Respiratory distress in newborns. Respiratory distress syndrome in children

Respiratory distress syndrome of the newborn, hyaline membrane disease, is a severe respiratory disorder in premature newborns caused by immature lungs and primary surfactant deficiency.

Epidemiology
Respiratory distress syndrome is the most common cause emergence respiratory failure in the early neonatal period in premature newborns. Its occurrence is higher, the lower the gestational age and body weight of the child at birth. Carrying out prenatal prevention when there is a threat of premature birth also affects the incidence of respiratory distress syndrome.

In children born before 30 weeks of gestation and who did not receive prenatal prophylaxis with steroid hormones, its frequency is about 65%, in the presence of prenatal prophylaxis - 35%; in children born at a gestational age of 30-34 weeks without prophylaxis - 25%, with prophylaxis - 10%.

In premature babies born at more than 34 weeks of gestation, its frequency does not depend on prenatal prevention and is less than 5%.

Etiology and pathogenesis
The main reasons for the development of respiratory distress syndrome in newborns are:
- disruption of the synthesis and excretion of surfactant by type 2 alveolocytes, associated with functional and structural immaturity of the lung tissue;
- a congenital qualitative defect in the structure of the surfactant, which is an extremely rare cause.

With a deficiency (or reduced activity) of surfactant, the permeability of the alveolar and capillary membranes increases, blood stagnation in the capillaries, diffuse interstitial edema and overstretching of the lymphatic vessels develop; alveoli collapse and atelectasis forms. As a result, the functional residual capacity, tidal volume and vital capacity of the lungs decrease.

As a result, the work of breathing increases, intrapulmonary shunting of blood occurs, and hypoventilation of the lungs increases. This process leads to the development of hypoxemia, hypercapnia and acidosis. Against the background of progressive respiratory failure, dysfunction occurs of cardio-vascular system: secondary pulmonary hypertension with a right-to-left blood shunt through functioning fetal communications, transient myocardial dysfunction of the right and/or left ventricles, systemic hypotension.

A postmortem examination revealed that the lungs were airless and sank in water. Microscopy reveals diffuse atelectasis and necrosis of alveolar epithelial cells. Many of the dilated terminal bronchioles and alveolar ducts contain fibrin-based eosinophilic membranes. It should be noted that hyaline membranes are rarely found in newborns who died from respiratory distress syndrome in the first hours of life.

Prenatal prevention
If there is a threat of premature birth, pregnant women should be transported to obstetric hospitals of the 2nd-3rd level, where there are neonatal intensive care units.

If there is a threat of premature birth at the 32nd week of gestation or less, transportation of pregnant women should be carried out to a 3rd level hospital (in perinatal center) (WITH).

Pregnant women at 23-34 weeks' gestation who are at risk of preterm birth should be prescribed a course of corticosteroids to prevent respiratory distress syndrome of prematurity and reduce the risk of possible adverse complications such as intraventricular hemorrhage and necrotizing enterocolitis (A).

Two alternative regimens for prenatal prevention of respiratory distress syndrome can be used:
- betamethasone - 12 mg intramuscularly every 24 hours, only 2 doses per course;
- dexamethasone - 6 mg intramuscularly every 12 hours, a total of 4 doses per course.

The maximum effect of steroid therapy develops after 24 hours and lasts a week. By the end of the second week, the effect of steroid therapy is significantly reduced. A second course of prophylaxis of respiratory distress syndrome with corticosteroids is indicated 2-3 weeks after the first in case of recurrent risk of premature birth at a gestation period of less than 33 weeks (A). It is also advisable to prescribe corticosteroid therapy for women at 35-36 weeks of gestation in case of planned caesarean section in the absence of a woman labor activity. Prescribing a course of corticosteroids to women in this category does not affect neonatal outcomes, but reduces the risk of children developing respiratory problems and, as a result, admission to the neonatal intensive care unit (B).

If there is a threat of premature birth in the early stages, it is advisable to use a short course of tocolytics to delay the onset of labor in order to transport pregnant women to the perinatal center, as well as to complete the full course of antenatal prophylaxis of respiratory distress syndrome with corticosteroids and the onset of complete therapeutic effect(IN). Premature rupture of amniotic fluid is not a contraindication to inhibition of labor and prophylactic administration of corticosteroids.

Antibacterial therapy is indicated for women with premature rupture membranes(premature rupture of amniotic fluid), since it reduces the risk of premature birth (A). However, the use of amoxicillin + clavulanic acid should be avoided due to the increased risk of necrotizing enterocolitis in premature infants. Widespread use of third-generation cephalosporins should also be avoided due to their pronounced influence on the formation of multidrug-resistant hospital strains in the hospital (C).

Diagnosis of respiratory distress syndrome
Risk factors
Predisposing factors for the development of respiratory distress syndrome, which can be identified before the birth of a child or in the first minutes of life, are:
- development of respiratory disorders in siblings;
- diabetes at the mother's;
- severe form hemolytic disease fetus;
- premature placental abruption;
- premature birth;
- male sex of the fetus in premature birth;
- caesarean section before the onset of labor;
- asphyxia of the fetus and newborn.

Clinical picture:
Shortness of breath that occurs in the first minutes - the first hours of life
Expiratory noises (“moaning breathing”) caused by the development of compensatory spasm of the glottis during exhalation.
Retraction chest on inspiration (retraction of the xiphoid process of the sternum, epigastric region, intercostal spaces, supraclavicular fossa) with the simultaneous occurrence of tension in the wings of the nose, swelling of the cheeks ("trumpeter" breathing).
Cyanosis when breathing air.
Decreased breathing in the lungs, crepitating wheezing on auscultation.
Increasing need for supplemental oxygenation after birth.

Clinical assessment of the severity of respiratory disorders
Clinical assessment of the severity of respiratory disorders is carried out using the Silverman scale in premature infants and the Downes scale in full-term newborns, not so much with diagnostic purpose, how much to assess the effectiveness of respiratory therapy or as an indication for its initiation. Along with assessing the newborn's need for additional oxygenation, this may be a criterion for changing treatment tactics.

X-ray picture
The X-ray picture of neonatal respiratory distress syndrome depends on the severity of the disease - from a slight decrease in pneumatization to “white lungs”. Characteristic signs are: a diffuse decrease in the transparency of the lung fields, a reticulogranular pattern and stripes of clearing in the region of the lung root (air bronchogram). However, these changes are nonspecific and can be detected in congenital sepsis and congenital pneumonia. X-ray examination in the first day of life is indicated for all newborns with respiratory disorders.

Laboratory research
For all newborns with respiratory disorders in the first hours of life, along with routine blood tests for acid-base status, gas composition and glucose levels, it is also recommended to carry out analyzes of markers of the infectious process in order to exclude the infectious genesis of respiratory disorders.
Conducting a clinical blood test with calculation of the neutrophil index.
Determination of the level of C-reactive protein in the blood.
Microbiological blood culture (the result is assessed no earlier than after 48 hours).
When conducting differential diagnosis with severe congenital sepsis in patients requiring strict modes of invasive artificial ventilation, with a short-term effect from repeated administrations of exogenous surfactant, it is recommended to determine the level of pro-calcitonin in the blood.

It is advisable to repeat the determination of the level of C-reactive protein and a clinical blood test after 48 hours if it is difficult to make a diagnosis of respiratory distress syndrome on the first day of the child’s life. Respiratory distress syndrome is characterized by negative inflammatory markers and negative microbiological blood cultures.

Differential diagnosis
Differential diagnosis is carried out with the following diseases. Transient tachypnea of newborns. The disease can occur at any gestational age of newborns, but is more common in full-term infants, especially after cesarean section. The disease is characterized by negative markers of inflammation and rapid regression of respiratory disorders. Nasal continuous positive pressure mechanical ventilation is often required. Characteristic rapid decline the need for additional oxygenation against the background of artificial ventilation of the lungs with constant positive pressure. Invasive artificial ventilation is extremely rarely required. There are no indications for the administration of exogenous surfactant. In contrast to respiratory distress syndrome, transient tachypnea on a chest x-ray is characterized by an increased bronchovascular pattern and signs of fluid in the interlobar fissures and/or pleural sinuses.
Congenital sepsis, congenital pneumonia. The onset of the disease may be clinically identical to respiratory distress syndrome. Characteristic are positive markers of inflammation, determined over time in the first 72 hours of life. Radiologically, with a homogeneous process in the lungs, congenital sepsis/pneumonia is indistinguishable from respiratory distress syndrome. However, focal (infiltrative shadows) indicate an infectious process and are not characteristic of respiratory distress syndrome
Meconium aspiration syndrome. The disease is typical for full-term and post-term newborns. Presence of meconium amniotic fluid and respiratory disorders since birth, their progression, absence laboratory signs infections, as well as characteristic changes X-ray of the chest organs (infiltrative shadows are interspersed with emphysematous changes, atelectasis, pneumomediastinum and pneumothorax are possible) support the diagnosis of “meconium aspiration syndrome”
Air leak syndrome, pneumothorax. The diagnosis is made based on the characteristic x-ray pattern in the lungs.
Persistent pulmonary hypertension. The chest x-ray shows no changes characteristic of respiratory distress syndrome. Echocardiographic examination reveals a right-to-left shunt and signs of pulmonary hypertension.
Aplasia/hypoplasia of the lungs. Diagnosis is usually made prenatally. Postnatally, the diagnosis is made on the basis of the characteristic x-ray pattern in the lungs. To clarify the diagnosis, a computed tomography scan of the lungs is possible.
Congenital diaphragmatic hernia. X-ray signs of organ translocation abdominal cavity into the chest indicates a diagnosis of “congenital diaphragmatic hernia”. Features of providing primary and resuscitation care to newborns from the group high risk on the development of respiratory distress syndrome in the delivery room To increase the effectiveness of the prevention and treatment of respiratory distress syndrome in the delivery room, a set of technologies is used

Prevention of hypothermia in the delivery room in premature newborns
Prevention of hypothermia is one of the key elements nursing critically ill and very premature children. If premature birth is expected, the temperature in the delivery room should be 26-28 °C. The main measures to ensure thermal protection are carried out in the first 30 seconds of life within the framework of initial events primary care newborn. The scope of hypothermia prevention measures differs in premature infants weighing more than 1000 g (gestation period 28 weeks or more) and in children weighing less than 1000 g (gestation period less than 28 weeks).

