To date, the problem of toxic pulmonary edema is not sufficiently covered; therefore, many issues of its diagnosis and treatment are little known to a wide range of doctors. Many doctors of different profiles, especially those working in multidisciplinary hospitals, very often deal with the symptom complex of acute respiratory failure.

This complex clinical situation poses a serious danger to the life of the patient. A lethal outcome can occur in a short time from the moment of occurrence, it directly depends on the correctness and timeliness of medical care provided by a doctor. Among the many causes of acute respiratory failure (atelectasis and collapse of the lung, massive pleural effusion and pneumonia involving large areas of the lung parenchyma, status asthmaticus, pulmonary embolism, etc.), doctors most often detect pulmonary edema - a pathological process in which the interstitial lung tissue, and later in the alveoli themselves, fluid accumulates in excess.

Toxic pulmonary edema is associated with damage, and in connection with this, an increase in the permeability of the alveolar-capillary membrane (in the literature, toxic pulmonary edema is referred to by the terms "shock lung", "non-coronary pulmonary edema", "adult respiratory distress syndrome or ARDS".

The main conditions leading to the development of toxic pulmonary edema are:

1) inhalation of toxic gases and fumes (nitric oxide, ozone, phosgene, cadmium oxide, ammonia, chlorine, fluoride, hydrogen chloride, etc.);

2) endotoxicosis (sepsis, peritonitis, pancreatitis, etc.);

3) infectious diseases (leptospirosis, meningococcemia, pneumonia.);

4) severe allergic reactions;

5) heroin poisoning.

Toxic pulmonary edema is characterized by a high intensity of clinical manifestations, a severe course and a serious prognosis.

The causes of toxic pulmonary edema during the period of hostilities can be extremely diverse. Most often it will occur during the destruction of chemical industries. It is also possible to develop it when inhaling toxic vapors of technical fluids in case of severe poisoning with various chemicals.

Diagnosis of toxic pulmonary edema should be based on a comparison of anamnesis data with the results of a comprehensive objective medical examination. First of all, it is necessary to establish whether the patient had contact with 0V or with other chemical agents and assess the initial manifestations of the lesion.

The clinic for the development of toxic pulmonary edema can be divided into 4 stages or periods:

one). The initial reflex stage.

2). Stage of hidden phenomena.

3). The stage of development of pulmonary edema.

four). Stage of outcomes and complications (reverse development).

one). It is known that after exposure to 0V asphyxiation or other irritating gases, a slight cough, a feeling of tightness in the chest, general weakness, headache, rapid shallow breathing with a distinct slowing of the pulse are noted. At high concentrations, suffocation and cyanosis appear due to reflex laryngo- and bronchospasm. The intensity of these symptoms may vary depending on the concentration of 0V and the state of the body. It is practically difficult to determine in advance whether poisoning will be limited to direct exposure reactions or whether pulmonary edema will develop in the future. Hence the need arises for the immediate evacuation of those affected by irritating gases to the emergency room or hospital, even in cases where the initial signs of poisoning seem harmless.

2). After 30-60 minutes, the unpleasant subjective sensations of the initial period disappear and the so-called hidden period, or period of imaginary well-being. The shorter it is, the more severe the clinical course of the disease is usually. The duration of this stage is on average 4 hours, but can vary from 1-2 to 12-24 hours. It is characteristic that in the latent period, a thorough examination of the affected allows them to reveal a number of symptoms of an increase in oxygen starvation: moderate emphysema, shortness of breath, cyanosis of the extremities, pulse lability. Poisonous substances that have a tropism for lipids (nitric oxides, ozone, phosgene, cadmium oxide, monochloromethane, etc.) are deposited mainly in the alveoli, dissolving in the surfactant and diffuse through thin alveolar cells (pneumocytes) to the endothelium of the pulmonary capillaries, damaging them. The capillary wall responds to chemical damage with increased permeability with the release of plasma and blood cells into the interstitium, which leads to a significant (several times) thickening of the alveolar-capillary membrane. As a result, the "diffuse path" of oxygen and carbon dioxide increases significantly (stage interstitial pulmonary edema)

3). As the pathological process progresses, dilatation of the pulmonary vessels increases, lymph drainage disorders through the septal and prevascular lymphatic slits, the edematous fluid begins to penetrate into the alveoli (alveolar stage of toxic edema). The resulting edematous foam fills and clogs the bronchioles and bronchi, which further impairs lung function. This determines the clinic of severe respiratory failure up to the onset of death (the lungs are buried in edematous fluid).

