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 defeat respiratory system has many serious implications. 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 internal cavity 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.
On this list possible causes 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:
- Developed (completed) form. In this case, the disease goes through 5 stages: reflex, latent, a period of increasing edema, completion and reverse development.
- abortion form. It is distinguished by the absence of the most difficult stage of completion.
- "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:
- "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.
- "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 last stage- reverse development: gradually cough, shortness of breath and sputum 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:
- Blockage of the airways. It occurs when excessive foam is released 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, 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 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 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 full 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 are taken, liver test. 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:
- Steroids;
- Diuretics;
- Bronchodilators;
- Glucose;
- Calcium chloride;
- 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.
Pulmonary edema is the cause of the painful death of many patients. It occurs most often as a complication of dysregulation of the amount of fluid that must circulate in the lungs.
At this moment, there is an active influx of fluid from the capillaries into the pulmonary alveoli, which overflow with exudate and lose the ability to function and take in oxygen. The person stops breathing.
This is an acute pathological condition that threatens life, requiring extremely urgent care, immediate hospitalization. The main characteristics of the disease are characterized acute lack of air, severe suffocation and death of the patient when no resuscitation measures are provided.
At this moment, there is an active filling of the capillaries with blood and the rapid passage of fluid through the walls of the capillaries into the alveoli, where there is so much of it that it greatly complicates the supply of oxygen. IN respiratory organs, gas exchange is disturbed, tissue cells experience acute insufficiency oxygen(hypoxia), the person suffocates. Often choking occurs at night during sleep.
Sometimes the attack lasts from 30 minutes to 3 hours, but often the excess accumulation of fluid in the extracellular tissue spaces increases at lightning speed, therefore resuscitation start immediately to avoid death.
Classification, from what happens
The causes and types of pathology are closely related, divided into two basic groups.
| Hydrostatic (or cardiac) pulmonary edema | |
It happens during diseases that are characterized by an increase in pressure (hydrostatic) inside the capillaries and further penetration of plasma from them into the pulmonary alveoli. The reasons for this form are:
|
|
| Non-cardiogenic pulmonary edema, which includes: | |
| iatrogenic | Occurs:
|
| Allergic, toxic (membranous) | It is provoked by the action of poisons, toxins that violate the permeability of the walls of the alveoli, when liquid penetrates into them instead of air, filling almost the entire volume. Causes of toxic pulmonary edema in humans:
Often passes without characteristic signs. The picture becomes clear only when X-rays are taken. |
| Infectious | Develops:
|
| aspiration | Occurs when a foreign body enters the lungs, the contents of the stomach. |
| Traumatic | Occurs with penetrating trauma chest. |
| Cancer | Occurs due to a malfunction of the functions of the pulmonary lymphatic system with difficulty in the outflow of lymph. |
| neurogenic | Main reasons:
|
Any asthma attack that occurs with such diseases is the basis for suspecting a state of acute swelling of the respiratory system.
Under these conditions alveoli become very thin, their permeability increases, integrity is broken, increases the risk of filling them with liquid.
At-risk groups
Since the pathogenesis (development) of pathology closely related to associated internal diseases , at risk are patients with diseases or factors provoking such a life-threatening condition.
The risk group includes patients suffering from:
- disorders of the vascular system, heart;
- damage to the heart muscle with hypertension;
- , respiratory systems;
- complex craniocerebral injuries, cerebral hemorrhages of various origins;
- meningitis, encephalitis;
- cancerous and benign neoplasms in brain tissues.
- pneumonia, emphysema, bronchial asthma;
- and increased blood viscosity; there is a high probability of separation of a floating (floating) clot from the wall of the artery with penetration into the pulmonary artery, which is blocked by a thrombus, which causes thromboembolism.
Doctors have found that athletes who actively practice excessive exercise have a serious chance of getting respiratory edema. These are scuba divers, climbers working at high altitudes (more than 3 km), marathon runners, divers, swimmers for long distances. For women, the risk of the disease is higher than for men.