In premature babies born at a gestation period of 28 weeks or more, as well as in full-term newborns, a standard amount of preventive measures is used: drying skin and wrapping in warm, dry diapers. The surface of the child's head is additionally protected from heat loss with a diaper or hat. To monitor the effectiveness of the measures and prevent hyperthermia, it is recommended that all premature infants carry out continuous monitoring of body temperature in the delivery room, as well as record the child’s body temperature upon admission to the intensive care unit. Prevention of hypothermia in premature infants born before the completion of the 28th week of gestation requires the mandatory use of plastic film (bag) (A).

Delayed umbilical cord clamping and cutting
Clamping and cutting of the umbilical cord 60 seconds after birth in premature newborns leads to a significant reduction in the incidence of necrotizing enterocolitis, intraventricular bleeding, and a reduction in the need for blood transfusions (A). Methods of respiratory therapy (stabilization of breathing)

Non-invasive respiratory therapy in the delivery room
Currently, for premature infants, initial therapy with continuous positive pressure artificial ventilation followed by prolonged inflation of the lungs is considered preferable. Creating and maintaining constant positive pressure in the airways is a necessary element of early stabilization of the condition of a very premature baby, both with spontaneous breathing and on mechanical ventilation. Continuous positive pressure in the airways helps to create and maintain functional residual lung capacity, prevents atelectasis, and reduces the work of breathing. Recent studies have shown the effectiveness of the so-called “extended lung inflation” as a start to respiratory therapy in premature newborns. The “extended inflation” maneuver is an extended artificial breath. It should be carried out in the first 30 s of life, in the absence of spontaneous breathing or during “gasping” breathing with a pressure of 20-25 cm H2O for 15-20 s (B). At the same time, residual lung capacity is effectively formed in premature babies. This technique is performed once. The maneuver can be performed using a hand-held device with a T-connector or automatic device artificial ventilation of the lungs, which has the ability to maintain the required pressure during inspiration for 15-20 s. It is not possible to perform prolonged inflation of the lungs using a breathing bag. A prerequisite for performing this maneuver is recording heart rate and SpCh using pulse oximetry, which allows you to evaluate its effectiveness and predict further actions.

If the child has been screaming and breathing actively since birth, then prolonged inflation should not be carried out. In this case, children born at a gestational age of 32 weeks or less should begin respiratory therapy using continuous positive pressure artificial ventilation with a pressure of 5-6 cm H2O. In preterm infants born at more than 32 weeks' gestation, continuous positive pressure ventilation should be administered if respiratory distress is present (A). The above sequence results in less need for invasive mechanical ventilation in preterm infants, which in turn leads to less use of surfactant therapy and a lower likelihood of complications associated with mechanical ventilation (C).

When conducting non-invasive respiratory therapy for premature babies in the delivery room, it is necessary to insert a decompression probe into the stomach at 3-5 minutes. Criteria for the ineffectiveness of the continuous positive pressure artificial lung ventilation mode (in addition to bradycardia) as a starting method of respiratory support can be considered the increase in the severity of respiratory disorders in dynamics during the first 10-15 minutes of life against the background of the constant positive pressure artificial lung ventilation mode: pronounced participation of auxiliary muscles, need for additional oxygenation (FiO2 >0.5). These clinical signs indicate a severe course of respiratory disease in premature infants, which requires the administration of exogenous surfactant.

The mode of mechanical ventilation of the lungs with constant positive pressure in the delivery room can be carried out by a mechanical ventilator with the function of artificial ventilation of the lungs with constant positive pressure, a manual ventilator with a T-connector, various systems of artificial ventilation of the lungs with constant positive pressure. The technique of artificial ventilation of the lungs with continuous positive pressure can be carried out using a face mask, a nasopharyngeal tube, an endotracheal tube (used as a nasopharyngeal tube) and binasal cannulas. At the stage of the delivery room, the method of performing artificial ventilation of the lungs with constant positive pressure is not significant.

The use of artificial pulmonary ventilation with continuous positive pressure in the delivery room is contraindicated for children:
- with choanal atresia or other congenital malformations of the maxillofacial region that prevent the correct application of nasal cannulas, a mask, or a nasopharyngeal tube;
- with diagnosed pneumothorax;
- with congenital diaphragmatic hernia;
- with congenital malformations that are incompatible with life (anencephaly, etc.);
- with bleeding (pulmonary, gastric, bleeding of the skin). Features of artificial ventilation of the lungs in the delivery room in premature infants

Artificial ventilation of the lungs in premature infants is carried out when constant positive pressure bradycardia persists against the background of artificial ventilation and/or during a long-term (more than 5 minutes) absence of spontaneous breathing.

Necessary conditions for effective mechanical ventilation in very premature newborns are:
- control of pressure in the respiratory tract;
- mandatory maintenance of Reer +4-6 cm H2O;
- the ability to smoothly adjust the oxygen concentration from 21 to 100%;
- continuous monitoring of heart rate and SpO2.

Starting parameters of artificial lung ventilation: PIP - 20-22 cm H2O, PEEP - 5 cm H2O, frequency 40-60 breaths per minute. The main indicator of the effectiveness of artificial ventilation is an increase in heart rate >100 beats/min. Such generally accepted criteria as visual assessment of chest excursion and assessment of skin color in very premature infants have limited information content, since they do not allow assessing the degree of invasiveness of respiratory therapy. Thus, a clearly visible excursion of the chest in newborns with extremely low body weight with a large share probability indicates excessive tidal volume ventilation and a high risk of volume injury.

Carrying out invasive mechanical ventilation in the delivery room under the control of tidal volume in very premature patients is a promising technology that allows minimizing mechanical ventilation-associated lung damage. When verifying the position of the endotracheal tube, along with the auscultation method in children with extremely low body weight, it is advisable to use the capnography method or the colorimetric method of indicating CO2 in exhaled air.

Oxygen therapy and pulse oximetry in premature newborns in the delivery room
The “gold standard” of monitoring in the delivery room when providing primary and resuscitation care to premature newborns is monitoring heart rate and SpO2 using pulse oximetry. Registration of heart rate and SaO2 using pulse oximetry begins from the first minute of life. A pulse oximetry sensor is installed in the wrist or forearm of the child’s right hand (“preductal”) during the initial activities.

Pulse oximetry in the delivery room has 3 main application points:
- continuous monitoring of heart rate starting from the first minutes of life;
- prevention of hyperoxia (SpO2 no more than 95% at any stage of resuscitation measures, if the child receives additional oxygen);
- prevention of hypoxia SpO2 by at least 80% by the 5th minute of life and by at least 85% by the 10th minute of life).

Initial respiratory therapy in children born at a gestation period of 28 weeks or less should be carried out with FiO2 0.3. Respiratory therapy in children of larger gestational age is carried out with air.

Starting from the end of 1 minute, you should focus on the pulse oximeter readings and follow the algorithm for changing the oxygen concentration described below. If the child’s indicators are outside the specified values, you should change (increase/decrease) the concentration of additional O2 in steps of 10-20% every subsequent minute until the target indicators are achieved. The exception is children who require chest compressions while undergoing artificial ventilation. In these cases, simultaneously with the start of chest compressions, the O2 concentration should be increased to 100%. Surfactant therapy

Surfactant administration may be recommended.
Prophylactically in the first 20 minutes of life for all children born at 26 weeks of gestation or less if they do not have a full course of antenatal steroid prophylaxis and/or the impossibility of non-invasive respiratory therapy in the delivery room (A).
All children of gestational age Premature children of gestational age >30 weeks requiring tracheal intubation in the delivery room. The most effective time of administration is the first two hours of life.
Premature babies undergoing initial respiratory therapy using artificial pulmonary ventilation with constant positive pressure in the delivery room with a need for FiO2 of 0.5 or more to achieve SpO2 85% by the 10th minute of life and the absence of regression of respiratory disorders and improvement of oxygenation in the next 10-15 minutes . By the 20-25th minute of life, you need to make a decision on the administration of surfactant or on preparation for transporting the child in artificial pulmonary ventilation mode with constant positive pressure. Children born at gestational age In the intensive care unit, children born at gestational age 3 points in the first 3-6 hours of life and/or FiO2 requirements up to 0.35 in patients 1000 g (B). Repeated administration is indicated.
Children of gestational age Children of gestational age
Repeated administration should be carried out only after a chest x-ray. A third administration may be indicated for mechanically ventilated children with severe respiratory distress syndrome (A). The intervals between administrations are 6 hours, but the interval may be shortened as children’s need for FiO2 increases to 0.4. Contraindications:
- profuse pulmonary hemorrhage (can be administered after relief if indicated);
- pneumothorax.

