Toxic pulmonary edema symptoms. Complication of acute poisoning – toxic pulmonary edema

Acute toxic-chemical damage to the respiratory system is divided into four periods (phases): the phase of primary reactions, the latent period (latent phase), the phase of extensive clinical reactions, and the outcome phase. The phase of primary reactions due to exposure to toxic chemical substances that are easily soluble in water is manifested by acute suffocating laryngospasm and bronchospasm, while substances that are sparingly soluble in water cause less vivid or even erased reactions, not disturbing in the victims.
The latent period (after the phase of primary reactions) lasts from 1-2 to 48 hours. It can end at any time (usually at night) with the rapid development of pulmonary edema, which is more typical for exposure to poorly soluble chemicals. Easily soluble substances are less likely to cause the development of acute toxic-chemical pulmonary edema, since they, to a lesser extent, due to acute laryngo- and bronchospasm, reach the bronchioloalveolar (distal) parts of the lung when inhaled. Thus, patients in the latent period are subject to constant medical supervision in the emergency room or hospital, otherwise they may die in the prehospital stage.
The period of extensive clinical reactions often begins with acute toxic-chemical pulmonary edema or acute toxic-chemical tracheobronchitis (when exposed to chemicals that are easily soluble in water). Acute toxic-chemical edema of the lungs is distinguished between blue (with a picture of acute hypoxia and hypercapnia) and gray (with acute hypoxia and hypocapnia) type.
Blue-type pulmonary edema is characterized by the presence of a pronounced alveolar phase and obstructive syndrome (with damage to small bronchi) with a predominance of inspiratory dyspnea. Against the background of fine-bubble and then large-bubble wheezing, affecting the receptors of the reflexogenic cough zone, foamy sputum appears, colored pinkish-orange (when exposed to nitrogen oxides on the mucous membranes respiratory tract, causing a xanthoprotein reaction with the protein contents of the bronchial tree).
In toxic-chemical pulmonary edema of the gray type with a predominance of the interstitial phase of edema with severe inspiratory dyspnea, the main clinical manifestation is cardiovascular failure. This is a more severe form of pulmonary edema, in which the alveolar-capillary membrane is affected to its full depth.
After relief of pulmonary edema, the clinical picture of acute toxic-chemical alveolitis or pneumonitis remains. In some cases, acute toxic-chemical pneumonia may develop.
In case of acute toxic-chemical injury, with substances easily soluble in water, when acute toxic-chemical pulmonary edema was not observed during the period of clinically developed reactions, injuries are recorded upper sections respiratory organs (toxic-chemical rhinitis, pharyngolaryngotracheitis), as well as acute bronchitis with predominant damage to the mucous membranes of large bronchial structures.
With a favorable course and treatment of respiratory pathology caused by acute toxic-chemical damage, the total duration of the disease is 2-3 weeks.
An unfavorable prognosis for toxic-chemical damage to the respiratory system is possible when aseptic inflammation is complicated by a bacterial: infectious-inflammatory process, accompanied by an increase in body temperature, hematological and biochemical changes. Such a complication is always dangerous and can be observed from the 3-4th day of injury. The addition of infectious-inflammatory reactions against the background of toxic-chemical damage to the lungs often leads to persistent infection and subsequent chronicization of the pathological process in the lungs, despite carefully administered anti-inflammatory therapy. This is explained by the fact that in similar cases the infectious-inflammatory process in the lungs is layered on destructively altered bronchial-pulmonary structures.

Pulmonary edema is the cause of painful death for many patients. It occurs most often as a complication when the regulation of fluid volumes that should circulate in the lungs is impaired.

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

It's spicy pathological condition threatening life, requiring extreme urgent help, immediate hospitalization. The main characteristics of the disease are characterized by acute lack of air, severe suffocation and death of the patient when resuscitation measures are not provided.

At this moment, the capillaries are actively filled with blood and fluid quickly passes through the walls of the capillaries into the alveoli, where so much of it collects that it greatly impedes the supply of oxygen. IN respiratory organs, gas exchange is disrupted, tissue cells experience acute failure oxygen(hypoxia), a person suffocates. Choking often occurs at night while sleeping.

