Respiratory failure in children: forms, degrees and treatment. What parents need to know about respiratory failure
Acute respiratory failure is an extremely dangerous condition that is accompanied by a sharp decrease in oxygen levels in the blood. Such a pathology can arise from various reasons, but regardless of the mechanism of development, it poses a serious threat to human life. That is why it is useful for every reader to learn about what such a condition is. What symptoms does it accompany? What are the rules of first aid?
What is respiratory failure?
Acute respiratory failure is a pathological syndrome that accompanies a change in the normal blood gas composition. In patients in similar condition there is a decrease in oxygen levels with a simultaneous increase in the amount carbon dioxide in blood. The presence of respiratory failure is indicated if the partial pressure of oxygen is below 50 mm Hg. Art. In this case, the partial pressure of carbon dioxide, as a rule, is above 45 - 50 mm Hg. Art.
In fact, a similar syndrome is characteristic of many diseases of the respiratory, cardiovascular and nervous systems. Developing hypoxia (oxygen starvation) is most dangerous for the brain and heart muscle - these are the organs that suffer first.
The main mechanisms of respiratory failure
Today, there are several classification systems for this condition. One of them is based on the development mechanism. If we take this particular criterion into account, then respiratory failure syndrome can be of two types:
- Respiratory failure type 1 (pulmonary, parenchymal, hypoxemic) is accompanied by a decrease in oxygen levels and partial pressure in arterial blood. This form of pathology is difficult to treat with oxygen therapy. Most often, this condition develops against the background of cardiogenic pulmonary edema, severe pneumonia or respiratory distress syndrome.
- Respiratory failure of the second type (ventilation, hypercapnic) is accompanied by a significant increase in the level and partial pressure of carbon dioxide in the blood. Naturally, there is a decrease in oxygen levels, but this phenomenon is easily eliminated with oxygen therapy. As a rule, this form of failure develops against the background of weakness of the respiratory muscles, as well as when the functioning of the respiratory center is disrupted or the presence of mechanical defects of the chest.
Classification of respiratory failure by causes
Naturally, many people are interested in the reasons for the development of such dangerous condition. And it’s immediately worth noting that many diseases of the respiratory system (and not only) can lead to a similar result. Depending on the cause of occurrence, respiratory system failure is usually divided into the following groups:
- The obstructive form of insufficiency is associated primarily with difficulty in the passage of air through the respiratory tract. A similar condition occurs with diseases such as inflammation of the bronchi, entry of foreign substances into the airways, as well as pathological narrowing of the trachea, spasm or compression of the bronchi, and the presence of a tumor.
- There are other respiratory diseases that lead to failure. For example, restrictive type this state occurs against the background of a limitation in the ability of lung tissue to expand and collapse - the depth of inspiration is significantly limited in patients. Failure develops with pneumothorax, exudative pleurisy, as well as the presence of adhesions in the pleural cavity, pneumosclerosis, kyphoscoliosis, and limited rib mobility.
- Accordingly, mixed (combined) failure combines both factors (changes in lung tissue and obstruction of air flow). Most often, this condition develops against the background of chronic cardiopulmonary diseases.
- Naturally, there are other reasons. Respiratory failure of the hemodynamic type is associated with a violation normal circulation blood. For example, a similar phenomenon is observed with thromboembolism and some heart defects.
- There is also a diffuse form of insufficiency, which is associated with significant thickening of the capillary-alveolar wall. In this case, the penetration of gases through tissues is disrupted.
Severity of respiratory failure
The severity of the symptoms that accompany respiratory failure also depends on the severity of the condition. The degrees of severity in this case are as follows:
- The first or minor degree of insufficiency is accompanied by shortness of breath, which, however, occurs only with significant physical activity. At rest, the patient's pulse is about 80 beats per minute. Cyanosis at this stage is either absent altogether or mildly expressed.
- Second or moderate degree insufficiency is accompanied by the appearance of shortness of breath already at normal levels physical activity(for example, when walking). You can clearly see a change in skin color. The patient complains of a constant increase in heart rate.
- At the third, severe degree of respiratory failure, shortness of breath appears even at rest. At the same time, the patient’s pulse increases sharply and cyanosis is pronounced.
In any case, it is worth understanding that, regardless of the severity, such a condition requires qualified medical care.
Features and causes of acute respiratory failure in children
Unfortunately, respiratory failure in children in modern medicine is not considered uncommon, since this condition develops when various pathologies. Moreover, some anatomical and physiological characteristics child's body increase the likelihood of such a problem occurring.
For example, it is no secret that in some babies the respiratory muscles are very poorly developed, which leads to impaired ventilation of the lungs. In addition, respiratory failure in children may be associated with narrow airways, physiological tachypnea, and less surfactant activity. At this age, insufficient functioning of the respiratory system is the most dangerous, because the baby’s body is just beginning to develop, and a normal blood gas balance for tissues and organs is extremely important.
Main symptoms of acute respiratory failure
It’s worth saying right away that clinical picture and the intensity of symptoms directly depend on the type of deficiency and the severity of the patient’s condition. Of course, there are several main signs that you should definitely pay attention to.
The first symptom in this case is shortness of breath. Breathing difficulties can occur both during physical activity and at rest. Due to such difficulties, the number breathing movements increases significantly. As a rule, cyanosis is also observed. First, a person’s skin turns pale, after which it acquires a characteristic bluish tint, which is associated with oxygen deficiency.
Acute respiratory failure of the first type is accompanied by a sharp decrease in the amount of oxygen, which leads to disruption of normal hemodynamics, as well as severe tachycardia, a moderate decrease blood pressure. In some cases, there is a disturbance of consciousness, for example, a person cannot recreate recent events in his memory.