Surfactant administration methods
There are two main methods of insertion that can be used in the delivery room: traditional (through an endotracheal tube) and "non-invasive" or "minimally invasive".

Surfactant can be administered through a side-port endotracheal tube or through a catheter inserted into a conventional, single-lumen endotracheal tube. The child is placed strictly horizontally on his back. Tracheal intubation is performed under direct laryngoscopy control. It is necessary to check the symmetry of the auscultation pattern and the mark of the length of the endotracheal tube at the corner of the child’s mouth (depending on the expected body weight). Through the side port of the endotracheal tube (without opening the artificial ventilation circuit), inject surfactant quickly as a bolus. When using the insertion technique using a catheter, it is necessary to measure the length of the endotracheal tube, cut the catheter 0.5-1 cm shorter than the length of the ETT with sterile scissors, and check the depth of the ETT above the tracheal bifurcation. Inject surfactant through the catheter as a rapid bolus. Bolus administration provides the most effective distribution of surfactant in the lungs. In children weighing less than 750 g, it is permissible to divide the drug into 2 equal parts, which should be administered one after the other with an interval of 1-2 minutes. Under the control of SpO2, the parameters of artificial ventilation of the lungs, primarily the inspiratory pressure, should be reduced. The reduction in parameters should be carried out quickly, since a change in the elastic properties of the lungs after the administration of a surfactant occurs within a few seconds, which can provoke a hyperoxic peak and ventilator-associated lung damage. First of all, you should reduce the inspiratory pressure, then (if necessary) - the concentration of additional oxygen to the minimum sufficient numbers required to achieve SpO2 91-95%. Extubation is usually carried out after transporting the patient in the absence of contraindications. A non-invasive method of administering surfactant can be recommended for use in children born at a gestational age of 28 weeks or less (B). This method avoids tracheal intubation, reduces the need for invasive mechanical ventilation in very premature infants and, as a result, minimizes ventilator-associated lung damage. The use of a new method of surfactant administration is recommended after practicing the skill on a mannequin.

The “non-invasive method” is carried out against the background of spontaneous breathing of the child, whose respiratory therapy is carried out using the method of artificial ventilation of the lungs with constant positive pressure. With the child in the supine or lateral position against the background of mechanical ventilation with constant positive pressure (most often carried out through a nasopharyngeal tube), a thin catheter should be inserted under the control of direct laryngoscopy (it is possible to use Magill forceps to insert a thin catheter into the tracheal lumen). The tip of the catheter should be inserted 1.5 cm below the vocal cords. Next, under control of the SpO2 level, surfactant should be injected into the lungs as a slow bolus over 5 minutes, monitoring the auscultation pattern in the lungs, gastric aspirate, SpO2 and heart rate. During the administration of surfactant, respiratory therapy of artificial ventilation of the lungs with continuous positive pressure is continued. If apnea or bradycardia is registered, administration should be temporarily stopped and resumed after normalization of the heart rate and respiration levels. After administration of surfactant and removal of the tube, artificial ventilation of the lungs with continuous positive pressure or non-invasive artificial ventilation should be continued.

In the neonatal intensive care unit, children receiving mechanical ventilation with continuous positive pressure if there are indications for the administration of surfactant are recommended to administer surfactant using the INSURE method. The method consists of intubating the patient under the control of direct laryngoscopy, verifying the position of the endotracheal tube, rapid bolus administration of surfactant, followed by rapid extubation and transferring the child to non-invasive respiratory support. The INSURE method may be recommended for use in babies born after 28 weeks.

Surfactant preparations and doses
Surfactant preparations are not uniform in their effectiveness. The dosage regimen affects treatment outcomes. The recommended starting dosage is 200 mg/kg. This dosage is more effective than 100 mg/kg and leads to best results treatment of premature infants with respiratory distress syndrome (A). Repeated recommended dose of surfactant is not less than 100 mg/kg. Poractant-α is the drug with the highest concentration of phospholipids in 1 ml of solution.

Basic methods of respiratory therapy for neonatal respiratory distress syndrome
Objectives of respiratory therapy in newborns with respiratory distress syndrome:
- maintain a satisfactory blood gas composition and acid-base status:
- paO2 at the level of 50-70 mm Hg.
- SpO2 - 91-95% (B),
- paCO2 - 45-60 mm Hg,
- pH - 7.22-7.4;
- stop or minimize respiratory disorders;

The use of continuous positive pressure artificial ventilation and non-invasive artificial ventilation in the treatment of respiratory distress syndrome in newborns. Non-invasive mechanical ventilation through nasal cannulas or a nasal mask is currently used as the optimal initial method of non-invasive respiratory support, especially after surfactant administration and/or after extubation. The use of non-invasive mechanical ventilation after extubation in comparison with the mode of mechanical ventilation of the lungs with continuous positive pressure, as well as after the introduction of surfactant, leads to a lesser need for reintubation and a lower frequency of apnea (B). Non-invasive nasal mechanical ventilation has an advantage over continuous positive pressure mechanical ventilation as initial respiratory therapy in preterm infants with very and extremely low body weight. Registration of respiratory rate and assessment according to the Silverman/Downs scale is carried out before the start of artificial pulmonary ventilation with continuous positive pressure and every hour of mechanical ventilation with continuous positive pressure.

Indications:
- as a starting respiratory therapy after prophylactic minimally invasive administration of surfactant without intubation
- as respiratory therapy in premature infants after extubation (including after the INSURE method).
- apnea, resistant to mechanical ventilation therapy with continuous positive pressure and caffeine
- an increase in respiratory disorders on the Silverman scale to 3 or more points and/or an increase in the need for FiO2 >0.4 in premature infants under continuous positive pressure artificial ventilation.

Contraindications: shock, convulsions, pulmonary hemorrhage, air leak syndrome, gestation period over 35 weeks.

Starting parameters:
- PIP 8-10 cm H2O;
- PEEP 5-6 cm H2O;
- frequency 20-30 per minute;
- inhalation time 0.7-1.0 second.

Reducing parameters: when using non-invasive artificial ventilation for apnea therapy, the frequency of artificial breaths is reduced. When using non-invasive artificial ventilation to correct respiratory disorders, PIP is reduced. In both cases, a transfer is carried out from non-invasive artificial ventilation of the lungs to the mode of artificial ventilation of the lungs with constant positive pressure, with the gradual withdrawal of respiratory support.

Indications for transferring from non-invasive artificial ventilation to traditional artificial ventilation:
- paCO2 >60 mm Hg, FiО2>0.4;
- Silverman scale score of 3 or more points;
- apnea, repeated more than 4 times within an hour;
- air leak syndrome, convulsions, shock, pulmonary hemorrhage.

In the absence of a non-invasive artificial lung ventilation device, preference is given to the method of spontaneous breathing under constant positive pressure in the respiratory tract through nasal cannulas as a starting method of non-invasive respiratory support. In very preterm neonates, the use of continuous positive pressure ventilators with variable flow has some advantage over constant flow systems, as they provide the least work of breathing in such patients. Cannulas for performing artificial pulmonary ventilation with continuous positive pressure should be as wide and short as possible (A). Respiratory support using continuous positive pressure artificial lung ventilation in children with ELBW is carried out based on the algorithm presented below.

Definition and principle of operation. The mode of artificial ventilation of the lungs with constant positive pressure - continuous positive airway pressure - constant (that is, continuously maintained) positive pressure in the respiratory tract. Prevents the collapse of alveoli and the development of atelectasis. Continuous positive pressure increases functional residual capacity (FRC), reduces airway resistance, improves the compliance of lung tissue, and promotes stabilization and synthesis of endogenous surfactant. Can be an independent method of respiratory support in newborns with preserved spontaneous breathing

Indications for support of spontaneous breathing in newborns with respiratory distress syndrome using nasal continuous positive pressure ventilation:
- prophylactically in the delivery room for premature infants of gestational age 32 weeks or less;
- Silverman scale scores of 3 or more points in children of gestational age older than 32 weeks with spontaneous breathing.

Contraindications include: shock, convulsions, pulmonary hemorrhage, air leak syndrome. Complications of continuous positive pressure artificial ventilation.
Air leak syndrome. Prevention of this complication is a timely decrease in pressure in the respiratory tract when the patient’s condition improves; timely transition to artificial ventilation of the lungs when the parameters of the artificial lung ventilation mode with constant positive pressure are tightened.
Barotrauma of the esophagus and stomach. A rare complication that occurs in premature infants due to inadequate decompression. The use of gastric tubes with a large lumen helps prevent this complication.
Necrosis and bedsores of the nasal septum. With proper placement of nasal cannulas and proper care, this complication is extremely rare.

Practical advice on caring for a child using continuous positive pressure artificial ventilation and non-invasive artificial ventilation.
Appropriately sized nasal cannulas should be used to prevent loss of positive pressure.
The cap should cover the forehead, ears and back of the head.
The straps securing the nasal cannulas should be attached to the cap “back to front” to make it easier to tighten or loosen the fastening.
In children weighing less than 1000 g, a soft pad (cotton wool can be used) must be placed between the cheek and the fixing tape:
The cannulas should fit snugly into the nasal openings and should be held in place without any support. They should not put pressure on the child's nose.
During treatment, it is sometimes necessary to switch to cannulas bigger size due to an increase in the diameter of the external nasal passages and the inability to maintain stable pressure in the circuit.
You cannot sanitize the nasal passages due to possible trauma to the mucous membrane and the rapid development of swelling of the nasal passages. If there is discharge in the nasal passages, then you need to pour 0.3 ml of 0.9% sodium chloride solution into each nostril and sanitize through the mouth.
The humidifier temperature is set to 37 degrees C.
The area behind the ears should be inspected daily and wiped with a damp cloth.
The area around the nasal openings should be dry to avoid inflammation.
Nasal cannulas should be changed daily.
The humidifier chamber and circuit should be changed weekly.