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

Classification, what causes it

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

Any attack of suffocation that occurs during such diseases is grounds for suspicion of a state of acute swelling of the respiratory system.

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

At-risk groups

Since the pathogenesis (development) of pathology closely related to related internal diseases , at risk are patients with diseases or factors that provoke such a health and life-threatening condition.

The risk group includes patients suffering from:

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

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

Climbers have this dangerous condition happens when quickly ascending to a high altitude without pausing at intermediate high-rise levels.

Symptoms: how they manifest and develop in stages

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

First emergency first aid: what to do if

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

1. Help a person sit down or sit up halfway with their legs down
2. If possible, treat with diuretics (they give diuretics - Lasix, furosemide) - this removes it from the tissues excess liquid, however, for low blood pressure, small doses of medication are used.
3. Organize the possibility of maximum access of oxygen to the room.
4. The foam is suctioned and, if skillful, oxygen inhalations are performed through the solution. ethyl alcohol(96% of the vapor is for adults, 30% of alcohol vapor is for children).
5. Cooking hot bath for legs.
6. If skillful, apply tourniquets to the limbs, not too tightly squeezing the veins in the upper third of the thigh. Leave the tourniquets on for longer than 20 minutes, and 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, do so carefully, slowly loosening them.
7. Continuously monitor how the patient breathes and pulse rate.
8. For pain, they give analgesics, if available, promedol.
9. For high blood pressure, benzohexonium, pentamine are used, which promote the outflow of blood from the alveoli, and nitroglycerin, which dilates blood vessels (with regular pressure measurements).
10. If normal - small doses of nitroglycerin under the control of pressure indicators.
11. If the pressure is below 100/50 - dobutamine, dopmin, which increase the function of myocardial contraction.

What is dangerous, forecast

Pulmonary edema is a direct threat to life. Without taking extremely urgent measures, which must be carried out by the patient’s relatives, without subsequent urgent active treatment in the hospital, pulmonary edema is the cause of death in 100% of cases. A person will experience suffocation, coma, and death.

Attention! When the very first signs of an acute pathological situation appear, it is important to provide qualified assistance at 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 must be taken: elimination of factors contributing to this condition:

1. For heart disease (angina, chronic failure) are taking medications to treat them and at the same time – hypertension.
2. For repeated swelling of the respiratory organs, the procedure of isolated blood ultrafiltration is used.
3. Prompt accurate diagnosis.
4. Timely adequate treatment of asthma, atherosclerosis, and other internal disorders that can cause such pulmonary pathology.
5. Isolate the patient from contact with any kind of toxins.
6. Normal (not excessive) physical and respiratory stress.

Complications

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

Long-term oxygen starvation has a negative effect on almost all organs. The most serious consequences are violations cerebral circulation, heart failure, cardiosclerosis, ischemic organ damage. These diseases pose a constant threat to life and cannot be avoided without intensive drug therapy.

These complications, despite stopping acute edema lungs - cause of death large quantity 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, causes, diseases and factors that can provoke it, as well as measures emergency care before the ambulance arrives can lead to favorable outcome and the absence of consequences even with such a serious threat to life.

is an acute inhalation injury to the lungs caused by inhalation of chemicals that have pulmonary toxicity. Clinical picture unfolds in stages; suffocation, cough, foamy sputum, chest pain, shortness of breath, severe weakness, collapse occur. Respiratory and cardiac arrest may occur. In a favorable scenario, toxic pulmonary edema reverses. The diagnosis is confirmed by anamnesis, chest X-ray, and blood tests. First aid consists of stopping contact with the pulmonary toxicant, performing oxygen therapy, administering steroidal anti-inflammatory, diuretic, oncotically active agents, and cardiotonics.