But with hypercapnia (failure of the second type), along with tachycardia, headaches, nausea, and sleep disturbances appear. A sharp increase in carbon dioxide levels can lead to the development of a coma. In some cases there is an increase cerebral circulation, sharp increase intracranial pressure, and sometimes cerebral edema.
Modern diagnostic methods
Acute respiratory failure requires correct diagnosis, which helps to determine the severity of such a condition and discover the causes of its occurrence. First, the doctor must examine the patient, measure blood pressure, determine the presence of cyanosis, count the number of respiratory movements, etc. In the future it will be necessary laboratory analysis blood gas composition.
After first aid is provided to the patient, additional studies are carried out. In particular, the doctor must study the functions of external respiration - tests such as peak flowmetry, spirometry and others are carried out functional tests. X-ray can detect lesions of the chest, bronchi, lung tissue, blood vessels, etc.
Acute respiratory failure: emergency care
Often this condition develops unexpectedly and very quickly. That is why it is important to know what it looks like first aid with respiratory failure. First of all, you need to give the patient's body the correct position - for this purpose, doctors recommend laying the person on a flat surface (floor), preferably on his side. In addition, you need to tilt the patient's head back and try to push lower jaw forward - this will help prevent the tongue from sinking and blocking respiratory tract. Naturally, call an ambulance, since further treatment only possible in a hospital setting.
There are some other measures that acute respiratory failure sometimes requires. Emergency care may also include cleansing oral cavity and pharynx from mucus and foreign substances (if you have such an opportunity). If respiratory movements stop, it is advisable to carry out artificial respiration"mouth to nose" or "mouth to mouth".
Chronic form of respiratory failure
Of course, this form of pathology is also quite common. Chronic respiratory failure, as a rule, develops over the years against the background of certain diseases. For example, the cause may be chronic or acute bronchopulmonary diseases. Failure may result from damage to the central nervous system, pulmonary vasculitis, as well as damage to peripheral muscles and nerves. Risk factors include some cardiovascular diseases, including hypertension of the pulmonary circulation. Sometimes the chronic form occurs after incorrect or incomplete treatment acute failure.
For quite a long time, the only symptom of this condition may be shortness of breath, which occurs during physical exertion. As the pathology progresses, the signs become brighter - pallor appears, and then cyanosis of the skin, observed frequent illnesses respiratory system, patients complain of constant weakness and fatigue.
As for treatment, it depends on the cause of development chronic failure. For example, patients are recommended to undergo therapy for certain diseases of the respiratory system, and medications are prescribed to correct the functioning of the respiratory system. of cardio-vascular system etc.
In addition, it is necessary to restore the normal gas balance of the blood - for this purpose oxygen therapy, special drugs that stimulate breathing, and also breathing exercises, special gymnastics, Spa treatment etc.
Modern methods of treatment
Respiratory failure syndrome in the absence of therapy will sooner or later lead to fatal outcome. That is why you should never refuse medical prescriptions or ignore the recommendations of a specialist.
Treatment of respiratory failure has two goals:
- First of all, it is necessary to restore and maintain normal blood ventilation and normalize the blood gas composition.
- In addition, it is extremely important to discover primary cause development of deficiency and eliminate it (for example, prescribe appropriate therapy for pneumonia, pleurisy, etc.).
The technique for restoring ventilation and blood oxygenation depends on the patient’s condition. First, oxygen therapy is performed. If the person can breathe on their own, additional oxygen is given through a mask or nasal catheter. If the patient is in comatose, then the doctor performs intubation, after which he connects an artificial respiration apparatus.
Further treatment directly depends on the cause of the deficiency. For example, in the presence of infections, antibacterial therapy is indicated. In order to improve drainage function bronchi, mucolytic and bronchodilator drugs are used. In addition, therapy may include chest massage, physical therapy, ultrasound inhalations and other procedures.
What complications are possible?
It is worth emphasizing once again that acute respiratory failure poses a real threat to human life. In the absence of timely medical care, the likelihood of death is high.
In addition, there are other dangerous complications. In particular, with oxygen deficiency, the central nervous system is primarily affected. Damage to the brain over time can lead to a gradual decline in consciousness until a coma.
Often, against the background of respiratory failure, so-called multiple organ failure develops, which is characterized by disruption of the intestines, kidneys, liver, and the appearance of gastric and intestinal bleeding.
No less dangerous is chronic insufficiency, which primarily affects the functioning of the cardiovascular system. Indeed, in such a condition, the heart muscle does not receive enough oxygen - there is a risk of developing right ventricular heart failure, hypertrophy of parts of the myocardium, etc.
That is why you should never ignore the symptoms. Moreover, it is extremely important to know about the main symptoms of such a dangerous condition, as well as what first aid looks like for acute respiratory failure - correct actions can save a person's life.
They call it a condition when the breathing process is not able to provide the body with a sufficient volume of oxygen and remove the required volume of carbon dioxide.
Clinical picture
This disease in children can cause serious consequences, so parents should know what factors influence the appearance of pathology. This condition occurs in childhood may be due to a number of reasons. Doctors consider the main ones to be:
Types of respiratory failure in children
By mechanism of appearance this problem divided into parenchymal and ventilation.
Respiratory failure can also be acute (AR) or chronic. The acute form develops within a short time, while chronic failure can last for several months or even years.
Degrees of respiratory failure
Based on their severity, it is customary to distinguish 4 degrees of this pathology, which differ in clinical manifestations.
Breathing disorders in newborns
Respiratory failure can also occur in infants. The reasons for this may be:
Respiratory failure in newborn premature babies is caused by respiratory distress syndrome.
All principles of treatment are aimed at restoring airway patency, getting rid of bronchospasms and pulmonary edema, as well as having a positive effect on the respiratory function of the blood and eliminating metabolic disorders.