Climbers have such a dangerous condition happens during rapid ascent to high altitude without pausing at intermediate levels.
Symptoms: how it manifests itself and develops in stages
Classification and symptoms are related to the severity of the disease.
| Severity | Severity of symptoms |
| 1 - on the border of development | Revealed:
|
| 2 - medium | Observed:
|
| 3 - heavy | Explicit symptoms:
|
| 4 degree - critical | Classic Manifestation critical condition:
|
First aid first aid: what to do if it occurs
Before the arrival of the ambulance, relatives, friends, colleagues don't waste a minute of time. To alleviate the patient's condition, do the following:
- Helping a person to sit up or half rise with their legs down
- If possible, they are treated with diuretics (they give diuretics - lasix, furosemide) - this removes excess fluid from the tissues, however, at low pressure, small doses of drugs are used.
- Organize the possibility of maximum access of oxygen to the room.
- The foam is sucked off and, if skillful, oxygen inhalations are performed through a solution of ethyl alcohol (96% of a couple - for adults, 30% alcohol vapor - for children).
- Prepare a hot foot bath.
- With skill - apply the imposition of tourniquets on the limbs, not too tightly pinching the veins in the upper third of the thigh. Leave tourniquets longer than 20 minutes, while the pulse should not be interrupted below the application sites. This reduces blood flow to the right atrium and prevents tension in the arteries. When the tourniquets are removed, it is done carefully, slowly loosening them.
- Continuously monitor the patient's breathing and pulse rate.
- For pain, give analgesics, if there is - promedol.
- With high blood pressure, benzohexonium, pentamine are used, which promote the outflow of blood from the alveoli, nitroglycerin, which dilates blood vessels (with regular measurement of pressure).
- In normal - small doses of nitroglycerin under the control of pressure indicators.
- If the pressure is below 100/50 - dobutamine, dopmin, which increase the function of myocardial contraction.
What is dangerous, the forecast
Pulmonary edema is a direct threat to life. Without taking extremely urgent measures, which should be carried out by the patient's relatives, without subsequent urgent active therapy in a hospital, pulmonary edema is the cause of death in 100% of cases. A person is waiting for suffocation, coma, death.
Attention! When the very first signs of an acute pathological situation appear, it is important to provide qualified assistance on the basis of a hospital as soon as possible, so an ambulance is called immediately.
Preventive measures
To prevent a threat to health and life, the following measures are necessarily assumed, meaning elimination of factors contributing to this condition:
- With heart disease (angina pectoris, chronic insufficiency) take funds for their treatment and at the same time - hypertension.
- With repeated edema of the respiratory organs, the procedure of isolated blood ultrafiltration is used.
- Prompt accurate diagnosis.
- timely adequate treatment asthma, atherosclerosis, other internal disorders that can cause such pulmonary pathology.
- Isolation of the patient from contact with any kind of toxins.
- Normal (not excessive) physical and respiratory stress.
Complications
Even if the hospital promptly and successfully managed to prevent suffocation and death of a person, therapy continues. After such a critical condition for the whole organism in patients often develop serious complications, most often in the form of constantly recurring pneumonia, difficult to treat.
Prolonged oxygen starvation has a negative effect on almost all organs. The most serious consequences are cerebrovascular accidents, heart failure, cardiosclerosis, ischemic organ damage. These diseases are a constant threat to life and can not do without intensive drug therapy.
These complications, despite the stopped acute pulmonary edema, are the cause of the death of a large number of people.
The greatest danger of this pathology is its speed and panic state. into which the patient and the people around him fall.
Knowledge of the basic signs of the development of pulmonary edema, the causes, diseases and factors that can provoke it, as well as emergency measures before the ambulance arrives, can lead to favorable outcome and the absence of consequences even with such a serious threat to life.