The initial signs of the development of pulmonary edema are general weakness, headache, weakness, tightness and heaviness in the chest, slight shortness of breath, dry cough (cough), increased breathing and heart rate. On the part of the lungs: omission of the borders, percussion sound acquires a tympanic tinge, X-ray determined heaviness and emphysema of the lungs. On auscultation - weakened breathing, and in the lower lobes - small bubbling moist rales or crepitus. From the side of the heart: moderate tachycardia, expansion of the boundaries to the right, accent of the second tone over the pulmonary artery - signs of stagnation in the pulmonary circulation. There is a slight cyanosis of the lips, nail phalanges, nose.

In the stage of clinically pronounced pulmonary edema, two different forms can be observed:

Blue form of hypoxia;

Gray form of hypoxia.

With edema occurring with "blue" hypoxemia, the main symptoms are: pronounced cyanosis, shortness of breath, in severe cases - noisy, "bubbling" breathing, cough with copious discharge of foamy sputum, sometimes pinkish or canary-yellow in color. On percussion, dull tympanitis is determined over the lower posterior sections of the lungs, a boxed shade of percussion sound over the anterior and lateral sections of the chest, and limitation of mobility of the pulmonary edge. On auscultation - a large number of small bubbling sonorous moist rales. The pulse is usually quickened, but its filling and tension remain satisfactory. BP - normal or slightly higher, muffled heart sounds. Body temperature can rise to 38 0 - 39 0 C. Blood tests reveal pronounced neutrophilic leukocytosis with lymphopenia and eosinopenia, and in more severe cases - blood clotting, increased clotting and viscosity.

Toxic pulmonary edema, proceeding as a "gray" hypoxemia, is clinically characterized by a pale gray color of the skin and mucous membranes; small, frequent, sometimes thready pulse, reduced blood pressure, severity of pulmonary changes, low carbon dioxide in the blood (hypocapnia); the respiratory center is depressed.

Usually, edema reaches full development by the end of the first day. Its pronounced signs are kept relatively stable for about a day. This period is the most dangerous, it falls a greater number of deaths. Starting from the third day, the general condition of patients improves markedly, the process enters the last phase - period of reverse development.

four). The onset of recovery is manifested by a decrease in shortness of breath, cyanosis, the number and prevalence of moist rales, normalization of body temperature, improvement in well-being, and the appearance of appetite. X-ray examination also indicates the regression of edema - large flaky shadows are not visible. In the peripheral blood, leukocytosis disappears, the number of neutrophils decreases with a simultaneous rise to a normal number of lymphocytes, and the normal gas composition of the blood is gradually restored.

Signs of expanded toxic pulmonary edema are quite characteristic and easily recognized. However, its severity varies from minimal clinical and radiographic symptoms to wheezing with copious frothy sputum.

Complications: often - secondary infectious pneumonia (in practice, we can assume that if after 3-4 days of illness the patient's condition does not improve, then pneumonia can be almost accurately diagnosed); less often - vascular thrombosis and embolism. And more often there are embolisms and pulmonary infarction, in which there are stabbing pains in the side and pure blood in the sputum. Pulmonary infarction is usually fatal. The development of a lung abscess is not ruled out. In persons who have suffered a severe injury, sometimes there are long-term consequences in the form of chronic bronchitis and emphysema, interstitial pneumonia and pneumosclerosis.

Clinical forms of the lesion. Depending on the concentration of 0V vapors and SDYAV, exposure and the state of the body, there may be mild, moderate and severe lesions.

With a mild degree of damage, the initial stage is poorly expressed, the latent period is longer. After this, the phenomena of pulmonary edema are usually not detected, and only changes in the type of tracheobronchitis are noted. There is slight shortness of breath, weakness, dizziness, chest tightness, palpitations, slight cough. Objectively, a runny nose, hyperemia of the pharynx, hard breathing and single dry rales are noted. All these changes pass in 3-5 days.

With a moderate lesion, after the latent stage, pulmonary edema develops, but it does not capture all the lobes or is more moderately expressed. Shortness of breath and cyanosis are moderate. Slight clotting of blood. On the second day begins resorption and improvement. But it must be borne in mind that in these cases, complications are possible, mainly bronchopneumonia, and if the regimen or treatment is violated, the clinic may be aggravated with dangerous consequences.

The clinical picture of a severe lesion was described above. In addition, there may be damage of an extremely severe degree when exposed to very high concentrations or prolonged exposures. In these cases, in the initial stage, the irritating effect of the vapors is pronounced, there is no latent period, and death occurs in the first hours after the defeat. Moreover, pulmonary edema is not very pronounced, and in some cases it still does not have time to develop, but destruction and death of the epithelium of the pulmonary alveoli occurs as a result of a “cauterizing” action.

