling", which is detected only by X-ray examination of the lungs, while 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 symptoms of irritation of the mucous membranes respiratory tract: slight cough, sore throat, chest pain. As a rule, these mild subjective disorders do not have a significant impact on the well-being of the victim and soon pass.

The latent period begins after the irritation subsides and can have varying durations (from 2 to 24 hours), usually 6-12 hours. During this period, the victim feels healthy, but upon careful examination, the first symptoms of increasing oxygen deficiency can be noted: shortness of breath, cyanosis , 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 lung tissue, so the absence is clear clinical manifestations does not yet indicate the absence of emerging pathology.

The period of increasing edema manifests itself clinically, which is associated with the accumulation of edematous fluid in the alveoli and a more pronounced impairment of respiratory function. Victims experience increased breathing, it becomes shallow and is accompanied by paroxysmal, painful coughing. Objectively, slight cyanosis is noted. In the lungs, ringing, fine, moist rales and crepitus are heard. During X-ray examination in this period, one can note vagueness and blurriness of the pulmonary pattern, small branches are poorly differentiated blood vessels, there is some thickening of the interlobar pleura. The roots of the lungs are somewhat expanded and have unclear contours.

Identifying signs of increasing toxic pulmonary edema is very important for carrying out appropriate treatment and preventive measures to prevent the development of edema.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

With the “gray” type of toxic edema, the clinical picture is more severe due to the addition of pronounced vascular disorders. The patient is usually lethargic, adynamic, and does not answer questions well. The skin becomes pale gray in color. The face is covered with cold sweat. Extremities are cold to the touch. The pulse becomes frequent and small. There is a drop in blood pressure. The gas composition of the blood in these cases is characterized by a decrease in carbon dioxide (hypoxemia with hypocapnia).

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

Treatment of acute intoxications.

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

If the upper respiratory tract is affected, rinsing or warm-moist inhalations with a 2% solution of sodium bicarbonate, mineral waters or infusions of medicinal herbs are prescribed. The administration of antitussives is indicated.

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

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

Anti-inflammatory drugs are prescribed to prevent infection. Patients with manifestations of bronchobronchiolitis require inpatient treatment. Shown bed rest, intermittent oxygen therapy. The treatment complex includes bronchodilators (teopec, berotec, atrovent, aminophylline, etc.) in combination with secretolytics and expectorants (bromhexine, lasolvon, etc.), and antihistamines. IN early dates active antibiotic therapy is prescribed.

Treatment of toxic pulmonary edema requires the greatest attention. Even if toxic edema is suspected, it is necessary to give the patient complete rest. Transportation to 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 clinical manifestations of edema, 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, inhalations of antifomsilan in a 10% alcohol solution can be used repeatedly for 10-15 minutes.

To dehydrate the lung tissue, saluretics are prescribed: Lasix or 30% urea solution intravenously.

In the early stages, corticosteroid drugs are used intravenously up to 150 ml in terms of prednisolone per day and antibiotics wide range actions.

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

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

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

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

In the case of severe pulmonary edema, intensive therapy methods are used - intubation with secretion suction, mechanical ventilation; hemosorption and plasmaphoresis are used for detoxification.

Treatment of patients with toxic edema most effective when these patients are admitted to poison control centers or intensive care units.

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

Toxic pulmonary edema can develop as a result of inhalation of certain aggressive substances, such as nitric oxide, ozone, ammonia, chlorine, etc. It can be caused by certain infectious lesions, for example, pneumonia, leptospirosis and meningococcemia, as well as endotoxicosis, for example, sepsis, peritonitis, pancreatitis, etc. In some cases similar condition provoked by severe allergic diseases or poisoning.
Toxic pulmonary edema is characterized by a number of intense clinical manifestations, especially severe course and often a 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 likelihood of further pulmonary edema at this stage. After half an hour or an hour, the unpleasant symptoms completely disappear, and a period of hidden well-being may begin. But the progression of pathological processes leads to the gradual appearance of negative symptoms.