ICD-10

J68.1 Acute pulmonary edema caused by chemicals, gases, fumes and vapors

General information

Toxic pulmonary edema - serious condition, caused by inhaled pulmonotropic poisons, the inhalation of which causes structural and functional disorders of the respiratory system. There may be cases of both isolated and mass casualties. Pulmonary edema is the most severe form of toxic damage to the respiratory tract: during intoxication mild degree acute laryngotracheitis develops, medium degree- bronchitis and tracheobronchitis, severe - toxic pneumonia and pulmonary edema. Toxic pulmonary edema is accompanied by a high mortality rate from acute cardiovascular failure and associated complications. Studying the problem of toxic pulmonary edema requires coordination of efforts on the part of clinical pulmonology, toxicology, resuscitation and other specialties.

Causes

The development of toxic pulmonary edema is preceded by inhalation of pulmonary toxicants - irritating gases and vapors (ammonia, hydrogen fluoride, concentrated acids) or suffocating effects (phosgene, diphosgene, chlorine, nitrogen oxides, combustion smoke). In peacetime, such poisonings most often occur due to non-compliance with safety precautions when working with these substances, violations of production process technology, as well as man-made accidents and disasters at industrial facilities. Possible damage from chemical warfare agents in military operations.

Pathogenesis

The direct mechanism of toxic pulmonary edema is caused by damage to the alveolar-capillary barrier by toxic substances. Following the primary biochemical changes in the lungs, the death of endothelial cells, alveocytes, bronchial epithelium, etc. occurs. Increased permeability of capillary membranes is facilitated by the release and formation in tissues of histamine, norepinephrine, acetylcholine, serotonin, angiotensin I, etc., and neuro-reflex disorders. The alveoli are filled with edematous fluid, which causes disruption of gas exchange in the lungs and contributes to an increase in hypoxemia and hypercapnia. Characteristic changes in the rheological properties of blood (thickening and increase in blood viscosity), accumulation of acidic metabolic products in tissues, and a shift in pH to the acidic side. Toxic pulmonary edema is associated with systemic disorders functions of the kidneys, liver, central nervous system.

Symptoms

Clinically, toxic pulmonary edema can occur in three forms - developed (complete), abortive and “silent”. The developed form includes a successive change of 5 periods: reflex reactions, latent, increasing edema, completion of edema and reverse development. In the abortive form of toxic pulmonary edema, 4 periods are noted: initial phenomena, latent course, increase in edema, and reverse development of edema. "Silent" edema is detected only on the basis X-ray examination lungs, clinical manifestations are practically absent.

Over the next few minutes and hours after inhalation of harmful substances, phenomena of irritation of the mucous membranes occur: sore throat, cough, mucous discharge from the nose, pain in the eyes, lacrimation. During the reflex stage of toxic pulmonary edema, sensations of tightness and pain in the chest, difficulty breathing, dizziness, and weakness appear and increase. In some poisonings (nitric acid, nitric oxide), dyspeptic disorders may occur. These disturbances do not have a significant impact on the well-being of the victim and soon subside. This marks the transition of the initial period of toxic pulmonary edema to latent.

The second stage is characterized as a period of imaginary well-being and lasts from 2 hours to one day. Subjective sensations are minimal, but physical examination reveals tachypnea, bradycardia, and decreased pulse pressure. The shorter the latent period, the more unfavorable the outcome of toxic pulmonary edema. In case of severe poisoning, this stage may be absent.

After a few hours, the period of imaginary well-being is replaced by a period of increasing swelling and pronounced clinical manifestations. A paroxysmal painful cough, difficulty breathing, shortness of breath, and cyanosis reappear. The victim's condition quickly deteriorates: weakness and headache, pain increases in chest. Breathing becomes frequent and shallow, moderate tachycardia and arterial hypotension are noted. During the period of increasing toxic pulmonary edema, abundant foamy sputum appears (up to 1 liter or more), sometimes mixed with blood; bubbling breathing audible from a distance.

During the period of completion of toxic pulmonary edema pathological processes continue to progress. A further scenario may develop according to the type of “blue” or “gray” hypoxemia. In the first case, the patient is excited, groans, rushes about, cannot find a place for himself, and greedily gasps for air. Pinkish foam is released from the mouth and nose. The skin is bluish, the vessels of the neck are pulsating, the consciousness is darkened. “Grey hypoxemia” is prognostically more dangerous. It is associated with a sharp disruption of the respiratory and cardiovascular systems(collapse, weak arrhythmic pulse, decreased breathing). The skin has an earthy gray tint, the limbs become colder, and facial features become sharper.