Diagnostics. X-ray examination plays an important role in the diagnosis of toxic edema. The first radiographic changes are detected already 2-3 hours after the lesion, reaching a maximum by the end of the first - the beginning of the second day. The severity of changes in the lungs corresponds to the severity of the lesion. They are most significant at the height of intoxication and consist in a decrease in the transparency of the lung tissue, the appearance of large-focal confluent opacities, usually recorded in both lungs, and also in the presence of emphysema in the supradiaphragmatic areas. In the initial stages and in the abortive form of edema, the number and size of darkening is less. In the future, as the resolution of pulmonary edema, the intensity of focal blackouts weakens, they decrease in size and disappear completely. Other x-ray changes also undergo reverse development.

Pathological changes in death: the lungs are sharply enlarged in volume. Their mass is also increased and reaches 2-2.5 kg instead of 500-600 g in the norm. The surface of the lungs has a characteristic mottled (marble) appearance due to the alternation of pale pink protruding areas of emphysema, dark red depressed areas of atelectasis and bluish areas of edema.

On incision, a copious amount of serous foamy fluid is released from the lungs, especially when pressed.

The trachea and bronchi are filled with edematous fluid, but their mucosa is smooth and shiny, slightly hyperemic. Microscopic examination reveals an accumulation of edematous fluid in the alveoli, which turns pink with azure-eosin.

The heart is moderately dilated, with dark blood clots in its cavities. Parenchymal organs are congestively plethoric. The meninges and brain substance are plethoric, in some places there are pinpoint hemorrhages, sometimes vascular thrombosis and softening foci.

In the case of later death (3-10 days), the lungs take on a picture of confluent bronchopneumonia, in the pleural cavities there is a small amount of serous-fibrinous fluid. The heart muscle is flabby. Other organs are stagnantly plethoric.

The mechanism of occurrence and development of toxic pulmonary edema.

The development of toxic pulmonary edema is a very complex process. The chain of cause-and-effect relationships consists of the main links:

Violation of the main nervous processes in the reflex arc (receptors of the vagus nerve of the lungs, hypothalamus-sympathetic nerves of the lungs);

Inflammatory-trophic disorders in the lung tissue, increased vascular permeability;

Accumulation of fluid in the lungs, displacement of the mediastinal organs, stagnation of blood in the vessels of the pulmonary circulation;

Oxygen starvation: the stage of "blue hypoxia" (with compensated circulation) and "gray hypoxia" (in case of collapse).

Treatment of toxic pulmonary edema.

Pathogenetic and symptomatic therapy is used, aimed at reducing pulmonary edema, combating hypoxia and stopping other symptoms, as well as combating complications.

1. Providing maximum rest and warming - the body's need for oxygen decreases and the body's ability to tolerate oxygen starvation is facilitated. In order to stop neuro-psychic excitation, they give phenazepam or seduxen in tablets.

2. Pathogenetic and symptomatic therapy:

A) drugs that reduce the permeability of the pulmonary capillaries;

B) dehydration agents;

B) cardio - vascular funds;

D) oxygen therapy.

A) Glucocorticoids: intravenous prednisolone at a dose of 30-60 mg or drip at a dose of up to 150-200 mg. Antihistamines (pipolphen, diphenhydramine). Ascorbic acid (5% solution 3-5 ml). Calcium chloride or calcium gluconate 10 ml of a 10% intravenous solution in the first hours, during the period of increasing edema.

B) 20-40 mg of lasix is ​​injected intravenously (2-4 ml of a 1% solution). Furosemide (lasix) 2-4 ml of a 1% solution is injected intravenously under the control of the acid-base state, the level of urea and electrolytes in the blood, 40 mg initially after 1-2 hours, 20 mg after 4 hours during the day;

AT). With the appearance of tachycardia, ischemia, sulfocamphocaine, corglicon or strophanthin, aminofillin are administered to reduce stagnation in the pulmonary circulation. With a decrease in blood pressure - 1 ml of a 1% solution of mezaton. With the phenomena of blood clotting - heparin (5000 IU), you can use trental.

D) Inhalations of an oxygen-air mixture with a content of 30-40% oxygen for 15-30 minutes are effective, depending on the patient's condition. When foaming edematous fluid, antifoaming surface-active agents (ethyl alcohol) are used.

With pulmonary edema, sedatives are indicated (phenazepam, seduxen, elenium). The introduction of adrenaline, which can increase edema, morphine, which depresses the respiratory center, is contraindicated. It may be advisable to introduce an inhibitor of proteolytic enzymes, in particular kininogenases, which reduce the release of bradykinin, trasylol (kontrykal) 100,000 - 250,000 IU in isotonic glucose solution. In severe pulmonary edema, in order to prevent secondary infectious pneumonia, especially with an increase in body temperature, antibiotics are prescribed.