Actually toxic pulmonary edema is associated with damage by toxicants to cells involved in the formation of the alveolar-capillary barrier. Military-grade toxicants capable of causing toxic pulmonary edema are called asphyxiant HIT.
The main cause of disorders of many functions of the body in case of poisoning with pulmonotoxicants is oxygen starvation. Oxygen starvation that develops when affected by asphyxiants can be characterized as mixed type hypoxia: hypoxic (impairment external respiration), circulatory (impaired hemodynamics), tissue (impaired tissue respiration).
Hypoxia underlies severe violations energy exchange. At the same time, organs and tissues with high level energy consumption (nervous system, myocardium, kidneys, lungs). Violations on the part of these organs and systems underlie the clinic of intoxication with asphyxiating OVTV.
Chlorine
Chlorine was the first substance used in the war as an agent. On April 22, 1915, near the city of Ypres, the German units released it from cylinders (about 70 tons), directing a stream of gas driven by the wind towards the positions of the French troops. This chemical attack caused the death of more than 7,000 people. Later, the substance was widely used on the fronts of the 1st World War, and therefore the clinic of the lesion is well studied.
At present, chlorine is not considered as an OM. Nevertheless, millions of tons of substances are produced annually and used for technical needs: water purification (2 - 6%), bleaching of cellulose and fabrics (up to 15%), chemical synthesis (about 65%), etc. Chlorine is the most common cause industrial accidents.
Physicochemical characteristics. Toxicity
Chlorine is a yellowish-green gas with a characteristic suffocating odor, about 2.5 times heavier than air. Spreading in the contaminated atmosphere, it follows the terrain, flowing into pits and shelters. Well adsorbed activated carbon. Chemically very active. Chlorine is neutralized with an aqueous solution of hyposulfite. It is stored and transported in liquefied form under high blood pressure. In the event of accidents at production, storage, transportation and use facilities, mass injury to people is possible.
The mechanism of the damaging effect of chlorine on the cells of the respiratory system is associated with its high oxidative activity, the ability to form hydrochloric acid (a sharp change in the pH of the medium and denaturation of macromolecules) and hypochlorous acid when interacting with water. Hypochlorous acid forms chloramines in the cytosol of cells, which have a sufficiently high biological activity, can interact with unsaturated fatty acid bonds of phospholipids and form peroxides, block sulfhydryl groups of oligopeptides and proteins. Data have been obtained that in the reactions of hypochlorous acid with biomolecules, a superoxide radical is formed - the initiator of the process of free radical oxidation in cells.
The main manifestations of intoxication
In rare cases (with inhalation of extremely high concentrations), death can occur already at the first breaths of contaminated air. The cause of death is a reflex stop of breathing and cardiac activity. Another cause of rapid death of victims (within 20 - 30 minutes after inhalation of the substance) is lung burns. In these cases, the color skin the victim acquires a greenish tint, clouding of the cornea is observed.
More often, in cases of severe poisoning, at the time of exposure, the victims felt a sharp burning sensation in the area of the eyes and upper respiratory tract, and shortness of breath. The poisoned person seeks to ease breathing by tearing the collar of his clothes. At the same time, extreme weakness is noted, the poisoned fall and are unable to leave the affected area. Almost from the beginning of exposure, a hysterical, painful cough appears, later shortness of breath joins, and additional respiratory muscles. The affected person tries to take a position that facilitates breathing. Speech is impossible. Sometimes there is vomiting.
Some time after leaving the affected area, some relief of the condition (latent period) may occur, but more often (unlike phosgene damage), complete remission does not occur: cough persists, pain along the trachea and in the region of the diaphragm.