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

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

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

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

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

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

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

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

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

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

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

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

Additional Information

Patients who have suffered toxic pulmonary edema may benefit from different means based on herbs and improvised means. They can be used for health purposes and only after consulting a doctor.

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

The feasibility of using funds traditional medicine follows in mandatory discuss with your doctor.

Poisoning with poisons is always unpleasant, but among all possible complications toxic pulmonary edema is one of the most dangerous. In addition to a high chance of death, this damage to the respiratory system has many serious consequences. It most often takes at least a year to achieve full recovery from illness.

How does pulmonary edema form?

Pulmonary edema begins in the same way as similar damage to other organs. The difference is that the liquid penetrates freely through the easily permeable tissue of the alveoli.

Accordingly, swelling of the lung, the same as, for example, with edema lower limbs, not happening. Instead, fluid begins to accumulate in the inner cavity of the alveoli, which normally serves to fill with air. As a result, the person gradually suffocates, and oxygen starvation causes serious damage to the kidneys, liver, heart and brain.

The peculiarity of toxic pulmonary edema is that the cause of this disease, instead of the disease, is poison. Toxic substances destroy organ cells, contributing to the filling of the alveoli with fluid. It can be:

carbon monoxide;
chlorine;
and diphosgene;
oxidized nitrogen;
hydrogen fluoride;
ammonia;
vapors of concentrated acids.

That's it for the list possible reasons toxic pulmonary edema is not limited. Most often, people with this diagnosis end up in the hospital due to non-compliance with safety precautions, as well as in the event of accidents at work.

Symptoms and stages of the disease

Depending on how the disease progresses, there are three types of edema:

Developed (completed) form. In this case, the disease goes through 5 stages: reflex, latent, period of increasing swelling, completion and reverse development.
Abortive form. It is distinguished by the absence of the most difficult stage of completion.
“Silent” edema is a hidden, asymptomatic type of the disease. It can only be determined by chance using an x-ray examination.

After inhaling the poison, the body becomes intoxicated, and the initial period of disease development begins—the reflex stage. It lasts from ten minutes to several hours. At this time, classic symptoms of mucous irritation and poisoning appear:

cough and sore throat;
pain in the eyes and lacrimation due to contact with toxic gases;
appearance heavy discharge nasal mucosa.

Also, the reflex stage is characterized by the appearance of chest pain and difficulty breathing, weakness and dizziness occur. In some cases, they are accompanied by disturbances in the digestive system.

Next comes the hidden period. At this time, the symptoms listed above disappear, the person feels much better, but upon examination, the doctor may note bradycardia, rapid shallow breathing and a drop in blood pressure. This condition lasts from 2 to 24 hours, and the longer it is, the better for the patient.

In severe intoxication, the latent period of pulmonary edema may be completely absent.

When the calm is over, a rapid increase in symptoms begins. Appears paroxysmal cough, breathing becomes very difficult and the person suffers from shortness of breath. Cyanosis, tachycardia and hypotension develop, even greater weakness sets in, and pain in the head and chest intensifies. This stage of toxic pulmonary edema is called the growth period; from the outside it is easy to recognize due to the wheezing that occurs when the patient breathes. At that time chest cavity gradually fill with foamy sputum and blood.

The next period is the end of the swelling. It is characterized by the maximum manifestation of the symptoms of the disease and has 2 forms:

"Blue" hypoxemia. Due to suffocation, a person rushes about and tries to breathe harder. He is very excited, moans, and his consciousness is clouded. The body reacts to swelling by turning blue, pulsating blood vessels, and secreting pinkish foam from the mouth and nose.
"Gray" hypoxemia. It is considered more dangerous for the patient. Because of sharp deterioration the activity of the cardiovascular and respiratory systems collapses. The breathing and heart rate noticeably decrease, the body becomes colder, and the skin takes on an earthy tint.

If a person was able to survive toxic pulmonary edema, then the last stage begins - reverse development: gradually cough, shortness of breath and sputum production recede. A long rehabilitation period begins.