At gray form of hypoxia therapeutic measures are aimed at removing from the collaptoid state, excitation of the respiratory center and ensuring airway patency. The introduction of corglicon (strophanthin), mezaton, lobelin or cytiton, inhalation of carbogen (a mixture of oxygen and 5-7% carbon dioxide) is shown. To thin the blood, an isotonic 5% glucose solution is administered with the addition of mezaton and vitamin C 300-500 ml intravenously. If necessary, intubation, suction of fluid from the trachea and bronchi and transfer of the patient to controlled breathing.

First aid and assistance at the stages of medical evacuation.

First and pre-medical care. The affected person is released from restrictive uniforms and equipment, provided with maximum peace (any movements are strictly prohibited), placed on a stretcher with a raised head end, and protect the body from cooling. The respiratory tract is freed from the accumulated fluid by giving the victim an appropriate position, the fluid is removed from the oral cavity with a gauze swab. With anxiety, fear, especially with combined lesions (pulmonary edema and chemical burns), an analgesic is administered from an individual first-aid kit. In the case of reflex respiratory arrest, artificial ventilation of the lungs is performed using the “mouth-to-mouth” method. With shortness of breath, cyanosis, severe tachycardia, oxygen is inhaled for 10-15 minutes using an inhaler, cardiovascular agents (caffeine, camphor, cordiamine) are administered. The victim is transported on a stretcher. The main requirement is to deliver the victim to the MCP as quickly as possible under conditions of a calm situation.

First aid. If possible, do not disturb or shift the patient. Inspection is carried out, pulse and number of breaths are counted, blood pressure is determined. Assign peace, warmth. With the rapid development of toxic pulmonary edema, foamy fluid is aspirated from the upper respiratory tract through a soft rubber catheter. Apply oxygen inhalation with defoamers, bloodletting (200 - 300 ml). 40 ml of a 40% glucose solution, strophanthin or corglicon are injected intravenously; subcutaneously - camphor, caffeine, cordiamine.

After carrying out first aid measures, the affected person should be taken to the emergency room or hospital as soon as possible, where he will be provided with qualified and specialized therapeutic assistance.

Qualified and specialized medical care.

In the omedb (hospital), the efforts of doctors should be aimed at eliminating the effects of hypoxia. At the same time, it is required to determine the sequence in the implementation of a complex of therapeutic measures that affect the leading mechanisms of edema.

Violation of the airway is eliminated by giving the patient a posture in which their drainage is facilitated due to the natural outflow of transudate, in addition, fluid is suctioned from the upper respiratory tract and antifoam agents are used. As defoamers, ethyl alcohol is used (30% solution in patients who are unconscious and 70-90% in persons with preserved consciousness) or a 10% alcohol solution of antifomsilan.

Continue the introduction of prednisolone, furosemide, diphenhydramine, ascorbic acid, corglycone, aminophylline and other agents, depending on the patient's condition. Persons with severe edema within 1-2 days are considered non-transportable, require constant medical supervision and treatment.

In the therapeutic hospital, specialized medical care is provided in full until recovery. After stopping the dangerous symptoms of pulmonary edema, reducing shortness of breath, improving cardiac activity and general condition, the main attention is paid to the prevention of complications and the complete restoration of all body functions. In order to prevent secondary infectious pneumonia with an increase in body temperature, antibiotic therapy is prescribed, periodic oxygen supply. In order to prevent thrombosis and embolism - control of the blood coagulation system, according to indications of heparin, trental, aspirin (weak anticoagulant).

medical rehabilitation is to restore the functions of organs and systems. In severe cases of poisoning, it may be necessary to determine the disability group and recommendations for employment.

Toxic pulmonary edema (TOL) is a symptom complex that develops with severe inhalation poisoning with asphyxiating and irritating poisons. TOL develops with inhalation poisoning: BOV (phosgene, diphosgene), as well as under the influence of SDYAV, for example, methyl isocyanate, sulfur pentafluoride, CO, etc. TOL easily occurs with inhalation of caustic acids and alkalis (nitric acid, ammonia) and is accompanied by a burn upper respiratory tract. This dangerous pathology of the lungs often occurs in emergency conditions, so any practicing physician may encounter such a serious complication of many inhalation poisonings in their work. Future doctors should be well aware of the mechanism of development of toxic pulmonary edema, the clinical picture and treatment of TOL in many pathological conditions.