Traditional artificial ventilation:
Objectives of traditional artificial lung ventilation:
- prosthetic function of external respiration;
- ensure satisfactory oxygenation and ventilation;
- do not damage the lungs.

Indications for traditional artificial ventilation:
- Silverman score of 3 or more points in children on non-invasive artificial ventilation/continuous positive pressure artificial ventilation mode;
- the need for high concentrations of oxygen in newborns in the mode of artificial ventilation of the lungs with continuous positive pressure / non-invasive artificial ventilation of the lungs (FiO2 >0.4);
- shock, severe generalized convulsions, frequent apneas during non-invasive respiratory therapy, pulmonary hemorrhage.

Carrying out artificial ventilation of the lungs in premature infants with respiratory distress syndrome is based on the concept of minimal invasiveness, which includes two provisions: the use of a “lung protection” strategy and, if possible, a rapid transfer to non-invasive respiratory therapy.

The “lung-protecting” strategy is to maintain the alveoli in an expanded state throughout the respiratory therapy. For this purpose, a PEER of 4-5 cm H2O is installed. The second principle of the “lung-protecting” strategy is to provide a minimum sufficient tidal volume to prevent volume injury. To do this, peak pressure should be selected under the control of tidal volume. For a correct assessment, the tidal volume of exhalation is used, since it is this volume that is involved in gas exchange. Peak pressure in premature newborns with respiratory distress syndrome is selected so that the tidal volume of exhalation is 4-6 ml/kg.

After installing the breathing circuit and calibrating the ventilator, select a ventilation mode. In premature newborns who have retained spontaneous breathing, it is preferable to use triggered artificial ventilation, in particular, the assist/control mode. In this mode, every breath will be supported by a respirator. If there is no spontaneous breathing, then the A/C mode automatically becomes the forced ventilation mode - IMV when a certain hardware breathing frequency is set.

In rare cases, the A/C mode may be excessive for a child when, despite all attempts to optimize the parameters, the child has persistent hypocapnia due to tachypnea. In this case, you can switch the child to SIMV mode and set the desired frequency of the respirator. In neonates born at 35 weeks of gestation and beyond, it is more appropriate to use acute mandatory ventilation (IMV) or SIMV if tachypnea is not severe. There is evidence of benefit from using volume-controlled ventilation modes compared with the more common pressure-controlled ventilation modes (B). After the modes are selected, the starting parameters of artificial ventilation are set before connecting the child to the device.

Starting parameters of artificial pulmonary ventilation in low birth weight patients:
- FiO2 - 0.3-0.4 (usually 5-10% more than with continuous positive pressure artificial ventilation);
- Tin - 0.3-0.4 s;
- ReeR- +4-5 cm water column;
- RR - in assist/control (A/C) mode, the respiratory rate is determined by the patient.

The hardware frequency is set to 30-35 and is only insurance for cases of apnea in the patient. In SIMV and IMV modes, the physiological frequency is set to 40-60 per minute. PIP is usually set in the range of 14-20 cmH2O. Art. Flow - 5-7 l/min when using the “pressure limited” mode. In "pressure control" mode, the flow is set automatically.

After connecting the child to a ventilator, the parameters are optimized. FiO2 is set so that the saturation level is within 91-95%. If the mechanical ventilation device has a function for automatically selecting FiO2 depending on the saturation level of the patient, it is advisable to use it to prevent hypoxic and hyperoxic peaks, which in turn is the prevention of bronchopulmonary dysplasia, retinopathy of prematurity, as well as structural hemorrhagic and ischemic brain damage .

Inspiratory time is a dynamic parameter. The inhalation time depends on the disease, its phase, the patient’s breathing rate and some other factors. Therefore, when using conventional time-cyclic ventilation, it is advisable to set the inspiratory time under the control of graphic monitoring of the flow curve. The inhalation time should be set so that on the flow curve, exhalation is a continuation of inhalation. There should be no inhalation pause in the form of blood retention at the isoline, and at the same time, exhalation should not begin before the inhalation ends. When using ventilation that is cyclic in flow, the inhalation time will be determined by the patient himself if the child is breathing independently. This approach has some advantage, since it allows the very premature patient to determine the comfortable inhalation time. In this case, the inspiratory time will vary depending on the patient’s respiratory rate and inspiratory activity. Flow-cyclic ventilation can be used in situations where the child is breathing spontaneously, there is no significant exudation of sputum and there is no tendency to atelectasis. When performing cyclic flow ventilation, it is necessary to monitor the patient's actual inspiratory time. In case of formation of an inadequately short inspiratory time, such a patient should be transferred to the time-cyclic artificial ventilation mode and ventilated with a given, fixed inspiratory time.

The selection of PIP is carried out in such a way that the tidal volume of exhalation is in the range of 4-6 ml/kg. If the mechanical ventilation device has a function for automatically selecting peak pressure depending on the patient’s tidal volume, it is advisable to use it in seriously ill patients in order to prevent artificial ventilation of associated lung damage.

Synchronization of a child with a ventilator. Routine drug synchronization with a respirator leads to worse neurological outcomes (B). In this regard, it is necessary to try to synchronize the patient with the ventilator by adequately selecting parameters. The vast majority of patients with extreme and very low body weight, with properly performed artificial ventilation, do not require drug synchronization with a ventilator. As a rule, newborns forcefully breathe or “struggle” with the respirator if the ventilator does not provide adequate minute ventilation. As is known, minute ventilation is equal to the product of tidal volume and frequency. Thus, it is possible to synchronize a patient with a ventilator by increasing the frequency of the respirator or tidal volume, if the latter does not exceed 6 ml/kg. Severe metabolic acidosis can also cause forced breathing, which requires correction of acidosis rather than sedation of the patient. An exception may be structural cerebral damage, in which shortness of breath is of central origin. If adjusting the parameters fails to synchronize the child with the respirator, painkillers and sedatives are prescribed - morphine, fentanyl, diazepam in standard doses. Adjustment of artificial ventilation parameters. The main correction of ventilation parameters is a timely decrease or increase in peak pressure in accordance with changes in tidal volume (Vt). Vt should be maintained between 4-6 ml/kg by increasing or decreasing PIP. Exceeding this indicator leads to lung damage and an increase in the length of time the child remains on a ventilator.

When adjusting parameters, remember that:
- the main aggressive parameters of artificial lung ventilation, which should be reduced first, are: PIP (Vt). and FiC2 (>40%);
- at one time the pressure changes by no more than 1-2 cm of water column, and the breathing rate by no more than 5 breaths (in SIMV and IMV modes). In Assist control mode, changing the frequency is meaningless, since in this case the frequency of breaths is determined by the patient, and not by the ventilator;
- FiO2 should be changed under the control of SpO2 in steps of 5-10%;
- hyperventilation (pCO2
Dynamics of artificial lung ventilation modes. If it is not possible to extubate the patient from the assist control mode in the first 3-5 days, then the child should be transferred to the SIMV mode with pressure support (PSV). This maneuver reduces the total mean airway pressure and thus reduces the invasiveness of mechanical ventilation. Thus, the patient's target inhalation rate will be delivered with inspiratory pressure set to keep the tidal volume between 4-6 ml/kg. The remaining spontaneous inspiration (PSV) support pressure should be set so that the tidal volume corresponds to the lower limit of 4 ml/kg. Those. ventilation in the SIMV+PSV mode is carried out with two levels of inspiratory pressure - optimal and maintenance. Avoidance of artificial ventilation is carried out by reducing the forced frequency of the respirator, which leads to a gradual transfer of the child to the PSV mode, from which extubation to non-invasive ventilation is carried out.

Extubation. It has now been proven that the most successful extubation of newborns occurs when they are transferred from artificial ventilation to continuous positive pressure artificial ventilation and to non-invasive artificial ventilation. Moreover, success in transferring to non-invasive artificial ventilation is higher than simply extubating to a continuous positive pressure artificial lung ventilation mode.

Rapid extubation from A/C mode directly to continuous positive pressure ventilation or non-invasive ventilation can be performed under the following conditions:
- absence of pulmonary hemorrhage, convulsions, shock;
- PIP - FiO2 ≤0.3;
- presence of regular spontaneous breathing. The blood gas composition before extubation should be satisfactory.

When using the SIMV mode, FiO2 gradually decreases to values less than 0.3, PIP to 17-16 cm H2O and RR to 20-25 per minute. Extubation to the binasal mode of artificial pulmonary ventilation with constant positive pressure is carried out in the presence of spontaneous breathing.