Complications

At severe forms toxic pulmonary edema death can occur within 24-48 hours. With a timely start intensive care, as well as in milder cases pathological changes are undergoing reverse development. The cough gradually subsides, shortness of breath and the amount of sputum decreases, wheezing weakens and disappears. In the most favorable situations recovery occurs within a few weeks. However, the period of resolution may be complicated by secondary pulmonary edema, bacterial pneumonia, myocardial dystrophy, and thrombosis. In the long-term period, after the toxic pulmonary edema subsides, toxic pneumosclerosis and pulmonary emphysema often develop, and an exacerbation of pulmonary tuberculosis is possible. Complications from the central nervous system (asthenoneurotic disorders), liver (toxic hepatitis), and kidneys (renal failure) develop relatively often.

Diagnostics

Physical, laboratory and x-ray morphological data vary depending on the period of toxic pulmonary edema. Objective changes are most pronounced in the stage of increasing edema. Moist fine bubbling rales and crepitus are heard in the lungs. X-ray of the lungs reveals vagueness of the pulmonary pattern, expansion and indistinctness of the roots.

During the period of completion of edema, the auscultatory picture is characterized by multiple moist rales of different sizes. Radiologically, the blurring of the pulmonary pattern increases, spotty foci appear, which alternate with foci of clearing (emphysema). A blood test reveals neutrophilic leukocytosis, an increase in hemoglobin content, increased coagulation, hypoxemia, hyper- or hypocapnia, and acidosis.

During the period of reverse development of toxic pulmonary edema, wheezing, large and then small focal shadows disappear, the clarity of the pulmonary pattern and the structure of the roots of the lungs are restored, and the peripheral blood picture is normalized. To assess damage to other organs, an ECG is performed, a study general analysis urine, biochemical analysis blood, liver tests.

Treatment of toxic pulmonary edema

All victims must receive first aid immediately. The patient must be kept at rest and prescribed sedatives and antitussives. To eliminate hypoxia, inhalations of an oxygen-air mixture passed through defoamers (alcohol) are performed. To reduce blood flow to the lungs, bloodletting or venous tourniquets are used on the limbs.

In order to combat the onset of toxic pulmonary edema, steroidal anti-inflammatory drugs (prednisolone), diuretics (furosemide), bronchodilators (aminophylline), oncotic drugs are administered active agents(albumin, plasma), glucose, calcium chloride, cardiotonics. As respiratory failure progresses, tracheal intubation and mechanical ventilation are performed. To prevent pneumonia, antibiotics are prescribed in normal dosages, and anticoagulants are used to prevent thromboembolic complications. Total duration Treatment can take from 2-3 weeks to 1.5 months. The prognosis depends on the cause and severity of toxic pulmonary edema, the completeness and timeliness of medical care. In the acute period, mortality is very high, and long-term consequences often lead to disability.

The cause of toxic pulmonary edema is damage to the pulmonary membrane by toxic substances. The result of exposure to poisons is inflammation with further development swelling of the lung tissue. Refers to a severe form of chemical lung damage. The most common pathological condition occurs when carbon monoxide, FOS, concentrated vapors of acids and alkalis or other chemicals with asphyxiating effects. Edema also develops if aggressive chemicals enter the digestive tract, causing a burn to the upper respiratory tract.

Symptoms of toxic pulmonary edema

The development of toxic pulmonary edema occurs in several stages:

1. Reflex.
2. Hidden.
3. A stage with pronounced symptoms of toxic pulmonary edema.
4. Stage of recovery or reverse development.

IN initial stage(reflex) the patient exhibits the first signs:

• pain in the eyes;
• sore throat;
• lacrimation;
• heaviness in the chest;
• difficulty breathing;
• decreased breathing.