Differential diagnosis of hypoxia.

Measures in the outbreak and at the stages of medical evacuation in case of damage to agents and SDYAV of asphyxiating action.

Physical properties of SDYAV, features of the development of toxic pulmonary edema (TOL).

Toxic pulmonary edema. Schematically, in the clinic of toxic pulmonary edema, the following stages are distinguished: reflex, latent, clinically expressed symptoms of pulmonary edema, regression of the lesion, stage of long-term consequences.

The reflex stage is manifested by symptoms of irritation of the mucous membranes of the eyes and respiratory tract, a dry, painful cough appears. Breathing quickens and becomes shallow. Reflex laryngobronchospasm and reflex respiratory arrest are possible.

After leaving the infected atmosphere, these symptoms gradually subside, the lesion passes into a latent stage, which is also called the stage of imaginary well-being. The duration of this stage is different and depends mainly on the severity of the lesion. On average, it is 4-6 hours, but can be shortened to half an hour or, conversely, increased to 24 hours.

The latent stage is replaced by the stage of pulmonary edema itself, the symptomatology of which, in principle, is similar to that of edema of any other etiology. Its features are: an increase in body temperature, sometimes up to 38-39 ° C; pronounced neutrophilic leukocytosis (up to 15-20 thousand per 1 mm3 of blood) with a shift of the formula to the left, a combination of pulmonary edema with manifestations of other signs of damage, in particular with reflex disorders and general intoxication of the body. Pulmonary edema leads to acute respiratory failure, which is then joined by cardiovascular failure.

The most dangerous condition of the victims is during the first two days after poisoning, during which a fatal outcome may occur. With a favorable course, a noticeable improvement begins on the 3rd day, which means a transition to the next stage of the lesion - the reverse development of pulmonary edema. In the absence of complications, the duration of the regressive stage is approximately 4-6 days. Usually, the affected remain in medical institutions for up to 15-20 days or more, which is most often associated with various complications, primarily with the occurrence of bacterial pneumonia.

In some cases, there is a milder course (abortive forms) of pulmonary edema, when exudation into the alveoli is less intense. The course of the pathological process is characterized by relatively rapid reversibility.

Toxic pneumonia and diffuse toxic bronchitis most often referred to as lesions of moderate severity. Toxic pneumonia is usually detected within 1-2 days after exposure to the gas. The main symptomatology of these pneumonias is common, but the peculiarity is that they occur against the background of toxic rhinolaringotracheitis or rhinolaringotracheobronchitis, the symptoms of which not only accompany, but initially prevail over signs of inflammation of the lung tissue. The prognosis of toxic pneumonia is usually favorable. Inpatient treatment lasts approximately 3 weeks.

However, the clinic of toxic pneumonia may be of a different nature. In acute poisoning with nitrogen dioxide and nitrogen tetroxide, cases of a peculiar course of this lesion were observed [Gembitsky E. V. et al., 1974]. The disease arose 3-4 days after the toxic effect, as if suddenly, against the background of the subsidence of the initial symptoms of acute inhalation poisoning and the emerging clinical recovery of patients. It was characterized by a violent onset, chills, cyanosis, shortness of breath, severe headaches, a feeling of general weakness, weakness, high leukocytosis, and eosinophilia.

X-ray examination of the lungs clearly revealed one or more pneumonic foci. Some patients noted the recurrence of the pathological process, its long and persistent course, the occurrence of complications and residual effects in the form of asthmatic conditions, hemoptysis, and the development of early pneumosclerosis.

The described features of the course of these pneumonias, namely: their occurrence some time after the lesion, recurrence of the pathological process, asthma-like conditions, eosinophilia - suggest that in their occurrence, along with the microbial factor, allergic reactions also play a certain role, apparently, autoimmune nature. Confirmation of this interpretation, in our opinion, is the fact that irritating substances cause significant alteration of the epithelium of the bronchopulmonary apparatus, which can lead to the formation of autoantibodies to the lung antigen.

The most common form of moderate inhalation poisoning is acute toxic bronchitis. Their clinical picture is usual for this disease. The duration in most victims is 5-10 days, and in diffuse bronchitis, especially with the involvement of the deep sections of the bronchial tree in the pathological process, it is 10-15 days. Perhaps the occurrence of toxic bronchiolitis, which, as a rule, occurs with the phenomena of acute respiratory failure and severe intoxication, which allows us to qualify it as a manifestation of a severe lesion.