Consequences of pulmonary edema

Despite the fact that the disease itself often ends in the death of the patient within 2 days, it can also occur with complications. Among them, the consequences of a toxic lung burn can be:

Airway obstruction. It occurs when excessive foam is produced and greatly impairs gas exchange.
Respiratory depression. When intoxicated, some poisons can additionally affect the respiratory center of the brain, negatively affecting the functioning of the lungs.
Cardiogenic shock. Due to edema, failure of the left ventricle of the heart develops, as a result of which blood pressure drops significantly and disrupts the blood supply to all organs, including the brain. In 9 out of 10 cases cardiogenic shock ends in death.
Fulminant form of pulmonary edema. This complication lies in the fact that all stages of the disease are compressed in time to a few minutes due to concomitant diseases of the liver, kidneys and heart. It is almost impossible to save the patient.

Even if a person managed to survive the complication, it is far from certain that everything will end in a complete recovery. The disease may return in the form of secondary pulmonary edema.

In addition, due to the weakening of the body as a result of the stress suffered, other consequences may appear. Most often they are expressed through the development of other diseases:

Pneumosclerosis. Damaged alveoli become overgrown and scarred, losing their elasticity. If thus affected Not a large number of However, the consequences are almost invisible. But with the widespread spread of the disease, the gas exchange process greatly deteriorates.
Bacterial pneumonia. When bacteria enter weakened lung tissue, microorganisms begin to actively develop, causing inflammation. Its symptoms are fever, weakness, shortness of breath, cough with expectoration of blood and purulent sputum.
Emphysema. This disease develops due to the expansion of the tips of the bronchioles, causing additional damage to the walls of the alveoli. A person's chest swells and makes a boxy sound when tapped. Another characteristic symptom- shortness of breath.

In addition to these diseases, pulmonary edema can provoke an exacerbation of other chronic ailments, including tuberculosis. Also, against the backdrop of deteriorating oxygen supply to tissues, the cardiovascular and central systems suffer greatly. nervous system, liver and kidneys.

Diagnosis and treatment

After intoxication, the development of the disease is determined by physical examination and radiography. These 2 diagnostic methods provide enough information for treatment, but in the final stages you cannot do without an ECG to monitor the condition of the heart.

If pulmonary edema has been controlled, then they give up lab tests blood (general and biochemical) and urine, liver tests. This is necessary to determine the damage caused to the body and prescribe treatment.

First aid for toxic pulmonary edema is to ensure rest and sedative injections. To restore breathing, oxygen inhalations are performed through alcohol solution to extinguish foam. To reduce swelling, you can apply tourniquets to the limbs and use the bloodletting method.

For treatment, doctors resort to the following set of medications:

Steroids;
Diuretics;
Bronchodilators;
Glucose;
Calcium chloride;
Cardiotonics.

As edema progresses, tracheal intubation and connection to a device may also be required. artificial respiration. After relief of symptoms, it is important to take a course of antibiotics to prevent bacterial infection. On average, rehabilitation after an illness takes about 1-1.5 months, and the chance of becoming disabled is very high.

A characteristic form of damage from pulmonary toxicants is pulmonary edema. The essence pathological condition- release of blood plasma into the wall of the alveoli, and then into the lumen of the alveoli and respiratory tract.

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

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

? regulation of pressure in the pulmonary circulation (normally 7-9 mm Hg; critical pressure - more than 30 mm Hg; blood flow speed - 2.1 l/min);
? barrier functions of the alveolar-capillary membrane, which separates the air located in the alveoli from the blood flowing through the capillaries.

Pulmonary edema can occur as a result of a violation of both regulatory mechanisms or each one separately. In this regard, there are three types of pulmonary edema:

Toxic (Fig. 5.1) - develops as a result of primary damage to the alveolar-capillary membrane, against the background normal pressure in the pulmonary circulation (in the initial period);

Rice. 5.1.