For successful extubation of low birth weight patients, the use of caffeine is recommended to stimulate regular breathing and prevent apnea. The greatest effect from the administration of methylxanthines is observed in children
A short course of low-dose corticosteroids can be used to more quickly convert from invasive mechanical ventilation to continuous positive pressure ventilation/non-invasive mechanical ventilation if the preterm infant cannot be removed from mechanical ventilation after 7-14 days (A) Necessary monitoring.
Parameters of artificial ventilation of the lungs:
- FiO2, RR (forced and spontaneous), inspiratory time PIP, PEER, MAP. Vt, leakage percentage.
Monitoring blood gases and acid-base status. Periodic determination of blood gases in arterial, capillary or venous blood. Permanent definition oxygenation: SpO2 and ТсСО2. In seriously ill patients and in patients on high-frequency mechanical ventilation, continuous monitoring of TcCO2 and TcO2 using a transcutaneous monitor is recommended.
Hemodynamic monitoring.
periodic assessment of chest radiograph data.

High-frequency oscillatory artificial ventilation
Definition. High-frequency oscillatory ventilation is mechanical ventilation of small tidal volumes with a high frequency. Pulmonary gas exchange during artificial ventilation is carried out through various mechanisms, the main of which are direct alveolar ventilation and molecular diffusion. Most often in neonatal practice, the frequency of high-frequency oscillatory artificial ventilation is used from 8 to 12 hertz (1 Hz = 60 oscillations per second). A distinctive feature of oscillatory artificial ventilation is the presence of active exhalation.

Indications for high-frequency oscillatory artificial ventilation.
Ineffectiveness of traditional artificial ventilation. To maintain acceptable gas composition blood required:
- MAP >13 cm water. Art. in children with b.t. >2500 g;
- MAP >10 cm water. Art. in children with b.t. 1000-2500 g;
- MAP >8 cm water. Art. in children with b.t.
Severe forms air leak syndrome from the lungs (pneumothorax, interstitial pulmonary emphysema).

Starting parameters of high-frequency oscillatory artificial ventilation for neonatal respiratory distress syndrome.
Paw (MAP) - average pressure in the respiratory tract, is set at 2-4 cm of water column than with traditional artificial ventilation.
ΔΡ is the amplitude of oscillatory oscillations, usually selected in such a way that the patient’s chest vibration is visible to the eye. The starting amplitude of oscillatory oscillations can also be calculated using the formula:

Where m is the patient’s body weight in kilograms.
Fhf - frequency of oscillatory oscillations (Hz). It is set to 15 Hz for children weighing less than 750 g, and 10 Hz for children weighing more than 750 g. Tin% (percentage of inspiratory time) - On devices where this parameter is adjusted, it is always set to 33% and does not change throughout the entire duration of respiratory support Increasing this parameter leads to the appearance of gas traps.
FiO2 (oxygen fraction). It is installed in the same way as with traditional artificial lung ventilation.
Flow (constant flow). On devices with adjustable flow, it is set within 15 l/min ± 10% and does not change in the future.

Adjusting parameters. Lung volume optimization. With normally expanded lungs, the dome of the diaphragm should be located at the level of the 8th-9th rib. Signs of hyperinflation (overinflated lungs):
- increased transparency of the lung fields;
- flattening of the diaphragm ( lung fields extend below the level of the 9th rib).

Signs of hypoinflation (underexpanded lungs):
- diffuse atelectasis;
- diaphragm above the level of the 8th rib.

Correction of high-frequency oscillatory artificial ventilation parameters based on blood gas values.
For hypoxemia (paO2 - increase MAP by 1-2 cm of water column;
- increase FiO2 by 10%.

For hyperoxemia (paO2 >90 mmHg):
- reduce FiO2 to 0.3.

In case of hypocapnia (paCO2 - reduce DR by 10-20%;
- increase the frequency (by 1-2 Hz).

With hypercapnia (paCO2 >60 mm Hg):
- increase ΔР by 10-20%;
- reduce the oscillation frequency (by 1-2 Hz).

Discontinuation of high-frequency oscillatory mechanical ventilation
As the patient's condition improves, FiO2 is gradually (in steps of 0.05-0.1) reduced, bringing it to 0.3. Also, stepwise (in increments of 1-2 cm of water column) the MAP is reduced to a level of 9-7 cm of water. Art. The child is then transferred to either one of the auxiliary modes of traditional ventilation or non-invasive respiratory support.

Features of caring for a child on high-frequency oscillatory artificial ventilation
To adequately humidify the gas mixture, it is recommended that sterile distilled water be continuously injected into the humidifier chamber. Because of high speed flow, the liquid from the humidification chamber evaporates very quickly. Sanitation of the respiratory tract should be carried out only if:
- weakening of visible vibrations of the chest;
- significant increase in pCO2;
- decreased oxygenation;
- the time to disconnect the breathing circuit for sanitation should not exceed 30 s. It is advisable to use closed systems for sanitation of the tracheobronchial tree.

After completing the procedure, you should temporarily (for 1-2 minutes) increase PAW by 2-3 cm of water column.
There is no need to administer muscle relaxants to all children on high-frequency ventilation. Your own respiratory activity helps improve blood oxygenation. The administration of muscle relaxants leads to an increase in sputum viscosity and contributes to the development of atelectasis.
Indications for sedatives include severe agitation and severe respiratory effort. The latter requires the exclusion of hypercarbia or obstruction of the endotracheal tube.
Children on high-frequency oscillatory ventilation require more frequent x-ray examination chest organs than children on traditional mechanical ventilation.
It is advisable to carry out high-frequency oscillatory artificial ventilation under the control of transcutaneous pCO2

Antibacterial therapy
Antibacterial therapy for respiratory distress syndrome is not indicated. However, during the period differential diagnosis respiratory distress syndrome with congenital pneumonia/congenital sepsis, carried out in the first 48-72 hours of life, it is advisable to prescribe antibacterial therapy followed by its rapid withdrawal in the event of negative markers of inflammation and a negative result of microbiological blood culture. Prescription of antibacterial therapy during the period of differential diagnosis may be indicated for children weighing less than 1500 g, children on invasive mechanical ventilation, as well as children in whom the results of inflammatory markers obtained in the first hours of life are questionable. The drugs of choice may be a combination of antibiotics penicillin series and aminoglycosides or one broad-spectrum antibiotic from the group of protected penicillins. Amoxicillin + clavulanic acid should not be prescribed due to the possible adverse effects of clavulanic acid on intestinal wall in premature babies.

MINISTRY OF HEALTH OF THE REPUBLIC OF UZBEKISTAN

TASHKENT PEDIATRIC MEDICAL INSTITUTE

RESPIRATORY DISTRESS SYNDROME IN NEWBORNS

Tashkent - 2010

Compiled by:

Gulyamova M.A., Rudnitskaya S.V., Ismailova M.A.,

Khodzhimetova Sh.H., Amizyan N.M., Rakhmankulova Z.Zh.

Reviewers:

1. Mukhamedova Kh. T.d. M.Sc., professor, head. Department of Neonatology TashIUV

2. Dzhubatova R.S. Doctor of Medical Sciences, Director of the Russian Scientific and Practical Medical Center of Pediatrics

3. Shomansurova E.A. associate professor, head Department of Outpatient Medicine TashPMI

"Respiratory distress syndrome in newborns"

1. At the Problem Commission of the Pediatric Council of TashPMI, protocol No.

2. At the Academic Council of TashPMI, protocol No.

Secretary of the Academic Council Shomansurova E.A.

List of abbreviations

CPAP- continuous positive airway pressure

FiO 2- oxygen content in the inhaled mixture

PaCO2- partial pressure of carbon dioxide in arterial blood

PaO2- partial pressure of oxygen in arterial blood

PCO 2- partial pressure of carbon dioxide in mixed (capillary) blood

P.I.P.- (PVP) peak (upper limit) pressure during inspiration

PO 2- partial pressure of oxygen in mixed (capillary) blood

SaO2- an indicator of hemoglobin oxygen saturation measured in arterial blood

SpO2- indicator of hemoglobin oxygen saturation measured by a transcutaneous sensor

HELL- arterial pressure

BGM- hyaline membrane disease

BPD- bronchopulmonary dysplasia

VFO IVL - high-frequency oscillatory artificial ventilation

ICE- disseminated intravascular coagulation

DN- respiratory failure

BEFORE- tidal volume

Gastrointestinal tract- gastrointestinal tract

mechanical ventilation- artificial ventilation

IEL- interstitial pulmonary emphysema

CBS- acid-base state

L/S - lecithin/sphingomyelin

IDA- average pressure in the respiratory tract, see water. Art.

MOS- cytochrome P-450 system

FLOOR- lipid peroxidation

RASPM - Russian Association perinatal medicine specialists

RDS- respiratory distress syndrome

MYSELF- meconium aspiration syndrome

HAPPY BIRTHDAY- respiratory distress syndrome

CCH- cardiovascular failure

SUV- air leak syndrome

LDP- tracheobronchial tree

FOE- functional residual capacity of the lungs

CNS - central nervous system

NPV- respiratory rate

ECG- electrocardiogram

YANEC- ulcerative-necrotizing enterocolitis

Definition

RESPIRATORY DISTRESS SYNDROME (English: distress, severe malaise, suffering; Latin: respiratio breathing; syndrome - a set of typical symptoms) - non-infectious pathological processes (primary atelectasis, hyaline membrane disease, edematous-hemorrhagic syndrome) that form in the prenatal and early neonatal periods of development child and manifested by breathing problems. A symptom complex of severe respiratory failure that occurs in the first hours of a child’s life due to the development of primary pulmonary atelectasis, hyaline membrane disease, and edematous hemorrhagic syndrome. It is more common in premature and immature newborns.