After some time (from several hours to a day), the condition worsens again, coughing and shortness of breath increase (up to 40 respiratory acts per minute), the face becomes cyanotic (blue type of hypoxia), and in extremely severe cases, ashy color. Wheezing is heard over the lungs. The victim constantly expectorates a foamy yellowish or reddish liquid (more than 1 liter per day). Severe headaches are observed, body temperature drops. The pulse is slow. Blood pressure drops. The victim loses consciousness and dies with symptoms of acute respiratory failure. If pulmonary edema does not lead to death, then after a few hours (up to 48), the condition begins to improve. However, in the future, the disease gradually passes into the next period - complications, during which the phenomena of bronchopneumonia usually develop.
This is the most severe form of lung toxicity.
The pathogenesis of toxic pulmonary edema cannot be considered definitive. Leading value in the development of toxic pulmonary edema belongs to an increase in the permeability of capillary membranes, which, apparently, can be facilitated by damage to the sulfhydryl groups of proteins in the lung tissue. The increase in permeability is carried out with the participation of histamine, active globulins and other substances released or formed in the tissue under the action of stimuli on it. Important in the regulation of capillary permeability belongs to the nervous mechanisms. So, for example, in the experiment it was shown that vagosympathetic novocaine blockade can reduce or even prevent the development of pulmonary edema.
Based on the clinical picture of toxic edema with the presence of leukocytosis and temperature reaction, as well as pathoanatomical data indicating the presence of confluent catarrhal inflammation, in the absence of microbial flora, some researchers consider pulmonary edema as one of the variants of toxic pneumonia, in which exudation processes are ahead of cellular infiltration.
The development of pulmonary edema causes a violation of gas exchange in the lungs. At the height of the edema, when the alveoli are filled with edematous fluid, the diffusion of oxygen and carbon dioxide is possible only due to the solubility of gases. At the same time, hypoxemia and hypercapnia gradually increase. At the same time, there is a thickening of the blood, an increase in its viscosity. All these factors lead to insufficient supply of tissues with oxygen - hypoxia. accumulate in tissues sour foods metabolism, the reserve alkalinity falls and the pH shifts to the acid side.
Clinically distinguish two forms of toxic pulmonary edema: developed, or completed, and abortive.
At developed form there is a consistent development of five periods: 1) initial phenomena (reflex stage); 2) hidden period; 3) the period of increase in edema; 4) the period of completed edema; 5) reverse development of edema.
Abortive form characterized by a change of four periods: 1) initial phenomena; 2) hidden period; 3) increase in edema; 4) reverse development of edema.
In addition to the two main ones, another form of acute toxic pulmonary edema is distinguished - the so-called " silent swelling”, which is detected only by X-ray examination of the lungs, while the clinical manifestations of pulmonary edema are practically absent.
The period of initial phenomena develops immediately after exposure to a toxic substance and is characterized by mild irritation of the mucous membranes of the respiratory tract: a slight cough, sore throat, chest pain. As a rule, these mild subjective disorders do not have a significant effect on the well-being of the victim and soon disappear.
The latent period follows the subsidence of irritation and can have a different duration (from 2 to 24 hours), more often 6-12 hours. During this period, the victim feels healthy, but with a thorough examination, the first symptoms of increasing oxygen deficiency can be noted: shortness of breath, cyanosis , pulse lability. It has been experimentally proven that in this "hidden" period from the very beginning it is possible to detect histological changes corresponding to edema of the interstitial tissue of the lung, therefore, the absence of clear clinical manifestations still does not indicate the absence of emerging pathology.
The period of increase in edema is clinically manifested, which is associated with the accumulation of edematous fluid in the alveoli and a more pronounced violation respiratory function. The victims have an increase in breathing, it becomes superficial and is accompanied by paroxysmal painful cough. Objectively, slight cyanosis is noted. In the lungs voiced fine bubbling wet rales and crepitus are heard. During X-ray examination in this period, one can note fuzziness, blurring of the pulmonary pattern, small ramifications of blood vessels are poorly differentiated, some thickening of the interlobar pleura is noted. The roots of the lungs are somewhat dilated, have fuzzy contours.
Identification of signs of increasing toxic pulmonary edema is very important for appropriate therapeutic and preventive measures to prevent the development of edema.