A significant part of inhalation poisoning is mild. Most often in this case, acute toxic rhinolaringotracheitis is diagnosed. Along with this, another clinical variant of the course of mild poisoning is also possible, when signs of damage to the bronchopulmonary apparatus are slightly expressed and disorders associated with the resorptive effect of the poisonous substance come to the fore: dizziness, stupor, short-term loss of consciousness, headache, general weakness, nausea, sometimes vomit. The duration of the lesion in this case is 3-5 days.

Clinical picture in chronic lesions these substances most often manifests itself in the form of chronic bronchitis. At the beginning of the disease, the pathological process is purely toxic ("irritant bronchitis"), later on, the resulting pathological changes are maintained and aggravated by the activated own facultative-virulent microflora of the respiratory tract. Some authors note that a characteristic feature of such bronchitis is dystrophic changes in the mucosa, as well as the early addition of a bronchospastic component [Ashbel S. M. et al., Zertsalova V. I. et al., Pokrovskaya E. A. 1978]. The deeper parts of the bronchopulmonary apparatus also suffer. So, in an experiment on animals, Polish authors found that chronic exposure to nitrogen oxides, destroying surfactant, leads to a decrease in static compliance and vital capacity of the lungs and an increase in their residual volume.

In the clinic of the lesion, changes in other organs and systems are also noted. These changes are very similar and are manifested by neurological disorders such as asthenoneurotic and asthenovegetative syndromes, hemodynamic changes with the predominant development of hypotonic conditions, various degrees of disorders of the gastrointestinal tract from dyspeptic disorders to chronic gastritis, and toxic liver damage.

Toxic pulmonary edema is a pathological condition that develops due to their inhalation exposure to chemicals. At the initial stages, clinical symptoms are manifested by suffocation, dry cough, foaming from the mouth. If first aid is not provided to the victim in a timely manner, then there is a high probability of respiratory arrest, severe violations of the heart. Drug therapy of toxic edema includes the use of corticosteroids, cardiotonic drugs, diuretics. Oxygen therapy is also practiced.

Types of pulmonary edema

Toxic damage to the lungs is acute pulmonary insufficiency (ICD-10 code - J81). This condition develops as a result of a massive release of transudate from small blood vessels into the lung tissue.

More often, patients are diagnosed with a developed, completed form of pathology, which is characterized by a successive change of five periods. Somewhat less often, the lungs are affected by the abortive form of toxic edema, which has 4 stages of development. The "silent" form is detected exclusively during X-ray diagnostics, mainly during the next medical examination.

In pulmonology and other areas of medicine, edema is classified depending on the speed of the pathological process:

• fulminant. It develops rapidly - several minutes pass from the moment chemicals enter the lungs to death;
• spicy. Usually lasts no more than 4 hours, so only immediate resuscitation can prevent the death of the patient;
• subacute. From the onset to the reverse development of toxic edema, it takes from several hours to 1-2 days. Symptoms are mild, irreversible lung damage is not observed.

The causes of pulmonary edema must be established to determine the methods of future therapy. Differential diagnostics is carried out to exclude other types of pathology. In addition to toxic, cardiogenic pulmonary edema occurs. It is provoked by myocardial infarction, severe arrhythmia, hypertension, cardiomyopathy, myocarditis. The release of transudate from the capillaries also occurs with anaphylactic shock - a dangerous type of systemic allergy. Eclampsia during pregnancy also sometimes leads to the development of toxic pulmonary edema.

Determine the tactics of treatment helps to determine the mechanism of development of lung pathology. Alveolar edema is accompanied by sweating of the walls of the alveoli with blood plasma. And with the interstitial form, only the lung parenchyma swells.

Causes of toxic pulmonary edema

Swelling of the lungs occurs due to the inhalation of substances that are toxic to their structures. First, primary biochemical changes are noted: endotheliocytes, alveocytes, and bronchial epithelium die. And then the work of the entire respiratory system is upset, including as a result of blood clotting.

Toxic pulmonary edema occurs as a result of exposure to such chemicals:

• irritant -, hydrogen fluoride, a pair of concentrated acids (, nitric, and others);
• suffocating action - phosgene, diphosgene, nitric oxide, smoke from the combustion of certain substances.

Poisoning by asphyxiating chemicals is usually noted only in case of a man-made accident, a catastrophe at an industrial facility. Previously, toxic edema developed from inhalation of phosgene in military exercises or in combat conditions. Damage to the lungs is also possible in case of violation of technological processes in industries, poor-quality treatment facilities.

Subacute edema is often a sign of an occupational disease. The lungs are slowly destroyed by the constant inhalation of small doses of chemicals. Often a person does not suspect what caused rapid fatigue and weakness.

Radiation therapy, smoking, alcohol abuse, and taking certain medications can act as factors provoking lung damage. Pulmonary edema is not uncommon in bedridden patients due to slow blood circulation.