? hemodynamic - it 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 - in victims there is a violation of the properties of both the alveolar-capillary barrier and the myocardium.

Actually, toxic pulmonary edema is associated with damage by toxicants to cells involved in the formation of the alveolar-capillary barrier. The mechanisms of damage to lung tissue cells by asphyxiating agents are different, but the processes that develop after this are quite similar.

Cell damage and death leads to increased barrier permeability and biological metabolic disorders active substances in the lungs. The permeability of the capillary and alveolar parts of the barrier does not change simultaneously. First, the permeability of the endothelial layer increases, vascular fluid sweats into the interstitium, where it temporarily accumulates. This phase of the development of pulmonary edema is called interstitial, during which lymphatic drainage is compensatory, approximately 10 times accelerated. However, this adaptive reaction turns out to be insufficient, and the edematous fluid gradually penetrates through the layer of destructively altered alveolar cells into the cavities of the alveoli, filling them. The considered 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 gas exchange process 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 in the lung tissue (norepinephrine, acetylcholine, serotonin, histamine, angiotensin I, prostaglandins Ej, E 2 , F 2, kinins), which leads to an additional increase in the permeability of the alveolar-capillary barrier, impaired hemodynamics in lungs. The speed 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 turbulent air movement in the respiratory tract, foam is formed, stabilized by washed away alveolar surfactant. Experiments on laboratory animals show that the content of surfactant in lung tissue decreases immediately after exposure to toxicants. This explains early development peripheral atelectasis in those affected.

Diagnostics The defeat of the suffocating effect during the development of pulmonary edema is based on the uncharacteristic symptoms of this condition: pulmonary edema, which developed as a result of cardiac failure. Anamnesis and chemical reconnaissance data help to make a correct diagnosis.

Objective signs of pulmonary edema: characteristic odor from clothes, pallor of the skin and mucous membranes or their cyanosis, increased breathing and pulse with minor physical effort, often aversion to tobacco smoke(smoking), phenomena of irritation of the mucous membrane of the eyelids, nasopharynx, larynx (if affected by chloropicrin). Only the simultaneous presence of several signs can serve as a basis for diagnosing a lesion.

The most difficult cases for diagnosis are those when there are only complaints about the lesion, and there are no objective, sufficiently convincing symptoms. Such affected people must be monitored during the first 24 hours, since even with severe damage in the first time after exposure to chemical agents, almost no signs are often detected.

Severe injuries from asphyxiating agents are characterized by the development of toxic pulmonary edema in the coming hours and days after exposure. In case of mustard gas intoxication, toxic pulmonary edema practically does not occur; with inhalation lesions of lewisite, pulmonary edema may develop, which is accompanied by a pronounced hemorrhagic component (acute serous-hemorrhagic pneumonia).

Depending on the physical and chemical properties OS clinical picture of the lesion has significant differences. Thus, in the case of damage by phosgene and diphosgene, the irritant effect at the time of contact with the poison is insignificant, the presence of a latent period and the development of toxic pulmonary edema in cases of moderate and severe damage are characteristic. When affected by poisons that have a pronounced irritating and cauterizing effect, lacrimation, rhinorrhea, cough develop immediately at the moment of contact with the agent, and laryngo-bronchospasm is possible. The latent period when affected by these agents is masked by the clinical picture chemical burn respiratory tract. Toxic pulmonary edema develops in 12-20% of people with severe disease.

IN clinical picture intoxication with asphyxiating poisons are isolated following periods: reflex, hidden phenomena (imaginary well-being), development of the main symptoms of the disease (pulmonary edema), resolution of edema, long-term consequences.

Reflex period equal to the time of contact with the poison. When affected by phosgene, more often at the moment of contact, a feeling of tightness in the chest, shallow rapid breathing, cough, and nausea develop. In some cases, the victim’s contact with poison can only be detected by the initial sensation of the smell of an agent (rotten apples or rotten hay), which then becomes dull.