The incidence of respiratory distress depends on the degree of prematurity, and averages 60% in children born at a gestational age of less than 28 weeks, 15-20% - at a period of 32-36 weeks. and 5% - for a period of 37 weeks. and more. With rational care of such children, the mortality rate approaches 10%.

Epidemiology.

RDS is the most common cause of respiratory failure in the early neonatal period. Its occurrence is higher, the lower the gestational age and body weight of the child at birth. However, the incidence of RDS is strongly influenced by methods of prenatal prevention when there is a threat of preterm birth.

In premature babies born at more than 34 weeks of gestation, its frequency does not depend on prenatal prevention and is less than 5%. (Volodin N.N. et al. 2007)

Etiology.

· deficiency of surfactant formation and release;

· quality defect of surfactant;

· inhibition and destruction of surfactant;

· immaturity of the lung tissue structure.

Risk factors.

Risk factors for RDS are all conditions leading to surfactant deficiency and lung immaturity, namely: asphyxia of the fetus and newborn, morpho-functional immaturity, impaired pulmonary-cardiac adaptation, pulmonary hypertension, metabolic disorders (acidosis, hypoproteinemia, hypofermentosis, changes electrolyte metabolism), untreated diabetes mellitus in pregnancy, bleeding in pregnancy, cesarean section, male sex of the newborn, and being born second of twins.

Intrauterine development of the lungs.

The tracheobronchial tree system begins as a lung bud, which subsequently continuously divides and develops, penetrating the mesenchyme, and expanding to the periphery. This process goes through 5 development phases (Fig. 1):

1. Embryonic phase (< 5 недели)

2. Pseudograndular phase (5-16 weeks)

3. Canalicular phase (17-24 weeks)

4. Developmental phase of the terminal sac (24-37 weeks)

5. Alveolar phase (from the end of 37 weeks to 3 years).

The rudiment of the respiratory tract appears in a 24-day embryo; in the next 3 days, two primary bronchi are formed. The first cartilaginous elements in the bronchi appear at the 10th week, and at the 16th week the intrauterine formation of all generations of the bronchial tree practically ends, although cartilage continues to appear until the 24th week of the gestational period.

Figure 1. Five phases of tracheobronchial airway development. ( adapted from Weibel ER: Morphomeiry of the Human Lung. Berlin, Springer-Verlag, 1963.)

Asymmetry of the main bronchi has been observed since the first days of their development; the rudiments of the lobar bronchi are visible in the embryo at 32 days, and the segmental bronchi at 36 days. By the 12th week, the pulmonary lobes are already distinguishable.

Differentiation of lung tissue begins from the 18th-20th week, when alveoli with capillaries appear in the walls. At the age of 20 weeks, the bronchial drainage usually accumulates, the lumen of which is lined with cuboidal epithelium.

Alveoli appear as outgrowths on the bronchioles, and from the 28th week they increase in number. Since new alveoli can form throughout the prenatal period, terminal air spaces lined by cuboidal epithelium can be found in the lungs of newborns.

The lung primordium is initially supplied with blood through paired segmental arteries arising from the dorsal part of the aorta. The vascular elements of the lung begin to form from the mesenchyme from 20 weeks of age as branches of these arteries. Gradually, the pulmonary capillaries lose connection with the segmental arteries, and their blood supply is provided by the branches of the pulmonary artery, which generally follow the branching of the respiratory tube. Anastomoses between the pulmonary and bronchial artery systems persist until birth and can function in premature infants in the first weeks of life.

Already in the 28-30 day embryo, blood from the lungs flows into the left atrium, where the venous sinus is formed.

At 26-28 weeks of the intrauterine period capillary network the lung closely meets the alveolar surface; At this point, the lung acquires the ability to exchange gases.

The development of the pulmonary arteries is accompanied by a progressive increase in their lumen, which initially does not exceed several micrometers. The lumen of the lobar arteries increases only at the 10th week of the intrauterine period, and the lumen of the terminal and respiratory arterioles - only at the 36-38th week. A relative increase in the lumen of the arteries is observed during the first year of life.

Lymphatic vessels surrounding the bronchi, arteries and veins reach the alveoli by the time of birth; this system is formed in the 60-day-old vibrio.

Mucous glands in the trachea are formed by secondary invagination of the epithelium at 7-8 weeks, goblet cells - at 13-14 weeks. At the 26th week of intrauterine life, the mucous glands begin to secrete mucus containing acidic glycosaminoglycans (mucopolysaccharides).

Epithelial cilia in the trachea and main bronchi appear around the 10th week, and in the peripheral bronchi - from the 13th week. In the bronchioles along with the cells ciliated epithelium there are cylindrical cells containing secretory granules in the apical part.

The most peripheral layer of the inner lining of the respiratory tract is represented by alveolocytes of two types, appearing from the 6th month of the intrauterine period. Type I alveolocytes cover up to 95% of the surface of the alveoli; the remainder of the area is occupied by type II alveolocytes, which have a developed lamellar complex (Golgi apparatus), mitochondria and osmiophilic inclusions. The main function of the latter is the production of surfactant, which appears in fruits weighing 500-1200 g; The lower the gestational age of the newborn, the higher the surfactant deficiency. Surfactant is primarily formed in upper lobes, then in the lower ones.

Another function of type II alveolocytes is proliferation and transformation into type I alveolocytes when the latter are damaged.

Surfactant produced by type II alveolocytes, which is based on phospholipids (mainly dipalmitoyl phosphatidylcholine), performs the most important function- stabilizes terminal air-containing spaces. Forming a thin continuous lining of the alveoli, the surfactant changes surface tension depending on the radius of the alveoli. With an increase in the radius of the alveoli during inspiration, surface tension increases to 40-50 dynes/cm, significantly increasing the elastic resistance to breathing. At low volumes alveolar tension drops to 1-5 dynes/cm, which ensures stability of the alveoli during exhalation. Surfactant deficiency in premature infants is one of the leading causes of RDS.

Respiratory distress syndrome in children, or “shock” lung, is a symptom complex that develops following stress and shock.

What Causes Respiratory Distress Syndrome in Children?

The triggering mechanisms of the RDS are gross violations microcirculation, hypoxia and tissue necrosis, activation of inflammatory mediators. Respiratory distress syndrome in children can develop with multiple trauma, severe blood loss, sepsis, hypovolemia (accompanied by shock), infectious diseases, poisoning, etc. In addition, the cause of respiratory distress syndrome in children can be the syndrome of massive blood transfusions, unskilled carrying out mechanical ventilation. It develops after undergoing clinical death and resuscitation measures as component post-resuscitation illness in combination with damage to other organs and systems (MODS).

It is believed that the formed elements of the blood, as a result of hypoplasmia, acidosis and changes in the normal surface charge, begin to deform and stick to each other, forming aggregates - a sludge phenomenon (English sludge - sludge, sludge), which causes embolism of small pulmonary vessels. Adhesion shaped elements blood between each other and with the vascular endothelium triggers the process of blood disseminated intravascular coagulation. At the same time, a pronounced reaction of the body begins to hypoxic and necrotic changes in tissues, to the penetration of bacteria and endotoxins (lipopolysaccharides) into the blood, which Lately interpreted as a syndrome of generalized inflammatory reaction(Sistemic inflammatory response syndrome - SIRS).

Respiratory distress syndrome in children, as a rule, begins to develop at the end of the 1st or beginning of the 2nd day after the patient is brought out of shock. There is an increase in blood supply in the lungs, and hypertension occurs in the pulmonary vascular system. Increased hydrostatic pressure against the background of increased vascular permeability contributes to the exudation of the liquid part of the blood into the interstitial, interstitial tissue, and then into the alveoli. As a result, lung compliance decreases, surfactant production decreases, and rheological properties are disrupted. bronchial secretions And metabolic properties lungs in general. Blood shunting increases, ventilation-perfusion relationships are disrupted, and microatelectasis of the lung tissue progresses. In advanced stages of “shock” lung, hyaline penetrates into the alveoli and hyaline membranes are formed, sharply disrupting the diffusion of gases through the alveolar capillary membrane.

Symptoms of respiratory distress syndrome in children

Respiratory distress syndrome in children can develop in children of any age, even in the first months of life against the background of decompensated shock and sepsis, but this diagnosis is rarely made in children, interpreting the detected clinical and radiological changes in the lungs as pneumonia.

There are 4 stages of respiratory distress syndrome in children.

In stage I (1-2 days) euphoria or anxiety is observed. Tachypnea and tachycardia increase. Hard breathing can be heard in the lungs. Hypoxemia develops, controlled by oxygen therapy. An X-ray of the lungs reveals an increased pulmonary pattern, cellularity, and finely focal shadows.
In stage II (days 2-3), patients are excited, shortness of breath and tachycardia intensify. The shortness of breath is inspiratory in nature, the inhalation becomes noisy, “with strain,” and auxiliary muscles are involved in the act of breathing. Zones of weakened breathing and symmetrical scattered dry rales appear in the lungs. Hypoxemia becomes resistant to oxygenation. An x-ray of the lungs reveals a picture of “air bronchography” and confluent shadows. Mortality reaches 50%.
Stage III (4-5 days) is manifested by diffuse cyanosis of the skin, oligopnea. In the posterior lower parts of the lungs, moist rales of various sizes are heard. There is severe hypoxemia, responsive to oxygen therapy, combined with a tendency to hypercapnia. An X-ray of the lungs reveals a “snow storm” symptom in the form of multiple merging shadows; pleural effusion is possible. Mortality reaches 65-70%.
In stage IV (after the 5th day), patients experience stupor, pronounced hemodynamic disturbances in the form of cyanosis, cardiac arrhythmias, arterial hypotension, gasping breathing. Hypoxemia in combination with hypercapnia becomes resistant to mechanical ventilation with a high oxygen content in the supplied gas mixture. Clinically and radiologically, a detailed picture of alveolar pulmonary edema is determined. Mortality reaches 90-100%.