Symptoms of acute and chronic respiratory failure
Symptoms acute form diseases are:
With chronic deficiency, the same symptoms occur as in children, only they do not appear immediately, but gradually. But it is worth noting that children this pathology develops much faster than in adults. This can be explained by the peculiarities of the anatomy of the child’s body.
Children are more susceptible to swelling of the mucous membrane, their secretions form faster, and the muscles of the respiratory system are not as developed as in adults.
Children's oxygen needs are much greater than those of adults, so the consequences of respiratory failure can be more serious. With chronic insufficiency, the timbre of the child’s voice changes, a cough appears, and wheezing is heard when breathing.
Complications of pathology
Respiratory failure is a very serious disorder that can lead to serious consequences. From the cardiovascular system, ischemia, arrhythmia, pericarditis, and hypotension may occur.
This condition also affects the nervous system. It can cause psychosis, polyneuropathy, decreased mental activity, muscle weakness and even coma.
Also, respiratory failure can cause stomach ulcers, bleeding in digestive tract, disruption of the liver and gallbladder. Acute respiratory failure even threatens the child's life.
Treatment of respiratory failure in children
First, all treatment is aimed at restoring pulmonary ventilation and clearing the airways. For this purpose, oxygen treatment is used, which helps normalize the blood gas composition. Oxygen is prescribed even to those patients who breathe on their own.
To treat chronic failure, in most cases, respiratory therapy is prescribed, which includes:
- inhalation;
- respiratory physiotherapy;
- oxygen therapy;
- aerosol therapy;
- taking antioxidants.
If breathing problems in young patients are caused by infections, they are prescribed antibiotics. The choice of these drugs occurs only after a sensitivity test has been performed.
In order to clear the bronchi of secretions accumulated there, the patient is prescribed expectorants - a mixture from the Altai root, Mucaltin. Doctors can also remove sputum from the bronchi through the nose or mouth using an endobronchoscope.
After the child's breathing has returned to normal, doctors begin symptomatic therapy. If a child has had pulmonary edema, he is prescribed diuretics. Furosemide is most often used. To eliminate pain, the child is prescribed painkillers - Panadol, Ibufen, Nimesil.
Basic diagnostic methods
First of all, the doctor studies the patient’s medical history and learns about disturbing symptoms. It is very important to determine if the child has diseases that could cause the development of deficiency.
Next is carried out general examination. During it, a specialist examines the chest and skin the patient, counts the respiratory rate and heartbeat, listens to the lungs with a phonendoscope.
Also mandatory research This pathology is diagnosed by analyzing the gas composition of the blood. It makes it possible to find out the degree of its saturation with oxygen and carbon dioxide. Also being studied acid-base balance blood.
Additional diagnostic methods are chest radiography and magnetic resonance imaging. In some cases, the doctor may prescribe a consultation with a pulmonologist for the child.
First aid for children with acute respiratory failure
This is dangerous pathological condition can develop very quickly, so every parent should know how to provide first aid to their child.
The baby should be placed on his right side and his chest should be freed from tight clothing. To prevent the tongue from sticking and further blocking the airway, the child’s head must be tilted back. If possible, you need to remove mucus and foreign bodies (if any) from the nasopharynx. This can be done using a gauze napkin. Next you need to wait for an ambulance.
Doctors will perform suction of secretions from the airway, intubation of the trachea, or other procedures to allow the child to start breathing again. Then the baby can be connected to a ventilator and continue treatment in the hospital.
Preventive measures
Since respiratory failure is not separate disease, but a symptom of others serious illnesses and a consequence of mechanical influences, then prevention of this condition lies in the timely treatment of these causes. It is also very important to limit the child from contact with allergens and toxic substances.
In addition, you need to regularly have your child examined by specialists so that they can identify any pathologies of the respiratory system as early as possible.
Respiratory failure is a very serious pathological condition that can lead to hypoxia and even death. Therefore, everyone needs to know what to do with this disease. If all measures are taken on time, then eliminate this symptom can be done quite easily. The main thing is to pay attention to all the child’s complaints and not to delay going to the doctor.
79. Respiratory failure in children. Causes, clinic, severity. Urgent Care
Acute respiratory failure (ARF) is a situation in which the body is unable to maintain a partial pressure of oxygen and/or carbon dioxide in the blood that is adequate to tissue metabolism. In the mechanism of development of acute respiratory failure, the leading role is played by disturbances in ventilation and membrane gas exchange processes. In this regard, ODN are divided into the following types.
Type I. Pulmonary ARF:
· Obstructive-constrictive:
– top type;
– bottom type.
· Parenchymatous.
· Restrictive.
Type II. Ventilation unit:
· Central.
· Thoracoabdominal.
· Neuromuscular.
According to pathogenesis, respiratory failure is divided into hypoxic (lack of oxygen) and hypercapnic (excess carbon dioxide).
Hypoxic respiratory failure (type I, pulmonary) is characterized by a decrease in the partial pressure of oxygen in the blood (PaO2) to less than 60 mm Hg. Art. at normal or reduced partial pressure of carbon dioxide in the blood (PaCO2). A decrease in PaO2 can be caused by:
– discrepancy between ventilation of the lungs and their perfusion;
– intrapulmonary shunting of blood from right to left;
– a decrease in the partial pressure of oxygen in the inhaled air or barometric pressure;
– impaired diffusion of gases through the alveolo-capillary membrane: factors leading to a decrease in diffusion are an increase in the distance between the alveoli and erythrocytes during fibrosing pulmonary processes, a decrease in the oxygen gradient for diffusion, as well as a shortening of the time interval for the transit of erythrocytes through the capillaries;
– alveolar hypoventilation;
– decreased oxygen saturation of venous blood.