Symptoms of pulmonary edema

At the initial stage of the development of the pathological condition, signs of pulmonary edema in an adult are rather weakly expressed, less often moderately. The mucous membranes of the respiratory tract are irritated, so it tickles in the throat, it hurts the eyes, there is a constant desire to cough up. Then such symptoms weaken and even disappear, but this does not mean that the threat has passed. Edema moved to the next stage.

The subsequent damage to lung tissue manifests itself as follows:

• increased sweating;
• dry severe paroxysmal cough, which is aggravated by lying down;
• growing weakness;
• palpitations, heart rhythm disorder;
• acceptance by the victim of a forced position - sitting with legs hanging from the bed;
• anxiety due to a lack of understanding of what is happening;
• a feeling of lack of air when inhaling, severe shortness of breath;
• separation of frothy sputum with a pinkish tint;
• swelling of the veins in the neck;
• blue legs and hands due to outflow of blood;
• fainting, loss of consciousness.

The nature of breathing in alveolar pulmonary edema is whistling, then bubbling, wheezing. If the victim inhaled vapors of nitric acid, then the clinical picture is supplemented by dyspeptic disorders. These are attacks of nausea, bloating, pain in the epigastric region, heartburn. The temperature with toxic pulmonary edema decreases, the skin becomes cool to the touch. There are chills, cold perspiration on the forehead.

First aid for pulmonary edema

The most important first aid measure for toxic pulmonary edema is an emergency call of the ambulance team. It is necessary to constantly be in touch with the doctor, helping him to monitor the condition of the victim.

Before the arrival of the doctor, you should help the person, reducing the risk of death:

• help to take a sitting position, while shifting the legs down. It is advisable to place a thick pillow behind your back to facilitate breathing;
• unfasten fasteners on clothes and underwear, open windows or take the victim to fresh air;
• moisten cotton wool with ethyl alcohol (pure for adults, 30-degree for children), let the person periodically breathe in its vapors;
• fill the container with hot water for taking a foot bath;
• control breathing, pulse, blood pressure;
• put a couple of Nitroglycerin tablets under the tongue.

If the victim lost consciousness, fell into a coma, then if possible, you need to go towards the ambulance. It is equipped with everything necessary for emergency resuscitation procedures in case of toxic pulmonary edema.

Complications

The arriving doctor diagnoses the pathology according to the position of the patient, specific for pulmonary edema. It is forced, since it is easier for the victim to breathe while sitting with his legs dangling, and the intensity of other symptoms is maximally reduced. Diagnostic criteria for toxic edema are also a decrease in body temperature, a slowing of the pulse, bubbling rales in the lungs.

Before arriving at the hospital, the ambulance team stabilizes the condition of the victim:

In the treatment of pulmonary edema of toxic origin, before arriving at a medical facility, other drugs are also used to eliminate the most dangerous symptoms. If respiratory failure progresses, then tracheal intubation and mechanical ventilation are performed.

In emergency cases, bloodletting helps to reduce blood flow to lung structures. The imposition of tourniquets on the upper or lower limbs is also practiced.

Treatment

Treatment in the hospital for pulmonary edema is carried out in accordance with the clinical protocol.

X-ray diagnostics is performed to confirm the toxic damage to the respiratory system. On the obtained images, the pulmonary pattern is indistinct, and the roots of the lungs are significantly expanded. An ECG allows you to assess the degree of damage to the organs of the cardiovascular system. Liver tests and a general examination of urine, a biochemical blood test are also carried out. Diagnosis of toxic pulmonary edema also requires identification of the nature of the chemical that caused the disease state.

With pathology of severe and moderate severity, therapy is carried out in the intensive care unit. Medical staff constantly monitors the vital signs of the patient.

The following pharmacological preparations are used in the treatment:

• painkillers, including non-steroidal anti-inflammatory drugs;
• neuroleptics (Morphine, Fentanyl) to improve the psycho-emotional state of the patient, eliminate anxiety, restlessness, nervous excitability;
• diuretics (Lasix, Furosemide) to cleanse the body of toxic substances;
• cardiac glycosides with a cardiotonic effect - Strofantin, Korglikon.

Bronchodilators are required for the relief of bronchospasm. Intravenous administration of Eufillin is practiced for pulmonary edema or taking this drug in tablets. Hormonal drugs contribute to the rapid removal of fluid from the lung tissues, anesthetize, stop inflammation. Injectable solutions of vitamins are used to strengthen the general state of health. Pulmonary edema requires infusions (intravenous administration) of oncotic active agents - Albumin, Mannitol, Sorbitol, glucose solutions. With rapid resuscitation, timely initiation of therapy, the prognosis is favorable.