Period of hidden phenomena (imaginary well-being). Its duration varies from 1 to 24 hours and indicates the body’s ability to resist intoxication. During this period, the main disorders are formed: the shorter the latent period, the more severe the intoxication. At latent period within 1-3 hours severe lesions develop; from 3-5 to 12 hours - lesions medium degree; 12-24 hours - mild degree. In the latent period, those affected usually feel healthy, although various vague complaints of weakness and headache may be observed. One of the most important diagnostic signs development of pulmonary edema in the latent period is an increase in breathing in relation to the pulse, and its slight decrease is determined. Normally, the ratio of respiratory rate to pulse rate is 1:4, with damage it is 1: 3-1:2. This happens by next reason: Active inhalation continues until sufficient stretching occurs. maximum amount alveoli, then the receptors are irritated, a signal is triggered to stop inhalation, and passive exhalation occurs. Initially, shortness of breath develops as a result of increased excitability vagus nerve under the influence of a toxic agent. Subsequently, due to shallow breathing, the carbon dioxide content in the blood increases, hypercapnia, in turn, stimulates breathing, which increases shortness of breath.

Period of development of the main symptoms of the disease characterized primarily by deepening hypoxia. Reflex hypoxia turns into respiratory “blue”, subsequently the oxygen content in the blood decreases, hypercapnia and blood thickening increase. In the “blue” form of hypoxia, metabolic processes are disrupted, under-oxidized metabolic products (lactic, acetoacetic, γ-hydroxybutyric acid, acetone) accumulate in the blood, and the blood pH decreases to 7.2. Skin and visible mucous membranes due to stagnation in the peripheral venous system acquire a blue-purple color, the face is puffy. Shortness of breath intensifies, a large number of moist rales are heard in the lungs, the affected OB takes on a semi-sitting position. Blood pressure is slightly elevated or within normal limits, pulse is normal or moderately rapid. Heart sounds are muffled, the boundaries are expanded to the left and right. Sometimes enteritis and an increase in the size of the liver and spleen are observed. The amount of urine excreted decreases, and in some cases complete anuria occurs. Consciousness is preserved, and sometimes signs of excitation are noted.

Blood thickening, increased viscosity, hypoxia, increased stress on cardiovascular system complicate the functioning of the circulatory apparatus and contribute to the development of circulatory hypoxia, respiratory-circulatory (“gray”) hypoxia develops. An increase in blood clotting creates conditions for the occurrence of thromboembolic complications. Changes in blood gas composition intensify, hypoxemia increases, and hypocapnia occurs. As a result of a drop in carbon dioxide levels in the blood, depression of the respiratory and vasomotor centers develops. Those affected by phosgene are often in unconscious. The skin is pale, blue-gray, facial features are pointed. Sudden shortness of breath, shallow breathing. The pulse is thread-like, very frequent, arrhythmic, and weak in filling. Blood pressure dropped sharply. Body temperature decreases.

Having reached a maximum by the end of the first day, the symptoms of pulmonary edema remain at the height of the process for two days. This period accounts for 70-80% deaths from phosgene damage.

Period of swelling resolution. With a relatively successful process, on the 3rd day, as a rule, the condition of the patient affected by phosgene improves, and over the next 4-6 days, pulmonary edema resolves. The absence of positive dynamics of the disease on days 3-5 and a rise in body temperature may indicate the development of pneumonia. It is by joining bacterial pneumonia causes the second peak of mortality, recorded on the 9-10th day.

When affected by suffocating poisons with a pronounced irritating effect for poisoning mild degree The development of toxic tracheitis, bronchitis, and tracheobronchitis is typical. In case of defeat medium degree Toxic tracheobronchitis and toxic pneumonia with respiratory failure of I-II degrees develop. In case of defeat severe- toxic bronchitis, toxic pneumonia with respiratory failure P-III degrees, in 12-20% of cases toxic pulmonary edema develops.

Sanitary losses due to suffocating agent damage are distributed as follows: severe damage - 40%, moderate - 30%, mild - 30%.