Hypoxemia in ARF is most often caused by a violation of the pulmonary ventilation/blood flow ratio (Va/Q), intrapulmonary shunting of blood from right to left and a decrease in residual oxygenation - pVO2. Diffusion disorders and hypoventilation play a lesser role.
Hypercapnic respiratory failure (type II, ventilation) is characterized by an increase in PaCO2 to a level of more than 50 mmHg. Art. and develops when the body is unable to provide proper ventilation to the lungs. Hypercapnia is based on a discrepancy between alveolar ventilation and excessive accumulation of carbon dioxide in the blood and tissues. This condition can occur with obstructive and restrictive breathing disorders, disturbances in the regulation of breathing of central origin, a pathological decrease in the tone of the respiratory muscles of the chest, etc. In fact, it turns out that hypercapnia is superimposed on the patient’s existing hypoxia, and this, in turn, is accompanied by the development respiratory acidosis, which in itself worsens the patient's condition. Excessive accumulation of CO2 in the body disrupts the dissociation of oxyhemoglobin and causes hypercatecholaminemia. The latter causes arteriolospasm and an increase in heart rate (HR). Carbon dioxide is a natural stimulant of the respiratory center, therefore, in the initial stages, hypercapnic syndrome is accompanied by the development of hyperpnea, but as it accumulates excessively in the arterial blood, depression of the respiratory center develops. Clinically, this is manifested by the development of hypopnea and the appearance of respiratory rhythm disturbances, bronchial secretion increases sharply, heart rate increases compensatoryly and blood pressure rises. In the absence of proper treatment, a coma develops. Death occurs from respiratory or cardiac arrest. An integral indicator of hypercapnic syndrome is an increased level of partial pressure of carbon dioxide in arterial blood (PaCO2).
When starting the treatment of acute respiratory failure, it is necessary first of all to highlight the cardinal criteria that determine the type of acute respiratory failure and the dynamics of its development. It is necessary to highlight the main symptoms that require priority correction. Hospitalization for any type of acute respiratory failure is mandatory.
There are quite a few causes of respiratory failure, including acute. These are diseases of the upper and lower respiratory tract, lung parenchyma; airway obstruction due to vomiting and regurgitation, foreign bodies, tongue retraction, pneumo- and pyothorax, as well as chest trauma. In addition, diseases and injuries of the central nervous system, damage to nerve pathways, muscular dystrophies, myasthenia gravis (Table 1).
The main manifestations of DN are hypoxemia, hypo- and hypercapnia. Moreover, hypercapnia never occurs without hypoxemia if the child breathes atmospheric air. Hypoxemia is often combined with hypocapnia.
Obstructive DN can be caused by mechanical reasons in the case of initially healthy airways (aspiration of a foreign body), the development of edema of the mucous membrane (subglottic laryngotracheitis), the presence of bronchiolospasm (an attack of bronchial asthma), compression of the airways from the outside (vascular ring or doubling of the aorta, foreign body esophagus, inflammatory diseases of the oropharynx, etc.), as well as congenital developmental defects (choanal atresia, laryngomalacia, cystic fibrosis). Often there is a combination of several factors (for example, inflammatory swelling of the mucous membrane with impaired sputum evacuation, etc.). When large airways are affected, inspiratory dyspnea is observed, and when the patency of small ones (bronchioles) is impaired, expiratory dyspnea is observed. A special mechanism of respiratory failure in children occurs when bronchial asthma or so-called valvular emphysema due to sudden overstretching of the alveoli by accumulated air. This causes disruption of capillary circulation. Reducing overextension of the alveoli after relieving bronchospasm helps eliminate respiratory failure.
Upper type of obstructive-constrictive ARF
Acute obstruction of the upper respiratory tract due to narrowing of the larynx and bronchi is the most common reason ODN in children. The following factors predispose it to its frequent occurrence: narrow airways, loose tissue of the subglottic space of the larynx, the tendency of children to laryngospasm, relative weakness of the respiratory muscles. In the subglottic space, with viral lesions, allergic conditions, and trauma, swelling quickly occurs and life-threatening stenosis progresses. Against the background of narrow airways in young children, edema of 1 mm leads to a narrowing of the lumen by up to 50%. In addition to edema, in the genesis of obstruction important role belongs to the spastic component and mechanical blockage (foreign body, mucus, fibrin). All three pathological factors are present in upper airway obstruction of any origin.
Atopic, exudative-catarrhal and lymphatic constitutional anomalies, polluted air (including passive smoking), iron deficiency conditions, and paratrophy also predispose to the development of upper respiratory tract obstruction syndrome.
The main cause of upper airway obstruction is viral infections, less often – bacterial. The first place in frequency is parainfluenza virus type I (75% of all cases), followed by the PC virus, adenovirus (in preschool children), influenza and measles viruses. Of the bacterial pathogens, the most common cause of obstruction was previously diphtheria bacillus, now it is Haemophilus influenzae type b and the epiglottitis caused by it. The causative agent of epiglottitis can also be streptococcus (more often with croup, which complicates the course of an acute respiratory infection at the end of the first week of the disease).
The listed etiological factors cause catarrhal (viruses), edematous (allergies), edematous-infiltrative (viruses, allergies, chemical and physical agents), fibrinous and fibrinous-purulent (diphtheria, streptococci), ulcerative-necrotic (diphtheria, staphylococci and other bacteria) changes in the mucous membrane of the larynx.
Inspiratory stridor is observed with the following changes in the respiratory tract.
· Narrowing of the nasal cavity: noise with stridor resembles sounds during sniffing, occurs with nonspecific rhinitis in infants, syphilitic rhinitis (congenital syphilis) in newborns and children in the first months of life, infectious and allergic rhinitis, when the nasal passages are blocked by a foreign body or choanal stenosis.