As a consequence of the disease, the victim, especially a child, may develop renal or hepatic insufficiency, toxic pneumosclerosis and emphysema. A serious consequence of the pathological condition can be lung cancer.

In the absence of treatment at the final stage, the manifestations of toxic pulmonary edema are most pronounced. There is a thready pulse, respiratory failure, tremor, convulsions. If resuscitation is not carried out at this stage, the victim dies.

The probability of death in toxic damage to the lungs is higher in the elderly, children, the elderly, debilitated patients.

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 usually takes at least a year to achieve full recovery after an illness.

How is pulmonary edema formed?

Pulmonary edema begins in the same way as a similar lesion of other organs. The difference lies in the fact that the liquid freely penetrates through the easily permeable tissues of the alveoli.

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

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

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

This list of possible causes of toxic pulmonary edema is not limited. Most often, people with this diagnosis end up in the hospital if safety precautions are not followed, as well as in case of accidents at work.

Symptoms and stages of the disease

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

1. Developed (completed) form. In this case, the disease goes through 5 stages: reflex, latent, a period of increasing edema, completion and reverse development.
2. abortion form. It is distinguished by the absence of the most difficult stage of completion.
3. "Silent" edema is a latent asymptomatic variety of the disease. It can only be determined by chance with the help of an X-ray examination.

After inhalation of the poison, intoxication of the body occurs, the initial period of the development of the disease begins - the reflex stage. It lasts from ten minutes to several hours. At this time, the classic symptoms of irritation of the mucous membranes and poisoning appear:

• cough and sore throat;
• pain in the eyes and tearing due to contact with toxic gases;
• the appearance of abundant secretions of the nasal mucosa.

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

Then comes the latency period. At this time, the symptoms listed above disappear, the person feels much better, but on 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 lasts, the better for the patient.

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

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

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

1. "Blue" hypoxemia. Because of suffocation, a person rushes about and tries to breathe harder. He is very excited, utters groans, while the consciousness is clouded. The body reacts to the edema with blueness, pulsation of blood vessels and the release of pinkish foam from the mouth and nose.
2. "Gray" hypoxemia. It is considered more dangerous for the patient. Due to a sharp deterioration in the activity of the cardiovascular and respiratory systems, collapse occurs. Respiration and pulse rate are noticeably reduced, the body becomes cold, and the skin acquires an earthy hue.

If a person was able to survive toxic pulmonary edema, then the last stage begins - the 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 burn of the lungs can be:

1. Blockage of the airways. It occurs when excessive foam is released and greatly impairs gas exchange.
2. Respiratory depression. When intoxicated, some poisons can additionally affect the respiratory center of the brain, negatively affecting the functioning of the lungs.
3. Cardiogenic shock. Due to edema, insufficiency of the left ventricle of the heart develops, as a result of which blood pressure drops sharply, disrupts the blood supply to all organs, including the brain. In 9 out of 10 cases, cardiogenic shock is fatal.
4. Fulminant form of pulmonary edema. This complication lies in the fact that all stages of the disease are compressed in time to several minutes due to concomitant diseases of the liver, kidneys and heart. It is almost impossible to save the patient in this case.

Even if a person managed to survive a complication, it is far from a fact 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 stress, other consequences may appear. Most often they are expressed through the development of other diseases:

• Pneumosclerosis. Damaged alveoli overgrow and heal, losing their elasticity. If a small number of cells are affected in this way, the consequences are almost imperceptible. But with the widespread spread of the disease, the process of gas exchange greatly deteriorates.
• bacterial pneumonia. When bacteria enter the weakened tissues of the lungs, microorganisms begin to actively develop, provoking inflammation. Its symptoms are fever, weakness, shortness of breath, coughing up blood and purulent sputum.
• Emphysema. This disease develops due to the expansion of the tips of the bronchioles, provoking additional damage to the walls of the alveoli. A person's chest swells and makes a boxy sound when tapped. Another characteristic symptom is shortness of breath.

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

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, an ECG is indispensable to monitor the condition of the heart.

If the pulmonary edema has been stopped, then laboratory blood tests (general and biochemical) and urine, liver tests are taken. This is necessary to determine the damage caused to the body, and prescribe treatment.

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

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

1. Steroids;
2. Diuretics;
3. Bronchodilators;
4. Glucose;
5. Calcium chloride;
6. Cardiotonics.

With the progression of edema, tracheal intubation and connection to a ventilator may also be required. Once symptoms have resolved, 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, while the chance of getting a disability is very high.