Diagnosis and treatment of respiratory distress syndrome in children

Diagnosing RDS in children is a rather complex task, requiring the doctor to know the prognosis of the course of severe shock of any etiology, the clinical manifestations of the “shock” lung, and the dynamics of blood gases. The general treatment regimen for respiratory distress syndrome in children includes:

restoration of airway patency by improving rheological properties sputum (inhalation of saline, detergents) and evacuation of sputum by natural (cough) or artificial (suction) means;
ensuring gas exchange function of the lungs. Oxygen therapy is prescribed in the PEEP mode using a Martin-Bauer bag or according to the Gregory method with spontaneous breathing (through a mask or endotracheal tube). At stage III of RDS, the use of mechanical ventilation with the inclusion of the PEEP mode (5-8 cm of water column) is mandatory. Modern ventilators allow the use of inverted modes of regulation of the ratio of inhalation and exhalation time (1:E = 1:1,2:1 and even 3:1). Combination with high-frequency ventilation is possible. In this case, it is necessary to avoid high concentrations of oxygen in the gas mixture (P2 above 0.7). P02=0.4-0.6 is considered optimal when pa02 is at least 80 mmHg. Art.;
improvement of the rheological properties of blood (heparin, disaggregating drugs), hemodynamics in the pulmonary circulation (cardiotonics - dopamine, dobutrex, etc.), reduction of intrapulmonary hypertension in stage II-III RDS with the help of ganglion blockers (pentamine, etc.), a-blockers;
antibiotics in the treatment of RDS are of secondary importance, but are always prescribed in combination.

Respiratory distress syndrome of newborns – pathological condition, which occurs in the early neonatal period and is clinically manifested by signs of acute respiratory failure. In the medical literature, there are also alternative terms for this syndrome: “respiratory distress syndrome”, “hyaline membrane disease”.

The disease is usually detected in premature infants and is one of the most severe and common pathologies of the newborn period. Moreover, the lower the gestational age of the fetus and its birth weight, the higher the likelihood of developing respiratory disorders in the child.

Predisposing factors

The basis of RDS syndrome in newborns is the lack of a substance that covers the alveoli from the inside - surfactant.

The basis for the development of this pathology is the immaturity of the lung tissue and surfactant system, which explains the occurrence of such disorders mainly in premature infants. But children born at full term may also develop RDS. The following factors contribute to this:

intrauterine infections;
fetal asphyxia;
general cooling (at temperatures below 35 degrees, surfactant synthesis is disrupted);
multiple pregnancy;
incompatibility of blood type or Rh factor between mother and child;
(increases the likelihood of detecting RDS in a newborn by 4-6 times);
bleeding due to premature placental abruption or placental previa;
delivery by planned cesarean section (before the onset of labor).

Why is it developing?

The occurrence of RDS in newborns is due to:

impaired synthesis of surfactant and its excretion onto the surface of the alveoli due to insufficient maturation of lung tissue;
birth defects of the surfactant system;
its increased destruction during various pathological processes (for example, severe hypoxia).

Surfactant begins to be produced by the fetus during intrauterine development at 20-24 weeks. However, during this period it does not have all the properties of a mature surfactant, it is less stable (it is quickly destroyed under the influence of hypoxemia and acidosis) and has a short half-life. This system fully matures at the 35-36th week of pregnancy. A massive release of surfactant occurs during labor, which helps expand the lungs during the first breath.

Surfactant is synthesized by type II alveolocytes and is a monomolecular layer on the surface of the alveoli, consisting of lipids and proteins. Its role in the body is very large. Its main functions are:

preventing the alveoli from collapsing during inspiration (by reducing surface tension);
protection of the alveolar epithelium from damage;
improvement of mucociliary clearance;
regulation of microcirculation and permeability of the alveolar wall;
immunomodulatory and bactericidal effect.

In a child born prematurely, the reserves of surfactant are only sufficient to take the first breath and ensure respiratory function in the first hours of life; subsequently, its reserves are depleted. Due to the lag between the processes of surfactant synthesis and the rate of its decay, the subsequent increase in the permeability of the alveolo-capillary membrane and the sweating of fluid into the interalveolar spaces, a significant change in the functioning of the respiratory system occurs:

are formed in various parts of the lungs;
stagnation is observed;
interstitial develops;
hypoventilation increases;
intrapulmonary shunting of blood occurs.

All this leads to insufficient oxygenation of tissues, accumulation of carbon dioxide in them, and a change in the acid-base state towards acidosis. The resulting respiratory failure disrupts the functioning of the cardiovascular system. These children develop:

increased pressure in the pulmonary artery system;
system ;
transient myocardial dysfunction.

It should be noted that surfactant synthesis is stimulated by:

corticosteroids;
estrogens;
thyroid hormones;
adrenaline and norepinephrine.

Its maturation is accelerated by chronic hypoxia (with intrauterine growth retardation, late gestosis).

How it manifests itself and why it is dangerous

Depending on the time of onset of symptoms of this pathology and general condition in the child’s body at this moment, three main variants of its clinical course can be distinguished.

Some premature babies born in satisfactory condition, first clinical manifestations are registered 1-4 hours after birth. This variant of the disease is considered classic. The so-called “light gap” is associated with the functioning of an immature and rapidly disintegrating surfactant.
The second variant of the syndrome is typical for premature babies who have suffered severe hypoxia during childbirth. Their alveolocytes are not able to quickly accelerate the production of surfactant after expansion of the lungs. The most common cause of this condition is acute asphyxia. Initially, the severity of the condition of newborns is due to cardiorespiratory depression. However, once their condition has stabilized, they quickly develop RDS.
The third variant of the syndrome is observed in very premature infants. They have a combination of immature surfactant synthesis mechanisms with a limited ability of alveolocytes to increase the rate of its production after the first breath. Signs of respiratory distress in such newborns are noticeable from the first minutes of life.

In the classical course respiratory syndrome Some time after birth, the baby develops the following symptoms:

gradual increase in respiratory rate (against the background of the skin being of normal color, cyanosis appears later);
swelling of the wings of the nose and cheeks;
loud moaning exhalation;
retraction of the most pliable places of the chest during inspiration - supraclavicular fossa, intercostal spaces, lower part of the sternum.

As the pathological process progresses, the child’s condition worsens:

the skin becomes cyanotic;
there is a decrease blood pressure and body temperature;
muscle hypotonia and hyporeflexia increase;
chest rigidity develops;
Moist rales are heard above the lungs against the background of weakened breathing.

In extremely premature infants, RDS has its own characteristics:

an early sign of a pathological process is diffuse cyanosis;
immediately after birth, they experience swelling of the anterosuperior parts of the chest, which is later replaced by its retraction;
breathing disorders are manifested by attacks of apnea;
symptoms such as swelling of the wings of the nose may be absent;
symptoms of respiratory failure persist for a longer period of time.

In severe RDS, due to severe circulatory disorders (both systemic and local), its course is complicated by damage nervous system, gastrointestinal tract, kidneys.

Diagnostic principles

Women who are at risk undergo amniocentesis and the lipid content of the resulting amniotic fluid sample is examined.

Early diagnosis RDS is extremely important. In women at risk, it is recommended to prenatal diagnostics. To do this, the lipid spectrum of amniotic fluid is examined. Its composition is used to judge the degree of maturity of the fetal lungs. Taking into account the results of such a study, it is possible to timely prevent RDS in the unborn child.

In the delivery room, especially in the case of premature birth, the maturity of the main systems of the child’s body is assessed for its gestational age, and risk factors are identified. In this case, the “foam test” is considered quite informative (ethyl alcohol is added to the amniotic fluid or aspirate of gastric contents and the reaction is observed).

IN further diagnostics respiratory distress syndrome is based on an assessment of clinical data and the results of x-ray examination. Radiological signs of the syndrome include the following:

decreased pneumatization of the lungs;
air bronchogram;
blurred boundaries of the heart.

To fully assess the severity of respiratory disorders in such children, special scales are used (Silverman, Downs).

Treatment tactics

Treatment for RDS begins with proper care of the newborn. He should be provided with a protective regime with minimization of light, sound and tactile irritations, optimal temperature environment. Typically the baby is placed under a heat source or in an incubator. His body temperature should not be less than 36 degrees. At first, until the child’s condition stabilizes, parenteral nutrition is provided.

Treatment for RDS begins immediately and usually includes:

ensuring normal airway patency (suction of mucus, appropriate position of the child);
administration of surfactant preparations (carried out as early as possible);
adequate ventilation of the lungs and normalization of blood gas composition (oxygen therapy, CPAP therapy, mechanical ventilation);
combating hypovolemia (infusion therapy);
correction of acid-base status.

Considering the severity of RDS in newborns, the high risk of complications and the numerous difficulties of the therapy, special attention should be paid to the prevention of this condition. It is possible to accelerate the maturation of the fetal lungs by administering glucocorticoid hormones (dexamethasone, betamethasone) to a pregnant woman. Indications for this are:

high risk of premature birth and its initial signs;
complicated course of pregnancy, in which early delivery is planned;
premature rupture of amniotic fluid;
bleeding during pregnancy.