· The narrowing of the pharynx before entering the larynx causes a peculiar sound similar to snoring. It occurs when the tongue is retracted in unconscious children, with a deep position of the tongue due to lower micrognathia, especially with Pierre Robin syndrome; with abundant accumulation of secretion in the pharynx, obstructing the passage of air, which is observed in patients with laryngeal paralysis, retropharyngeal abscess, purulent epiglottitis.
· Narrowing of the larynx: characteristic signs – persistent barking cough and hoarseness of the voice that occurs with influenza croup, as well as croup against the background of measles, diphtheria and other diseases, with phlegmonous epiglottitis, congenital laryngeal and tracheal stridor with softening of the cartilaginous base of the trachea and bronchi and a peculiar stridorous sound reminiscent of chicken squealing; with rickets (laryngospasm as a manifestation of life-threatening spasmophilia) and the consequences of traumatic injuries to the larynx (external trauma or intubation with subsequent swelling of the mucous membrane and submucosal hemorrhage).
Mixed, inspiratory and expiratory stridor may indicate tracheobronchitis, including severe laryngotracheitis (viral croup), diphtheria croup with an abundance of pseudomembranes, goiter causing narrowing of the trachea in the form of a saber sheath, space-occupying processes in the upper mediastinum narrowing the trachea, tracheal strictures associated with stenosis or atresia of the esophagus, with the consequences of prolonged intubation (damage to the mucous membrane and cartilage of the trachea) or tracheotomy, malformations of the aortic arch (doubling of the aortic arch, left-sided origin of the right subclavian artery), anomalies of the pulmonary trunk (significant expansion), open ductus arteriosus.
More often in pediatric practice, acute stenosing laryngotracheitis, allergic laryngeal edema, laryngospasm, and epiglottitis are observed. Each of the listed conditions is characterized by its own history, development of the clinical picture of the disease and manifestations accompanying ARF.
The most common cause of high airway obstruction in children is acute stenosing laryngotracheitis (ASLT), which has a viral (parainfluenza virus, adenovirus, etc.) or combined viral-bacterial (staphylococcus or E. coli) etiology. Depending on the etiology and previous background of the disease, one of its three forms occurs: edematous, infiltrative, fibrinous-necrotic (obstructive). It is not always possible to clearly differentiate between acute stenosing laryngotracheitis and allergic laryngeal edema. This is explained by the fact that the virus often plays the role of a resolving factor in children with a predisposition to allergies. The morphofunctional basis of both pathological processes is swelling and spasm.
The edematous form usually develops at the onset of ARI (often parainfluenza), has an infectious-allergic nature and is not accompanied by signs of intoxication. Characterized by a rapid increase in symptoms, as well as relief of signs of stenosis, good effect when prescribing corticosteroids. In the infiltrative form, stenosis develops by the 2-3rd day from the onset of ARI, intoxication is moderate. The pathological process is caused by a combination of bacterial and viral infection. Stenosis increases slowly, but progresses to severe degrees. The obstructive form of OSLT often occurs in the form of laryngotracheobronchitis. The stenosis is caused predominantly by fibrin deposits rather than by subglottic narrowing, and the process is a descending bacterial fibrinous inflammation.
Foreign bodies of the larynx and trachea are one of the most common causes of asphyxia and sudden decompensation of breathing. Most often, foreign bodies are observed in children aged 1-3 years, in boys twice as often as in girls. The risk of aspiration of small objects, such as seeds, nuts, pebbles, etc. is especially high. During aspiration, food and gastric contents can enter the respiratory tract during vomiting or passive leakage (regurgitation) in children in the first months of life, premature babies, and deep comas. The child may also inhale pieces of solid food, resulting in rapid development of asphyxia. In approximately half of the cases, foreign bodies are localized in the trachea and can move from the subglottic space to the tracheal bifurcation, causing periodic attacks of suffocation. When a foreign body is localized in the bronchi, a reflex spasm of the bronchioles may occur, leading to the sudden appearance of symptoms bronchial obstruction with a sharp prolongation of exhalation.
Lower type of obstructive-constrictive ARF
Acute bronchial obstruction syndrome (ABO) occurs more easily in children early age, since the lumen of their bronchi is significantly narrower than in adults. In the genesis of the BBO syndrome, swelling of the walls of the bronchioles, obstruction of the bronchi with accumulated secretions, mucus, purulent crusts (discrimination) and, finally, spasm of the bronchial muscles play a role. The ratio of the listed components varies depending on the causes of OBO and the age of the child. Most often, OBO in children is observed with infectious obstructive bronchitis (bronchiolitis), with ARI, an attack of bronchial asthma and status asthmaticus, congestive left ventricular heart failure (equivalent to cardiac asthma in adults), for example, with Kishsh toxicosis.
In children of the first three years of life, OBO, which occurs against the background of ARI, is almost always caused by inflammatory swelling of the mucous membrane of the bronchioles (bronchiolitis). The primary disease at 3-6 months of life is usually associated with rhinosyncytial infection, and at the age of 6 months to 3 years - with parainfluenza. Repeated attacks of ABO in ARI can be caused by any respiratory virus, since they occur against the background of previous sensitization of the bronchi with the inclusion of reagin mechanisms. In other words, in these cases bronchiolitis is combined with bronchospasm. Bronchospasm is always an indispensable component of acute respiratory syndrome in children over 3 years of age, which indicates that the patient has asthma. The pathological role of discrinia (obstruction due to the accumulation of mucus, desquamated epithelium, fibrin in the bronchi) should be taken into account when OBO develops towards the end of the first week of acute bronchopulmonary disease, especially in frequently ill children with severe concomitant pathology.