Subsequently, the victim's discomfort, however, breathing problems persist. This stage is called hidden or imaginary well-being. Its duration can be up to a day. During this period, pathological processes occur in the lungs, which manifest themselves with the following symptoms:

• wheezing;
• bubbling breathing;
• painful cough;
• discharge of foamy sputum from the patient’s mouth;
• increasing respiratory failure;
• blueness of the skin (cyanosis).

The patient's arterial pressure, the face becomes gray, the mucous membranes also take on an earthy tint. If the victim is not provided health care, toxic pulmonary edema will result in death.

Diagnosis and treatment of toxic pulmonary edema

Patients with suspected pulmonary edema are advised to undergo an X-ray examination, blood and urine tests. On x-ray vagueness and blurring of the contours of the lungs will be revealed. In the blood - leukocytosis, increased hemoglobin, excess blood clotting parameters.

Treatment of patients with respiratory failure due to poisoning occurs in intensive care units and includes:

1. Artificial ventilation.
2. Oxygen therapy.
3. Detoxification of the body.
4. Prevention of infections.

If there is no spontaneous breathing, the patient is intubated and connected to a ventilator. In case of acute poisoning, treatment of toxic edema begins with the administration of a dehydrating drug, lyophilized urea. The medicine increases the osmotic pressure of the blood and promotes the absorption of fluid from the lungs, improves the function of the lung tissue, and prevents the congestion of other vital important organs. After administration of the drug, the patient’s heart muscle function improves. The diuretic Furosemide has almost the same effect.

Advice! If it is not possible to transport the patient to the hospital, in order to prevent the increase in edema and reduce the load of the small circle, bloodletting up to 300 ml is performed. Another way is to apply venous tourniquets to the limbs.

To reduce the permeability of the vascular wall and the development of edema, victims are administered glucocorticoid drugs (Prednisolone), as well as antihistamines. In combination with this purpose, they prescribe ascorbic acid in a solution of glucose, calcium chloride.

Oxygen therapy with inhalation of defoamers, which convert foam into liquid, plays an important role in relieving pulmonary edema. The drugs clear the respiratory surface of the lungs and prevent the development of acute respiratory failure. Ethyl alcohol is successfully used in intensive care units.

If the use of diuretics during acute intoxication does not have an effect, emergency blood filtration using an artificial kidney apparatus is indicated. It is also recommended to administer colloidal solutions (Gelofusin) simultaneously with diuretics (Furosemide).

After emergency care and elimination of pulmonary edema, patients are prescribed oxygen therapy with bronchodilators and glucocorticoids. Oxygen treatment begins with a low concentration. The procedure lasts 10–15 minutes. Patients with are indicated in pressure chambers.

Important! If the victim is affected, such therapy is contraindicated. Chemical substance when inhaled, it may cause repeated swelling of the lung tissue.

Since the patient after acute chemical poisoning with severe respiratory failure is in a state of stress, he is prescribed sedatives which help relieve emotional stress. Antipsychotics are administered to reduce shortness of breath and anxiety.

To prevent secondary infection, patients are prescribed antibiotics. Drugs that prevent thrombosis (anticoagulants) are also indicated. For a speedy recovery from hypoxic conditions, patients are administered B vitamins, ascorbic acid, and vitamin P in large doses. Vitamin therapy accelerates tissue regeneration and accelerates redox processes, which is important for toxic lesions.

Find out what to do if it occurs: causes, treatment at home and in a hospital setting.

Read why they appear and how to help a person.

Read why and what to do to help the victims to him.

Prognosis for patients' lives

Severe forms of pulmonary edema often result in death if assistance is not provided in a timely manner or the victim is treated inadequately. If the patient received treatment on time and in full, changes in the lung tissue begin to reverse. A person is able to fully restore health within a few weeks.

The recovery period may be complicated by repeated pulmonary edema, infection and the development of pneumonia or thrombosis that occurred against the background of blood thickening in the acute period of the disease.

After the patient is discharged from the hospital, more late complications related to the respiratory and central organs nervous system: emphysema, pneumosclerosis, autonomic disorders, asthenia. Depending on the concentration of the toxic substance and the degree of damage to the body, the victim is likely to develop problems with the liver and kidneys.