The period of completed edema corresponds to further progression pathological process. During toxic pulmonary edema, two types are distinguished: "blue hypoxemia" and "gray hypoxemia". With the "blue" type of toxic edema, pronounced cyanosis of the skin and mucous membranes is noted, pronounced shortness of breath - up to 50-60 breaths per minute. In the distance, bubbling breathing is heard. Cough with large amounts of frothy sputum, often containing blood. During auscultation, a mass of different-sized wet rales is found throughout the lung fields. Tachycardia is noted, blood pressure remains normal or even slightly increased. When examining blood, its significant thickening is revealed: the content of hemoglobin increases. Coagulation is enhanced. The arterialization of blood in the lungs is disturbed, which is manifested by a deficiency in arterial blood oxygen saturation with a simultaneous increase in carbon dioxide content (hypercapnic hypoxemia). Compensated gaseous acidosis develops.
With the "gray" type of toxic edema, the clinical picture is more severe due to the addition of pronounced vascular disorders. The skin becomes pale gray in color. Face covered with cold sweat. The limbs are cold to the touch. The pulse becomes frequent and small. There is a drop in blood pressure. The gas composition of the blood in these cases is characterized by a decrease in oxygen saturation and reduced content carbon dioxide (hypoxemia with hypocapnia). The coefficient of oxygen utilization and its arteriovenous difference decrease. The state of "gray hypoxemia" may be preceded by a period of "blue hypoxemia". Sometimes the process begins immediately according to the type of "gray hypoxemia". This can be facilitated physical exercise, prolonged transportation of the victim.
Cardiac disorders vascular system with toxic pulmonary edema, they are caused by impaired blood flow in the pulmonary circulation with an overload of the "acute pulmonary heart" type, as well as myocardial ischemia and autonomic changes. Regardless of the type of edema in the stage of completed edema, an increase in the blurring of the lung pattern and the appearance in the lower and middle sections of small (2-3 mm) spotted shadows at first, which later increase in size due to the merging of individual foci, form fuzzy contoured shadows resembling "flakes of melting snow" Areas of darkening alternate with enlightenments due to emerging foci of bullous emphysema. The roots of the lungs become even wider with fuzzy contours.
The transition of the period of increasing to expanded pulmonary edema often occurs very quickly, characterized by a rapidly progressive course. Severe forms of pulmonary edema can be fatal in 24-48 hours. In milder cases and with timely intensive care, a period of regression of pulmonary edema occurs.
During the reverse development of edema, coughing and the amount of sputum discharge gradually decrease, shortness of breath subsides. Cyanosis decreases, weaken, and then wheezing in the lungs disappears. X-ray studies indicate the disappearance of first large and then small focal shadows, only the fuzziness of the lung pattern and the contours of the roots of the lungs remains, and after a few days the normal X-ray morphological picture of the lungs is restored, the composition of the peripheral blood is normalized. Recovery can have significant variability in terms - from several days to several weeks.
The most common complication of toxic pulmonary edema is the addition of infection and the development of pneumonia. During the period of subsiding of the clinical manifestations of edema and improvement 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 mucopurulent sputum. In the lungs, areas of finely bubbling wet rales appear or increase. In the blood, leukocytosis increases and an acceleration of ESR appears. Radiologically, small pneumonic foci of the type of small-focal pneumonia are noted. Another serious complication of toxic edema is the so-called "secondary" pulmonary edema, which can develop at the end of the 2nd - the middle of the 3rd week, as a result of the onset of acute heart failure. In the long-term follow-up after toxic pulmonary edema, toxic pneumosclerosis and pulmonary emphysema may develop. An exacerbation of previously latent pulmonary tuberculosis and other chronic infections may occur.