All children, as a rule, experience hypoxemia, which persists for 5 weeks even as the condition improves. In a significant percentage of cases, as a result of increased work of breathing against high airway resistance due to muscle fatigue, the patient develops uncompensated respiratory acidosis with a PaCO2 level above 65 mm Hg. Art. The terminal stage of any ABO is pulmonary edema caused by significant negative intrathoracic pressure and secondary left ventricular heart failure.
The leading symptom of OBO is expiratory dyspnea, and in children in the first months and years of life it is mixed dyspnea. The more severe the degree of obstruction and the more pronounced the physical changes in the respiratory system, the more the clinical picture is dominated by signs of increased work of breathing. Children of the first years of life, not finding the optimal position for pushing out air, become restless and rush about. Exhalation is carried out with the participation of auxiliary muscles, and children over 3 years of age more often take a forced position. Characterized by bloating of the chest, physical signs of increased airiness of the lungs (weakened breathing and bronchophony, “boxy” percussion sound). The auscultatory picture varies depending on the predominance of one or another pathophysiological mechanism of obstruction. Thus, when the hypercrinic component predominates, mainly rough, buzzing rales are heard, while in the edematous version of ABO with significant transudation of fluid into the lumen of the bronchi and bronchioles, scattered fine-bubbly moist rales are heard on both sides. When OBO is combined with primary infectious toxicosis, along with excessive tachycardia (Kisch toxicosis), widespread fine moist rales in the lungs, waxy skin or periorbital edema, bronchiole stenosis due to peribronchial edema should be suspected.
Parenchymal DN is characterized by predominant damage to the alveoli and capillary bed of the pulmonary circulation. Its clinical equivalent is adult-type respiratory distress syndrome (ARDS). The pathophysiological basis of RDS is an alveolar-capillary block for oxygen diffusion, a decrease in compliance and functional residual capacity of the lungs. Most often it develops as a result of a systemic inflammatory response of the macroorganism to endotoxemia. Inflammatory lung diseases can also lead to parenchymal DN. This variant of DN is characterized by the appearance of early hypoxemia with hypocapnia and mixed shortness of breath.
Ventilation DN is caused by a violation of the neuromuscular control of external respiration. This may be due to inhibition of the respiratory center (barbiturate poisoning, injuries and tumors of the central nervous system, encephalitis, etc.), pathology of the nervous system pathways (Guillain-Barré syndrome - acute inflammatory demyelinating polyradiculoneuropathy; poliomyelitis, etc.), synaptic transmission (myasthenia gravis , residual effect of muscle relaxants), with changes in the respiratory muscles (muscular dystrophies, muscle proteolysis during hypercatabolism, etc.). Often, hypoventilation (this is the main clinical manifestation of this variant of DN) can be caused by pneumo-, hemo- or hydrothorax, a high position of the diaphragm (intestinal paresis) or chest trauma. Ventilatory DN is characterized by a combination of hypoxemia and hypercapnia.
Respiratory failure can occur when PaO2 decreases in the inhaled air (anoxic hypoxemia), which causes a decrease in blood oxygen saturation in the pulmonary capillaries and leads to tissue hypoxia (at high altitudes, when the oxygen supply to the incubator is disrupted when nursing newborns, etc.).
It is possible to develop respiratory failure when the transport of gases in the blood is impaired in severe anemia, changes in the structure of hemoglobin (met- or carboxyhemoglobinemia). In case of circulatory disorders due to slowing of blood flow in organs and tissues, stagnant hypoxia occurs. A special place is occupied by the so-called tissue hypoxia, which is explained by damage to the enzyme systems of cells involved in the utilization of oxygen diffusing from the blood (in case of poisoning, infection).
For all types of ARF, three pathogenetic stages can be distinguished:
· in the 1st stage, there are usually no disturbances in gas exchange due to a compensatory increase in breathing and blood circulation;
· in the 2nd stage, the first clinical and laboratory signs of decompensation appear in the form of symptoms of hypocapnia and hypoxia;
· in the 3rd stage, the aggravation of these changes leads to complete decompensation, during which the differences between the types of respiratory failure disappear.
The leading disorders during this period are mixed metabolic and respiratory acidosis, neurological disorders associated with cerebral edema, and cardiovascular failure.
Clinical picture of ARF
The clinical picture of DN in children consists of the symptoms of the underlying disease, the semiotics of changes in the function of the external respiratory apparatus, as well as signs of hypoxemia and hypercapnia, tissue hypoxia, and a violation of the acid-base composition of the blood (ABC). Decompensation during hypoxemia is manifested by neurological disorders and circulatory disorders, resulting in the development of secondary hypoventilation and hypercapnia.
Violations of the function of external respiration are manifested by symptoms characterizing compensation, increased work of the respiratory muscles and decompensation of the external respiratory apparatus. The main signs of compensation are shortness of breath and prolongation of inhalation or exhalation with a change in the ratio between them. Increased breathing is manifested by the inclusion of auxiliary muscles - cervical and deep intercostal muscles. Their participation is reflected by the retraction of the pliable places of the chest during inspiration (supra- and subclavian regions, jugular fossa, intercostal spaces, sternum), as well as nodding movements of the head in young children. Decompensation is indicated by bradyarrhythmia of breathing, its pathological types and signs of damage to the respiratory center.
Clinical signs of hypercapnia and hypoxemia can be early or late. Early ones, reflecting compensation, primarily from the cardiovascular system, are tachycardia, arterial hypertension, pale skin. They indicate the centralization of blood circulation necessary to maintain the oxygen regime of the central nervous system.