A promising direction for preventing RDS is the introduction of thyroid hormones into the amniotic fluid.

Respiratory function is vital, so at birth it is assessed using the Apgar score along with other important indicators. Breathing problems sometimes lead to serious complications, as a result of which in certain situations one has to literally fight for life.

One of these serious pathologies is neonatal respiratory distress syndrome, a condition in which respiratory failure develops in the first hours or even minutes after birth. In most cases, breathing problems occur in premature babies.

There is such a pattern: the shorter the gestational age (number full weeks from conception to birth) and the weight of the newborn, the greater the likelihood of developing respiratory distress syndrome (RDS). But why does this happen?

Causes of occurrence and mechanism of development

Modern medicine today believes that main reason the development of respiratory failure remains the immaturity of the lungs and the still imperfect functioning of the surfactant.

It may be that there is enough surfactant, but there is a defect in its structure (normally it consists of 90% fat, and the rest is protein), which is why it does not cope with its purpose.

The following factors may increase your risk of developing RDS:

Deep prematurity, especially for children born before the 28th week.
If the pregnancy is multiple. The risk exists for the second baby of twins and for the second and third of triplets.
Delivery by caesarean section.
Large blood loss during childbirth.
Serious illnesses in the mother, such as diabetes.
Intrauterine hypoxia, asphyxia during childbirth, infections (intrauterine and not only), such as streptococcal, which contributes to the development of pneumonia, sepsis, etc.
Meconium aspiration (a condition when a child swallows amniotic fluid with meconium).

The important role of surfactant

Surfactant is a mixture of surfactants that lies in an even layer on the pulmonary alveoli. It plays an indispensable role in the breathing process by reducing surface tension. In order for the alveoli to work smoothly and not collapse during exhalation, they need lubrication. Otherwise, the child will have to expend a lot of effort to straighten his lungs with each breath.

Surfactant is vital for maintaining normal breathing

While in the mother’s womb, the baby “breathes” through the umbilical cord, but already at the 22-23rd week the lungs begin to prepare for full work: the process of producing surfactant begins, and they talk about the so-called maturation of the lungs. However, enough of it is produced only by 35-36 weeks of pregnancy. Children born before this period are at risk for developing RDS.

Types and prevalence

WITH respiratory distress Approximately 6% of children struggle. RDS occurs in approximately 30-33% of premature babies, in 20-23% - in those born too late and only in 4% of cases - in full-term ones.

There are:

Primary RDS occurs in premature infants due to surfactant deficiency.
Secondary RDS - develops due to the presence of other pathologies or the addition of infections.

Symptoms

The clinical picture unfolds immediately after birth, within a few minutes or hours. All symptoms indicate acute respiratory failure:

Tachyapnea - breathing with a frequency above 60 breaths per minute, with periodic stops.
Inflating of the wings of the nose (due to reduced aerodynamic resistance), as well as retraction of the intercostal spaces and the chest as a whole when inhaling.
Blueness of the skin, blueness of the nasolabial triangle.
Breathing is heavy, and “grunting” noises are heard when exhaling.

To assess the severity of symptoms, tables are used, for example the Downs scale:

A score of up to 3 points indicates mild respiratory distress; if the score is > 6, then we're talking about O in serious condition requiring immediate resuscitation measures

Diagnostics

Respiratory distress syndrome in newborns is, one might say, a symptom. For treatment to be effective, it is necessary to establish the true cause of this condition. First, they check the “version” of possible immaturity of the lungs, lack of surfactant, and also see if there is congenital infections. If these diagnoses are not confirmed, they are examined for the presence of other diseases.

To make a correct diagnosis, consider the following information:

History of pregnancy and general condition of the mother. Pay attention to the age of the woman in labor, whether she has chronic diseases(in particular, diabetes), infectious diseases, how the pregnancy progressed, its duration, results of ultrasound and tests during gestation, what medications the mother took. Is there polyhydramnios (or oligohydramnios), what kind of pregnancy is it, how did the previous ones proceed and end.
Labor was spontaneous or by cesarean section, fetal presentation, characteristics of amniotic fluid, anhydrous interval time, heart rate of the child, whether the mother had fever, bleeding, whether she was given anesthesia.
Condition of the newborn. The degree of prematurity, the condition of the large fontanel are assessed, the lungs and heart are listened to, and an Apgar score is assessed.

The following indicators are also used for diagnosis:

X-ray of the lungs is very informative. There are shadows in the image, usually they are symmetrical. The lungs are reduced in volume.
Determination of the coefficient of lecithin and sphingomyelin in amniotic fluid. It is believed that if it is less than 1, then the likelihood of developing RDS is very high.
Measurement of saturated phosphatidylcholine and phosphatidylglycerol levels. If their quantity is sharply reduced or there are no substances at all, there is a high risk of developing RDS.

Treatment

The choice of therapeutic interventions will depend on the situation. Respiratory distress syndrome in newborns is a condition that requires resuscitation measures, including ensuring airway patency and restoring normal breathing.

Surfactant therapy

One of the effective methods of treatment is the introduction of surfactant into the trachea of a premature baby in the first so-called golden hour of life. For example, they use the drug Kurosurf, which is a natural surfactant obtained from pig lungs.

The essence of the manipulation is as follows. Before administration, the bottle with the substance is heated to 37 degrees and turned upside down, being careful not to shake it. This suspension is drawn up using a syringe with a needle and injected into lower section trachea through an endotracheal tube. After the procedure, manual ventilation is performed for 1-2 minutes. If the effect is insufficient or absent, a second dose is administered after 6-12 hours.

This type of therapy has good results. It increases the survival rate of newborns. However, the procedure has contraindications:

arterial hypotension;
state of shock;
pulmonary edema;
pulmonary hemorrhage;
low temperature;
decompensated acidosis.

One of the surfactant preparations

In such critical situations, it is first necessary to stabilize the baby’s condition, and then begin treatment. It is worth noting that the most effective results surfactant therapy gives in the first hours of life. Another drawback is the high cost of the drug.

CPAP therapy

This is a method of creating continuous positive pressure in the respiratory tract. It is used for mild forms of RDS, when the first signs of respiratory failure (RF) only develop.

mechanical ventilation

If CPAP therapy is ineffective, the child is transferred to mechanical ventilation (artificial pulmonary ventilation). Some indications for mechanical ventilation:

increasing attacks of apnea;
convulsive syndrome;
score greater than 5 points according to Silverman.

It must be taken into account that the use of mechanical ventilation in the treatment of children inevitably leads to lung damage and complications such as pneumonia. When carrying out mechanical ventilation, it is necessary to monitor the vital signs and functioning of the baby’s body.

General principles of therapy

Temperature conditions. It is extremely important to prevent heat loss in a child with RDS, as cooling can reduce surfactant production and increase the frequency of sleep apneas. After birth, the baby is wrapped in a warm sterile diaper, the remaining amniotic fluid on the skin is blotted and placed under a radiant heat source, after which it is transported to the incubator. You definitely need to put a cap on your head, since there is a large loss of heat and water from this part of the body. When examining a child in an incubator, you should avoid sharp changes temperatures, so the inspection should be as short as possible, with minimal touching.
Sufficient humidity in the room. The baby loses moisture through the lungs and skin, and if born with a small weight (
Normalization of blood gas parameters. For this purpose, oxygen masks, a ventilator and other options for maintaining breathing are used.
Proper feeding. In severe form Newborn RDS on the first day they are “fed” by introducing infusion solutions parenterally (for example, glucose solution). The volume is administered in very small portions, since fluid retention is observed at birth. Breast milk or adapted milk formulas are included in the diet, focusing on the baby’s condition: how well developed is his sucking reflex, whether there is prolonged apnea, regurgitation.
Hormone therapy. Glucocorticoid drugs are used to accelerate the maturation of the lungs and the production of their own surfactant. However, today such therapy is being abandoned due to many side effects.
Antibiotic therapy. All children with RDS are prescribed a course of antibiotic therapy. This is due to the fact that the clinical picture of RDS is very similar to the symptoms of streptococcal pneumonia, as well as the use of a ventilator in treatment, the use of which is often accompanied by infection.
Use of vitamins. Vitamin E is prescribed to reduce the risk of developing retinopathy (vascular disorders in the retina). Administration of vitamin A helps prevent the development of necrotizing enterocolitis. The administration of riboxin and inositol helps reduce the risk of bronchopulmonary dysplasia.

Placing the baby in an incubator and carefully caring for him is one of the basic principles of nursing premature babies.

Prevention

Women who are at risk of miscarriage at 28-34 weeks are prescribed hormone therapy (usually dexamethasone or betamethasone according to the regimen). It is also necessary timely treatment existing chronic and infectious diseases in a pregnant woman.

If doctors offer to go on preservation, you should not refuse. After all, increasing the gestational age and preventing premature birth allows you to gain time and reduce the risk of respiratory distress syndrome at birth.

Forecast

In most cases, the prognosis is favorable, and gradual recovery is observed by 2-4 days of life. However, childbirth at a short gestational age, the birth of infants weighing less than 1000 g, complications due to accompanying pathologies(encephalopathy, sepsis) make the prognosis less rosy. In the absence of timely medical care or the presence of these factors, the child may die. The fatality rate is approximately 1%.

In view of this, a pregnant woman should take responsibility for bearing and giving birth to a child, not neglect examination, observation at the antenatal clinic and promptly receive treatment for infectious diseases.