In addition to changes in the lungs and of cardio-vascular system, with toxic pulmonary edema, changes are often found nervous system. The victims complain of headache, dizziness. Relatively often, instability in the neuro-emotional sphere is revealed: irritability, anxiety, the predominance of depressive-hypochondriac reactions, in some victims - agitation and convulsions, and in severe cases - stupor, drowsiness, adynamia, loss of consciousness. In the future, the addition of asthenoneurotic and vegetative disorders is possible.
At the height of toxic edema, diuresis sometimes decreases, up to anuria. In the urine, traces of protein, hyaline and granular cylinders, erythrocytes are found. These changes are associated with the possibility of developing toxic kidney damage due to general vascular changes.
With pulmonary edema, liver damage is often noted - a slight increase in the organ, a change in functional liver tests by type toxic hepatitis. These changes in the liver can persist for quite some time. long terms, often combined with functional disorders gastrointestinal tract.
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 lung collapse, massive pleural effusion and pneumonia involving large areas of the lung parenchyma, status asthmaticus, pulmonary embolism, etc.) most often, doctors detect pulmonary edema - a pathological process in which excess fluid accumulates in the interstitial tissue of the lungs, and later in the alveoli themselves .
Toxic edema lungs are associated with damage, and in connection with this, an increase in the permeability of the alveolar-capillary membrane (in the literature, toxic pulmonary edema denoted 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) heavy 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 research. 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:
1). The initial reflex stage.
2). Stage of hidden phenomena.
3). The stage of development of pulmonary edema.
4). Stage of outcomes and complications (reverse development).
1). It is known that after exposure to 0V asphyxiation or other irritating gases, there is a slight cough, a feeling of tightness in the chest, general weakness, headache, rapid shallow breathing with a distinct slowing of the pulse. 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 organism. 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 unpleasant subjective feelings initial period pass and comes the so-called hidden period, or period of imaginary well-being. The shorter it is, the heavier it is. clinical course illness. 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 by increased permeability with plasma release and shaped elements blood 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).
Initial signs 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 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 various forms:
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 more deaths. Starting from the third day, the general condition of patients improves markedly, the process enters the last phase - period of reverse development.
4). 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. People who have suffered a severe injury sometimes have long-term consequences in the form of chronic bronchitis and emphysema, interstitial pneumonia and pneumosclerosis.
Clinical forms defeat. Depending on the concentration of 0V vapors and SDYAV, exposure and the state of the body, there may be mild, moderate and severe lesions.
At lung injury degree, the initial stage is weakly 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 opacities confluent nature, usually recorded in both lungs, as well as the presence of emphysema in the supraphrenic 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 lethal outcome: 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. Meninges and the substance of the brain are full-blooded, in some places there are petechial hemorrhages, sometimes vascular thrombosis and softening foci.
In case of more late 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 vagus nerve 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;
IN). 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 agents are used superficially. active means(ethanol).
In case of pulmonary edema, sedatives(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). 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 medical assistance. 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. In this case, it is required to determine the sequence in the implementation of the complex medical measures acting on 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. Used as defoamers ethanol(30% solution in patients who are in 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, corglicon, aminofillin and other means, 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 cupping dangerous symptoms pulmonary edema, reduction of shortness of breath, improvement of cardiac activity and general condition, the main attention is paid to the prevention of complications and full recovery 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 hypoxia.
| № p p | Indicators | blue form | gray form |
| 1. | Coloration of the skin and visible mucous membranes | Cyanosis, blue-purple color | Pale, blue-gray or ash gray |
| 2. | Breathing state | Dyspnea | Sharp shortness of breath |
| 3. | Pulse | The rhythm is normal or moderately rapid, satisfactory filling | Threadlike, frequent, weak filling |
| 4. | Arterial pressure | Normal or slightly elevated | Dramatically lowered |
| 5. | Consciousness | Saved, sometimes excitation phenomena | Often unconscious, no arousal |
| Content in arterial and venous blood | Oxygen deficiency with excess in the blood (hypercapnia) | Acute insufficiency with a decrease in blood levels (hypocapnia) |
Measures in the outbreak and at the stages of medical evacuation in case of damage to agents and SDYAV of asphyxiating action.