Late clinical signs of hypercapnia and hypoxemia indicate decompensation in the cardiovascular and respiratory systems, and the central nervous system. This is cyanosis, sticky sweat, motor and mental restlessness of the child or lethargy. When assessing cyanosis, it is imperative to take into account its prevalence and changes under the influence of different oxygen concentrations in the inhaled air. If the reaction to 45% oxygen content in the inspired air persists, this indicates ventilation respiratory failure and the absence of shunt-diffuse disorders. A positive reaction to 100% oxygen content in the inspired air is characteristic of impaired diffusion through the alveolar-capillary membrane, but with intrapulmonary arteriovenous shunting, on the contrary, there is no effect.
Characteristic symptoms of another group are manifestations of decompensation of the central nervous system, blood circulation and respiration, developing as a result of tissue hypoxia and associated metabolic acidosis. Among these symptoms, the most threatening signs of hypoxic damage to the central nervous system, requiring emergency treatment, are coma and convulsions. At the same time, the cardiovascular system also reacts to tissue hypoxia in the form of arterial hypotension, bradycardia and other rhythm disorders. Subsequently, decompensated breathing disorders occur, ending in respiratory arrest.
In acute respiratory failure, unlike chronic, the body does not have time to activate long-term compensation mechanisms, so this condition is characterized by a clear relationship between the levels of PaCO2 and PaO2 in arterial blood and the clinical picture.
The first clinical signs of hypoxemia are cyanosis, tachycardia, behavioral disturbances, which appear when PaO2 decreases to 70 mm Hg. Art. Neurological disorders are typical for a patient with PaO2 below 45 mm Hg. Art. Death occurs when PaO2 reaches 20 mm Hg. Art. For blood PaCO2, this relationship is as follows: the deep cervical and intercostal muscles begin to participate in breathing when PaCO2 is above 60 mm Hg. Art., and signs of respiratory decompensation indicate an increase in PaCO2 of more than 90-120 mm Hg. Art.
Treatment methods for ARF
Oxygen therapy
The simplest and most direct way to improve oxygenation is to increase the oxygen content in the inhaled air-oxygen mixture (FіO2). Oxygen therapy makes it possible to maintain the partial pressure of oxygen in arterial blood, but it does not eliminate the main cause of gas exchange disorders.
Higher Fio2 values should be avoided due to the risk of damage to lung tissue and the development of retinopathy in premature infants. Direct pulmonary oxygen toxicity occurs at FiO2 values greater than 0.6-0.7.
If it is impossible to determine FiO2, the oxygen concentration should be minimal to eliminate the phenomena of hypoxia (cyanosis).
Kinds respiratory therapy
These are methods that improve the flow of gas into the alveoli (tracheal intubation, tracheotomy, ensuring patency of the trachea and bronchi, artificial ventilation, spontaneous breathing with continuous positive expiratory pressure (CPEP).
The main goal of tracheal intubation is to maintain alveolar gas exchange and oxygenation, prevent aspiration of gastric contents, eliminate adverse hemodynamic reactions and brain damage.
Depending on the age of the child, there are different sizes endotracheal tube and laryngoscope blade (Table 2).
In newborns and young children, it is more advisable to use a straight blade of a laryngoscope (Miller, Wis-Hippie); a curved blade (Macintosh) is more often used in children aged 2-15 years.
Technique of spontaneous breathing under increased pressure - SPPBP
Early use of the technique reduces the need for mechanical ventilation. In the case of the development of RDS in infants and children, SDPPD prevents atelectasis, reduces swelling of the alveolar-capillary membrane, and provides a functional feature of the surfactant.
Indications for performing SDPPD:
– for newborns and children with RDS to maintain PaO2 at the appropriate level; the oxygen concentration under the tent should be 40-50%;
– children with breathing disorders to maintain the required level of oxygenation; the oxygen concentration in the breathing mixture is 60%;
– if signs of respiratory failure are observed after extubation.
To carry out SDPPD, a mask, a plastic bag, an endotracheal tube, a nasopharyngeal tube, and nasal cannulas are used. The latter are most often used in newborns. This is the most convenient and safest way.
When determining airway pressure, it is necessary to achieve a balance between the positive effect of CPAP on lung tissue and its adverse effect on cardiac output (blood flow). SDPPD therapy begins with a pressure of 5-6 cm of water. Art. to ensure a flow of air-oxygen mixture that is 5-10 times greater than the minute volume of breathing. This rate of delivery of the mixture prevents the entry of exhaled gas into the lungs both during inhalation and exhalation. If necessary, the pressure can be increased (by 1 cm H2O) under the control of the child’s respiratory efforts, skin color and monitoring of PaO2 or SpO2 (hemoglobin oxygen saturation).
Artificial ventilation
In this article, we did not pursue the goal of talking in detail about mechanical ventilation and its types in children. This would require more time and, perhaps, more than one publication. In addition, this information will be useful only for a narrow circle of specialists who are seriously involved in this method of treating ARF in children. But I would like to present its basic basics, as well as algorithms for changing the parameters of the respirator, which will ensure adequate gas exchange and maintain PaO2 and PaCO2 in the blood.
Mechanical ventilation as a method of respiratory therapy for acute respiratory failure is intended to temporarily replace the function of external respiration. Timely and correct implementation of mechanical ventilation in the case of severe ARF leads to a favorable outcome of the disease. However, mechanical ventilation in newborns and young children remains a rather complex problem, which is primarily due to the anatomical and physiological characteristics of the respiratory system. In turn, this method of intensive respiratory therapy has a complex effect on various organs and systems. Therefore, without knowledge of changes in the body during mechanical ventilation, it is impossible to successfully perform mechanical respiration.
Indications for mechanical ventilation. The decision on the feasibility of carrying out and timing of the start of mechanical ventilation depends on the situation and does not fit into a specific scheme. Mechanical ventilation is indicated in cases where spontaneous breathing does not provide adequate supply of the required amount of oxygen or removal of carbon dioxide. This situation occurs during hypoventilation as a result of decreased alveolar ventilation, as well as in the event of impaired pulmonary circulation and a decrease in the alveolar surface through which gases diffuse. Sometimes these situations occur simultaneously.
Clinical indications for the need to start mechanical ventilation in children: in case of severe progressive respiratory failure, cyanosis of the skin during oxygen intake of more than 70% in the inhaled mixture, tachypnea more than 60-80 per minute or bradypnea.
The most reliable indications for mechanical ventilation are the following indicators of CBS and blood gas composition:
– PaO2 is lower than 60 mm Hg. Art. (8 kPa) with an oxygen concentration in the inhaled mixture of 80% even during SDPPD;
– PaCO2 above 60 mm Hg. Art. (8 kPa) or an increase in PaCO2 by more than 10 mm Hg. Art. in 1 hour;
– pH lower than 7.2.
In the treatment of DN, mechanical ventilation is an advantage to prevent severe disturbances of homeostasis.
Acute respiratory failure in children is a condition in which their lungs are unable to maintain normal blood gas composition, i.e. tissues do not receive enough oxygen and excess carbon dioxide accumulates in them. Therefore, the main mechanisms of damage in respiratory failure are hypoxemia (lack of oxygen) and hypercapnia (excess carbon dioxide), leading to metabolic shifts.
Respiratory distress syndrome is a consequence various conditions and diseases in childhood:
- Bronchial asthma (this is the most common cause in older children)
- Stenosing laryngotracheitis (most common cause in young children)
- Epiglottitis
- Obstructive bronchitis
- Entry of foreign bodies into the oropharynx or nasopharynx and their descent below
- Aspiration of vomit
- Prematurity, in which there is a true deficiency of surfactant (a substance that helps the lungs expand and not stick together when exhaling)
- Congenital defects lungs and heart
- Respiratory tract infections
- Heart diseases.
Stenosing laryngotracheitis is the main cause of acute respiratory failure in children aged one to 6 years. It often complicates influenza and other respiratory infections. Symptoms of stenosing laryngotracheitis appear on the 1st or 2nd day of the infectious disease.
Anatomical features of children predispose to frequent complication underlying disease of acute respiratory failure.
These features are:
- Raised position of the ribs, giving chest“expiratory” type, i.e. she is in a state of exhalation
- Initially reduced tidal volume
- Rapid breathing (compared to adults)
- Narrow airways
- Rapid fatigue of the respiratory muscles
- Reduced surfactant activity.
Therefore, parents should always be on guard for timely detection of acute respiratory failure if the child develops any causative factor(primarily respiratory infections).
Types of respiratory failure
Depending on the developing disorders of the blood gas composition, there are three main degrees of respiratory failure:
- Hypoxemic, in which there is a deficiency of oxygen in the blood (carbon dioxide tension may be normal or may be slightly elevated). This type of failure develops due to a violation between the alveoli and capillaries
- Hypercapnic– occurs due to sharply rapid breathing (excess carbon dioxide prevails over lack of oxygen)
- Mixed.
Degrees
The degree of respiratory failure in children determines the severity of their condition. At first degree the child's consciousness is clear, the skin normal color, but anxiety and shortness of breath appear, the heart rate increases (by 5-10% of normal).
The second degree is characterized by greater severity of symptoms:
- Retraction of the intercostal spaces, supraclavicular areas and the area above the jugular notch
- Noisy breathing heard from a distance
- Bluish skin color that appears when the child is excited
- Increased heart rate is 10-15% higher than normal for a given age.
The third degree represents serious danger for the child's health. Its characteristics are:
- Arrhythmic breathing due to suffocation
- Periodic loss of pulse
- Paroxysmal increased heart rate
- Constant (not only during excitement, but also at rest) cyanosis of the skin and mucous membranes.
Diagnostics
The final diagnosis of acute respiratory failure in children is made after determining blood gases. One of two signs is enough(determined in arterial blood):
- Oxygen tension 50 mm Hg. or less
- Carbon dioxide voltage 50 mm Hg. and more.
But often it is not possible to determine the gas composition. Therefore, doctors (and parents) focus on clinical manifestations, accessible to research in any situation.
Clinical signs of respiratory failure are:
- Increased breathing rate, followed by slower breathing
- Irregular pulse
- No breath sounds
- Stridorous and wheezing breathing
- Intercostal space retraction
- Participation of additional muscles in the act of breathing
- Bluish discoloration of the limbs, tip of the nose and nasolabial triangle
- Pre-fainting state, which may be followed by loss of consciousness.
Treatment
Treatment of respiratory failure in childhood is carried out in several areas:
- Restoring air flow through the respiratory tract (removing a foreign body that has entered there, removing inflammatory edema, etc.)
- Correction metabolic disorders, developed against the background of hypoxia
- Prescribing antibiotics to prevent infectious complications.
However, such treatment is only possible in a hospital. At home, parents should know emergency rules which should be immediately provided to the child:
Before following these rules, you should contact the ambulance service!
- Removing a foreign object from the throat or aspirated vomit
- Inhalation of a bronchodilator drug for bronchial asthma (it should always be in your home medicine cabinet)
- Ensuring a flow of oxygen-saturated air (open windows)
- Steam inhalation for laryngeal edema, which is the main symptom of stenosing laryngotracheitis
- Foot baths
- Warm drinks in large quantities.
In children, foreign bodies cannot be removed blindly, because this can lead to complete airway obstruction. It is recommended to place your hands on the epigastric region and push upward. The foreign body that appears can be removed.
Late referral of parents for medical care when symptoms of respiratory failure appear in children, this is the reason for the low effectiveness of pharmacological therapy. Therefore, in pediatric practice, indications for conicotomy (dissection of the larynx) and artificial ventilation lungs using tracheal intubation.