| Type of medical care | Normalization of the main nervous processes | Normalization of metabolism, elimination of inflammatory changes | Unloading the pulmonary circulation, reducing vascular permeability | Elimination of hypoxia by normalizing blood circulation and respiration |
| First aid | Putting on a gas mask; inhalation of ficilin under a gas mask | Shelter from the cold, warm with a medical cape and in other ways | Evacuation on a stretcher of all affected with a raised head end or in a sitting position | Artificial respiration reflex respiratory arrest |
| First aid | Inhalation of ficilin, abundant washing of the eyes, mouth and nose with water; promedol 2% i / m; phenazepam 5 mg orally | Warming | Tourniquets for compression of the veins of the extremities; evacuation with a raised head end of the stretcher | Removing the gas mask; inhalation of oxygen with alcohol vapors; cordiamine 1 ml IM |
| First aid | Barbamil 5% 5 ml IM; 0.5% solution of dicaine, 2 drops per eyelid (according to indications) | Diphenhydramine 1% 1 ml IM | Bloodletting 200-300 ml (with the blue form of hypoxia); lasix 60-120 mg IV; vitamin C 500 mg orally | Suction of fluid from the nasopharynx with the help of DP-2 inhalation of oxygen with alcohol vapor; strophanthin 0.05% solution 0.5 ml in glucose solution IV |
| Qualified help | Morphine 1% 2 ml subcutaneously, anaprilin 0.25% solution 2 ml IM (with blue form of hypoxia) | Hydrocortisone 100-150 mg IM, diphenhydramine 1% 2 ml IM, penicillin 2.5-5 million units per day, sulfadimethoxine 1-2 g/day. | 200-400 ml of 15% mannitol solution IV, 0.5-1 ml of 5% pentamin solution IV (with blue form of hypoxia) | Aspiration of fluid from the nasopharynx, inhalation of oxygen with alcohol vapor, 0.5 ml of 0.05% strophanthin solution intravenously in a glucose solution, inhalation of carbogen. |
| Specialized assistance | A complex of diagnostic, therapeutic and rehabilitation measures carried out in relation to the affected using complex techniques, using special equipment and equipment in accordance with the nature, profile and severity of the lesion | |||
| medical rehabilitation | A complex of medical and psychological measures to restore combat and working capacity. |
Physical properties SDYAV, features of the development of toxic pulmonary edema (TOL).
| Name | Physical properties | Poison entry routes | Industries where there may be contact with poison | LC100 | Feature of the PPE clinic. |
| Isocyanates (methyl isocyanate) | Liquid b / tsv. with a pungent odor Boil T=45°C | Inhalation ++++ H/c ++ | Paints, varnishes, insecticides, plastics | May cause instant death like HCN | Irritant effect on the eyes, upper. breath. way. Latent period up to 2 days, reduced body t. There is only an insulating gas mask in the hearth. |
| Sulfur pentafluoride | Liquid b / color | Inhalats. +++ H / c - V / gastrointestinal tract - | By-product of sulfur production | 2.1 mg/l | The development of TOL according to the type of phosgene poisoning, but with a more pronounced cauterizing effect on the lung tissue. Protects the filtering gas mask |
| Chloropicrin | B / color liquid with a pungent odor. t bale = 113°С | Inhalats. ++++ B/c++ V/GI++ | Educational AE | 2 g/m 3 10 minutes | Acute eye irritation, vomiting, shortened latency, methemoglobin formation, weakness of the cardiovascular system. Protects the filtering gas mask. |
| Phosphorus trichloride | B / color liquid with a strong odor. | Inhalats. +++ B/C++ Eyes++ | Receipt | 3.5 mg/l | Irritation of the skin, eyes, shortened latent period with TOL. Exceptionally insulated. mask. Skin protection is a must. |
